Authors,Title,Year,Source title,Volume,Issue,Art. No.,Page start,Page end,Page count,Cited by,Link,Affiliations,Abstract,Author Keywords,Index Keywords,Molecular Sequence Numbers,Chemicals/CAS,Tradenames,Manufacturers,References,Correspondence Address,Editors,Sponsors,Publisher,Conference name,Conference date,Conference location,Conference code,ISSN,ISBN,CODEN,DOI,Language of Original Document,Abbreviated Source Title,Document Type,Source "Gao M., Wang M., Zheng Q.-H.","Synthesis of carbon-11 labeled 1-(3,4-dimethoxybenzyl)-2,2-dimethyl-1,2,3,4-tetrahydroisoquinolinium derivatives as new potential PET SKCa channel imaging agents",2008,"Applied Radiation and Isotopes",66,2,,194,202,,,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-37149043294&partnerID=40&rel=R8.0.0","Department of Radiology, Indiana University School of Medicine, 1345 West 16th Street, L-3 Room 202, Indianapolis, IN 46202, United States","Small conductance Ca2+-activated K+ (SKCa) channels play an important role in many functions such as neuronal communication and behavioral plasticity, secretion, and cell proliferation. SKCa channel modulation is associated with various brain, heart, and cancer diseases. N-methyl-laudanosine and its structurally related derivatives, substituted 1-(3,4-dimethoxybenzyl)-2,2-dimethyl-1,2,3,4-tetrahydroisoquinoliniums, are reversible and selective SKCa channel blockers. Carbon-11 labeled N-methyl-laudanosine and its tetrahydroisoquinolinium derivatives may serve as new probes for positron emission tomography (PET) to image SKCa channels in the brain, heart, and cancer. The key intermediates, substituted isoquinolines (3a-c), were synthesized using a modification of the Pomeranz-Fritsch procedure. The precursors, substituted 1-(3,4-dimethoxybenzyl)-2-methyl-1,2,3,4-tetrahydroisoquinolines (8a-c), and their corresponding reference standards, substituted 1-(3,4-dimethoxybenzyl)-2,2-dimethyl-1,2,3,4-tetrahydroisoquinoliniums (9a-c), were synthesized from compounds 3a-c with 3,4-dimethoxybenzyl chloride (2) in multiple steps with moderate to excellent chemical yields. The precursor 6,7-dimethoxy-1-(3,4-dimethoxybenzyl)-2-methyl-1,2,3,4-tetrahydroisoquinoline (10) was commercially available, and the methylation of compound 10 with methyl iodide provided N-methyl-laudanosine (11). The target quaternary ammonium tracers, carbon-11 labeled 1-(3,4-dimethoxybenzyl)-2,2-dimethyl-1,2,3,4-tetrahydroisoquinoliniums ([11C]9a-c and [11C]11), were prepared by N-[11C]methylation of the tertiary amine precursors (8a-c and 10) with [11C]methyl triflate and isolated by a simplified solid-phase extraction (SPE) purification using a SiO2 or cation-exchange CM Sep-Pak cartridge in 40-65% radiochemical yields. © 2007 Elsevier Ltd. All rights reserved.","1-(3,4-Dimethoxybenzyl)-2,2-dimethyl-1,2,3,4-tetrahydroisoquinoliniums; Carbon-11; Imaging; N-methyl-laudanosine; Positron emission tomography (PET); Small conductance Ca2+-activated K+ (SKCa) channels",,,,,,"Doorty, K.B., Bevan, S., Wadsworth, J.D.F., Strong, P.N., A novel small conductance Ca2+-activated K+ channel blocker from oxyuranus scutellatus taipan venom (1997) J. Biol. Chem., 272, pp. 19925-19930; Gao, M., Miller, M.A., DeGrado, T.M., Mock, B.H., Lopshire, J.C., Rosenberger, J.G., Dusa, C., Zheng, Q.-H., Evaluation of [11C]hemicholinium-15 and [18F]hemicholinium-15 as new potential PET tracers for the high-affinity choline uptake system in the heart (2007) Bioorg. Med. Chem., 15, pp. 1289-1297; Graulich, A., Scuvee-Moreau, J., Alleva, L., Lamy, C., Waroux, O., Seutin, V., Liegeois, J.-F., Synthesis and radioligand binding studies of methoxylated 1,2,3,4-tetrahydroisoquinolinium derivatives as ligands of the apamin-sensitive Ca2+-activated K+ channels (2006) J. Med. Chem., 49, pp. 7208-7214; Graulich, A., Scuvee-Moreau, J., Seutin, V., Liegeois, J.-F., Synthesis and radioligand binding studies of C-5- and C-8-substituted 1-(3,4-dimethoxybenzyl)-2,2-dimethyl-1,2,3,4-tetrahydroisoquinoliniums as SK channel blockers related to N-methyl-laudanosine and N-methyl-noscapine (2005) J. Med. Chem., 48, pp. 4972-4982; Hendrickson, J.B., Rodriguez, C., An efficient synthesis of substituted isoquinolines (1983) J. Org. Chem., 48, pp. 3344-3346; Jewett, D.M., A simple synthesis of [11C]methyl triflate (1992) Appl. Radiat. Isot., 43, pp. 1383-1385; Mock, B.H., Mulholland, G.K., Vavrek, M.T., Convenient gas phase bromination of [11C]methane and production of [11C]methyl triflate (1999) Nucl. Med. Biol., 26, pp. 467-471; Popp, F.D., Developments in the chemistry of Reissert compounds (1968-1978) (1979) Adv. Heterocycl. Chem., 24, pp. 187-214; Snabaitis, A.K., D'Mello, R., Dashnyam, S., Avkiran, M., A novel role for protein phosphatase 2A in receptor-mediated regulation of the cardiac sarcolemmal Na+/H+ exchanger NHE1 (2006) J. Biol. Chem., 281, pp. 20252-20262; Tuteja, D., Xu, D., Timofeyev, V., Lu, L., Sharma, D., Zhang, Z., Xu, Y., Chiamvimonvat, N., Differential expression of small-conductance Ca2+-activated K+ channels SK1, SK2, and SK3 in mouse and ventricular myocytes (2005) Am. J. Physiol. Heart Circ. Physiol., 289, pp. H2714-H2723; Wang, J.-Q., Miller, M.A., Fei, X., Stone, K.L., Lopshire, J.C., Groh, W.J., Zipes, D.P., Zheng, Q.-H., Facile synthesis and initial PET imaging of novel potential heart acetylcholinesterase imaging agents [11C]pyridostigmine and its analogs (2004) Nucl. Med. Biol., 31, pp. 957-964; Wang, M., Lacy, G., Gao, M., Miller, K.D., Sledge, G.W., Zheng, Q.-H., Synthesis of carbon-11 labeled sulfonanilide analogues as new potential PET agents for imaging of aromatase in breast cancer (2007) Bioorg. Med. Chem. Lett., 17, pp. 332-336; Weaver, A.K., Bomben, V.C., Sontheimer, H., Expression and function of calcium-activated potassium channels in human glioma cells (2006) Glia, 54, pp. 223-233; Zheng, Q.-H., Mock, B.H., Purification of carbon-11 PET radiotracers from unlabeled precursors by preparative HPLC and SPE (2005) Biomed. Chromatogr., 19, pp. 671-676","Zheng, Q.-H.; Department of Radiology; Indiana University School of Medicine; 1345 West 16th Street, L-3 Room 202 Indianapolis, IN 46202, United States; email: qzheng@iupui.edu",,,,,,,,09698043,,ARISE,10.1016/j.apradiso.2007.08.011,"English","Applied Radiation and Isotopes",Article,Scopus "Forquer J.A., Harkenrider M., Fakiris A.J., Timmerman R.D., Cavaliere R., Henderson M.A., Lo S.S.","Brain metastasis from non-seminomatous germ cell tumor of the testis",2007,"Expert Review of Anticancer Therapy",7,11,,1567,1580,,,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-37449009309&partnerID=40&rel=R8.0.0","Indiana University Medical Center, Department of Radiation Oncology, 535 Barnhill Drive, Indianapolis, IN 46202, United States; Indiana University Medical Center, Department of Radiation Oncology, 35 Barnhill Drive, Indianapolis, IN 46202, United States; University of Texas Southwestern, Department of Radiation Oncology, 5801 Forest Park Road, Dallas, TX 75390-9183, United States; Ohio State University, Department of Neurology, Division of Neuro-Oncology, 1654 Upham Drive, Columbus, OH 43210, United States; Department of Radiation Medicine, Ohio State University Medical Medicine, Arthur G James Cancer Hospital, 300 West 10th Avenue, Columbus, OH 43210, United States","Brain metastasis occurs rarely in patients with testicular cancer in the modern era where cisplatin-based chemotherapy regimens are used. The occurrence of brain metastasis can be synchronous or metachronous (with or without concurrent systemic disease). Long-term survival can be achieved in some patients. The vast majority of testicular cancer cases with brain metastasis reported in the literature involve nonseminomatous germ cell tumor and this subtype will be the focus of this review. This article reviews the literature of the diagnosis and management of brain metastasis from nonseminomatous germ cell tumor of the testis. © 2007 Future Drugs Ltd.","Brain metastasis; Germ cell tumor; Nonseminomatous; Testis",,,,,,"Huyghe, E., Matsuda, T., Thonneau, P., Increasing incidence of testicular cancer worldwide: A review (2003) J. 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Phys, 63, pp. 37-46; Nicolato, A., Ria, A., Foroni, R., Gamma knife radiosurgery in brain metastases from testicular tumors (2005) Med Oncol, 22, pp. 45-56; Kulkarni, R.P., Reynolds, K.W., Newlands, E.S., Cytoreductive surgery in disseminated non-seminomatous germ cell tumours of testis (1991) Br. J. Surg, 78, pp. 226-229; Crabb, S.J., McKendrick, J.J., Mead, G.M., Brain as sanctuary site of relapse in germ cell cancer patients previously treated with chemotherapy (2002) Clin. Oncol. (R. Coll. Radiol.), 14, pp. 287-293; Cohn, D.A., Stuart-Harris, R., Isolated central nervous system relapse of non-seminomatous germ cell tumour of the testis. A case report and review of the literature (2001) Oncology, 6 l, pp. 184-188; Perry, J.J., Jelinek, J.S., Isolated central nervous system relapse of testicular cancer (1992) Med. Pediatr. Oncol, 20, pp. 68-70; James, P.P., Mead, G.M., Sanctuary site relapse in chemotherapy-treated testicular cancer (1992) Ann. Oncol, 3, pp. 41-43; Stolinsky, D.C., Prolonged survival after cerebral metastasis of testicular carcinoma (1981) Cancer, 47, pp. 978-981; Andrews, D.W., Scott, C.B., Sperduto, P.W., Whole brain radiation therapy with or without stereotactic radiosurgery boost for patients with one to three brain metastases: Phase III results of the RTOG 9508 randornised trial (2004) Lancet, 363, pp. 1665-1672; Budach, V., Schutz, U., Higi, M., Niederle, N., Radiotherapy in case of intracerebral formation of metastases of non-seminomatous testicle tumors (author's transl.) (1981) Strahlentherapie, 157, pp. 450-454; Logothetis, C.J., Samuels, M.L., Trindade, A., The management of brain metastases in germ cell tumors (1982) Cancer, 49, pp. 12-18; Schmoll, H.J., Souchon, R., Krege, S., European consensus on diagnosis and treatment of germ cell cancer: A report of the European Germ Cell Cancer Consensus Group (EGCCCG) (2004) Ann. Oncol, 15 (9), pp. 1377-1399; Azar, J.M., Schneider, B.P., Einhorn, L.H., Is the blood-brain barrier relevant in metastatic germ cell tumor? (2007) Int. J. Radiat. Oncol. Biol. Phys, 69 (1), pp. 163-166","Lo, S.S.; Ohio State University Medical Center; Arthur G. James Center Hospital; 300 West 10th Avenue Columbus, OH 43210, United States; email: simon.lo@osumc.edu",,,,,,,,14737140,,ERATB,10.1586/14737140.7.11.1567,"English","Expert Review of Anticancer Therapy",Review,Scopus "Kwee S.A., DeGrado T.R., Talbot J.N., Gutman F., Coel M.N.","Cancer Imaging With Fluorine-18-Labeled Choline Derivatives",2007,"Seminars in Nuclear Medicine",37,6,,420,428,,,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-34848926866&partnerID=40&rel=R8.0.0","University of Hawaii John A. Burns School of Medicine, Honolulu, HI, United States; Hamamatsu/Queen's PET Imaging Center, The Queen's Medical Center, Honolulu, HI, United States; Department of Radiology, Indiana University School of Medicine, Indianapolis, IN, United States; Department of Nuclear Medicine, Hôpital Tenon, AP-HP, Paris, France","The choline transporter and choline kinase enzyme frequently are overexpressed in malignancy. Therefore, positron-emitter-labeled compounds derived from choline have the potential to serve as oncologic probes for positron emission tomography. The fluorine-18 (18F)-labeled choline derivative fluorocholine (FCH) in particular has demonstrated potential utility for imaging of a variety of neoplasms, including those of the breast, prostate, liver, and brain. The pharmacokinetics of FCH and other choline tracers allow for whole-body imaging within minutes of injection while still achieving high tumor-to-background contrast in most organs, including the brain. These features, along with the possibility of imaging malignancies that have proved elusive with the use of 18F-fluorodeoxyglucose positron emission tomography support further clinical investigations of 18F-labeled choline tracers. © 2007 Elsevier Inc. 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Burns School of Medicine Honolulu, HI, United States; email: skwee@queens.org",,,,,,,,00012998,,SMNMA,10.1053/j.semnuclmed.2007.07.003,"English","Seminars in Nuclear Medicine",Review,Scopus "Zhong J., Yao W., Lee W.","Cesium chloride protects cerebellar granule neurons from apoptosis induced by low potassium",2007,"International Journal of Developmental Neuroscience",25,6,,359,365,,,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-35748966721&partnerID=40&rel=R8.0.0","Departments of Pediatrics, Anatomy and Cell Biology, Indiana University School of Medicine, Riley Hospital for Children, Indianapolis, IN, United States","Neuronal apoptosis plays a critical role in the pathogenesis of neurodegenerative disorders, and neuroprotective agents targeting apoptotic signaling could have therapeutic use. Here we report that cesium chloride, an alternative medicine in treating radiological poison and cancer, has neuroprotective actions. Serum and potassium deprivation induced cerebellar granule neurons to undergo apoptosis, which correlated with the activation of caspase-3. Cesium prevented both the activation of caspase-3 and neuronal apoptosis in a dose-dependent manner. Cesium at 8 mM increased the survival of neurons from 45 ± 3% to 91 ± 5% of control. Cesium's neuroprotection was not mediated by PI3/Akt or MAPK signaling pathways, since it was unable to activate either Akt or MAPK by phosphorylation. In addition, specific inhibitors of PI3 kinase and MAP kinase did not block cesium's neuroprotective effects. On the other hand, cesium inactivated GSK3β by phosphorylation of serine-9 and GSK3β-specific inhibitor SB415286 prevented neuronal apoptosis. These data indicate that cesium's neuroprotection is likely via inactivating GSK3β. Furthermore, cesium also prevented H2O2-induced neuronal death (increased the survival of neurons from 72 ± 4% to 89 ± 3% of control). Given its relative safety and good penetration of the brain blood barrier, our findings support the potential therapeutic use of cesium in neurodegenerative diseases. © 2007 ISDN.","Apoptosis; Cesium; GSK3β; Lithium; Neuron",,,,,,"Ankarcrona, M., Dypbukt, J.M., Bonfoco, E., Zhivotovsky, B., Orrenius, S., Lipton, S.A., Nicotera, P., Glutamate-induced neuronal death: a succession of necrosis or apoptosis depending on mitochondrial function (1995) Neuron, 15, pp. 961-973; Barnham, K.J., Masters, C.L., Bush, A.I., Neurodegenerative diseases and oxidative stress (2004) Nat. Rev. Drug Discov., 3, pp. 205-214; Bhat, R.V., Budd haeberlein, S.L., Avila, J., Glycogen synthase kinase 3: a drug target for CNS therapies (2004) J. Neurochem., 89, pp. 1313-1317; Borson, S., Leverenz, J.B., Basic mechanisms in neurodegenerative disease: implications for behavioral pathogenesis and treatment (1996) Semin. Clin. 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Neurosci., 17, pp. 1548-1560; D'Mello, S.R., Galli, C., Ciotti, T., Calissano, P., Induction of apoptosis in cerebellar granule neurons by low potassium: inhibition of death by insulin-like growth factor I and camp (1993) Proc. Natl. Acad. Sci. USA, 90, pp. 10989-10993; Datta, S.R., Brunet, A., Greenberg, M.E., Cellular survival: a play in three Akts (1999) Genes Dev., 13, pp. 2905-2927; Doble, B.W., Woodgett, J.R., GSK-3: tricks of the trade for a multi-tasking kinase (2003) J. Cell Sci., 116, pp. 1175-1186; Eldar-Finkelman, H., Glycogen synthase kinase 3: an emerging therapeutic target (2002) Trends Mol. Med., 8, pp. 126-132; Jope, R.S., Lithium and GSK-3: one inhibitor, two inhibitory actions, multiple outcomes (2003) Trends Pharmacol. Sci., 24, pp. 441-443; Journot, L., Villalba, M., Bockaert, J., PACAP-38 protects cerebellar granule cells from apoptosis (1998) Ann. N Y Acad. 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Commun., 350, pp. 905-910","Zhong, J.; Departments of Pediatrics, Anatomy and Cell Biology; Indiana University School of Medicine; Riley Hospital for Children Indianapolis, IN, United States; email: jizhong@iupui.edu",,,,,,,,07365748,,IJDND,10.1016/j.ijdevneu.2007.07.003,"English","International Journal of Developmental Neuroscience",Article,Scopus "Azar J.M., Schneider B.P., Einhorn L.H.","Is the Blood-Brain Barrier Relevant in Metastatic Germ Cell Tumor?",2007,"International Journal of Radiation Oncology Biology Physics",69,1,,163,166,,1,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-34547838168&partnerID=40&rel=R8.0.0","Department of Medicine, Division of Hematology and Oncology, Indiana University, Indianapolis, IN, United States; Walther Cancer Institute, Indianapolis, IN, United States","Purpose: Germ cell tumors are uniquely chemosensitive and curable, even with advanced metastatic disease. Central nervous system recurrence can terminate a complete remission in other chemosensitive tumors, such as small cell lung cancer, because of the blood-brain barrier (BBB). We propose to document that the BBB is also relevant in germ cell tumors despite their dramatic chemosensitivity. Methods and Materials: We present five cases illustrating the concept of the BBB in patients with metastatic testicular cancer treated with chemotherapy. Results: In our large series of patients with metastatic testicular cancer treated with chemotherapy, we identified 5 unique patients. These patients were rendered free of disease only to experience relapse in the brain alone. This included 1 patient who initially had good-risk metastatic disease by means of the International Germ Cell Collaborative Group staging system at the onset of chemotherapy. Conclusions: The BBB is relevant in patients with metastatic testicular cancer. © 2007 Elsevier Inc. All rights reserved.","Blood-brain barrier; Brain metastasis; Germ cell tumor; Testicular cancer",,,,,,"Einhorn, L.H., Curing metastatic testicular cancer (2002) Proc Natl Acad Sci U S A, 99, pp. 4592-4595; Spears, W., Morphis II, J., Lester, S., Brain metastases and testicular tumors: Long-term survival (1991) Int J Radiat Oncol Biol Phys, 22, pp. 17-22; Bokemeyer, C., Nowak, P., Haupt, A., Treatment of brain metastases in patients with testicular cancer (1997) J Clin Oncol, 15, pp. 1449-1454; Kollmannsberger, C., Nichols, C., Bamberg, M., First-line high dose chemotherapy ± radiation therapy in patients with metastatic germ-cell cancer and brain metastases (2000) Ann Oncol, 11, pp. 553-559; Nicolato, A., Ria, A., Foroni, R., Gamma knife radiosurgery in brain metastases from testicular tumors (2005) Med Oncol, 22, pp. 45-56; Bhatia, S., Abonour, R., Porcu, P., High-dose chemotherapy as initial salvage chemotherapy in patients with relapsed testicular cancer (2000) J Clin Oncol, 18, pp. 3346-3351; Cooper, M., Einhorn, L.H., Maintenance chemotherapy with daily oral etoposide following salvage therapy in patients with germ cell tumors (1995) J Clin Oncol, 13, pp. 1167-1169; Hinton, S., Catalano, P., Einhorn, L.H., Phase II study of paclitaxel plus gemcitabine in refractory germ cell tumors (E9897): A trial of the Eastern Cooperative Oncology Group (2002) J Clin Oncol, 1, pp. 1859-1863; Cohn, D., Stuart-Harris, R., Isolated central nervous system relapse of non-seminomatous germ cell tumour of the testis (2001) Oncology, 61, pp. 184-188; Mahalati, K., Bilen, C., Ozen, H., The management of brain metastasis in non-seminomatous germ cell tumours (1999) Brit J Urol Int, 83, pp. 457-461; Salvati, M., Cervoni, L., Vitale, A., Solitary cerebral metastasis from tumor of the testis: Some observations about treatment in two cases (1997) Ital J Neurol Sci, 18, pp. 173-175; Raina, V., Singh, S., Kamble, N., Brain metastasis as the site of relapse in germ cell tumor of testis (1993) Cancer, 72, pp. 2182-2185; James, P., Mead, G., Sanctuary site relapse in chemotherapy-treated testicular cancer (1992) Ann Oncol, 3, pp. 41-43; Perry, J., Jelinek, J., Isolated central nervous system relapse of testicular cancer (1992) Med Pediatr Oncol, 20, pp. 68-70; Lester, S., Morphis, J., Hornback, N., Brain metastases and testicular tumors: Need for aggressive therapy (1984) J Clin Oncol, 2, pp. 1397-1403; Logothetis, C., Samuels, M., Trindade, A., The management of brain metastases in germ cell tumors (1982) Cancer, 49, pp. 12-18; Bart, J., Groen, H., Hendrikse, N., The blood-brain barrier and oncology: New insights into function and modulation (2000) Cancer Treat Rev, 26, pp. 449-462; Warren, K., Gervais, A., Aikin, A., Pharmacokinetics of carboplatin administered with lobradimil to pediatric patients with brain tumors (2004) Cancer Chemother Pharmacol, 54, pp. 206-212; Redina, A., Demeule, M., Laplante, A., Multidrug resistance in brain tumors: Roles of the blood-brain barrier (2001) Cancer Metastasis Rev, 20, pp. 13-25; Mathews, V., Broome, D., Smith, R., Neuroimaging of disseminated germ cell neoplasms (1990) AJNR Am J Neuroradiol, 11, pp. 319-324","Azar, J.M.; Department of Medicine; Division of Hematology and Oncology; Indiana University Indianapolis, IN, United States; email: jazar@iupui.edu",,,,,,,,03603016,,IOBPD,10.1016/j.ijrobp.2007.02.042,"English","International Journal of Radiation Oncology Biology Physics",Article,Scopus "Berk L., Berkey B., Rich T., Hrushesky W., Blask D., Gallagher M., Kudrimoti M., McGarry R.C., Suh J., Mehta M.","Randomized Phase II Trial of High-Dose Melatonin and Radiation Therapy for RPA Class 2 Patients With Brain Metastases (RTOG 0119)",2007,"International Journal of Radiation Oncology Biology Physics",68,3,,852,857,,1,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-34249326606&partnerID=40&rel=R8.0.0","Department of Radiation Oncology, H. Lee Moffitt Cancer Center, University of South Florida, Tampa, FL, United States; Department of Statistics, Radiation Therapy Oncology Group, Philadelphia, PA, United States; Department of Radiation Oncology, University of Virginia, Charlottesville, VA, United States; Laboratory of Experimental Neuroendocrinology/Oncology, W. J. B. Dorn Veterans Administration Medical Center, University of South Carolina Arnold School of Public Health, Columbia, SC, United States; Medical Chronobiology Laboratory, S. C. Bassett Research Institute, Cooperstown, NY, United States; Scranton Radiation Medicine Association, Scranton, PA, United States; Department of Radiation Oncology, University of Kentucky, Lexington, KY, United States; Department of Radiation Oncology, Indiana University, Indianapolis, IN, United States; Department of Radiation Oncology, Cleveland Clinic, Cleveland, OH, United States; Department of Radiation Oncology, University of Wisconsin, Madison, WI, United States","Purpose: To determine if high-dose melatonin for Radiation Therapy Oncology Group (RTOG) recursive partitioning analysis (RPA) Class 2 patients with brain metastases improved survival over historical controls, and to determine if the time of day melatonin was given affected its toxicity or efficacy. RTOG 0119 was a phase II randomized trial for this group of patients. Methods and Materials: RTOG RPA Class 2 patients with brain metastases were randomized to 20 mg of melatonin, given either in the morning (8-9 am) or in the evening (8-9 pm). All patients received radiation therapy (30 Gy in 10 fractions) in the afternoon. Melatonin was continued until neurologic deterioration or death. The primary endpoint was overall survival time. Neurologic deterioration, as reflected by the Mini-Mental Status Examination, was also measured. Results: Neither of the randomized groups had survival distributions that differed significantly from the historic controls of patients treated with whole-brain radiotherapy. The median survivals of the morning and evening melatonin treatments were 3.4 and 2.8 months, while the RTOG historical control survival was 4.1 months. Conclusions: High-dose melatonin did not show any beneficial effect in this group of patients. © 2007 Elsevier Inc. All rights reserved.","Brain metastases; Chronobiology; Melatonin; Randomized trial; Survival","Brain; Neurology; Oncology; Toxicity; Brain metastases; Chronobiology; Melatonin; Randomized trials; Radiotherapy; melatonin; adult; aged; allergy; analytic method; article; blood toxicity; bone marrow toxicity; brain metastasis; cancer chemotherapy; cancer radiotherapy; cancer survival; chronobiology; clinical article; clinical trial; controlled clinical trial; controlled study; drug megadose; drug response; eye toxicity; fatigue; febrile neutropenia; female; gastrointestinal symptom; headache; hearing disorder; human; infection; male; mini mental state examination; musculoskeletal disease; nausea; neurotoxicity; outcome assessment; pain; phase 2 clinical trial; priority journal; randomized controlled trial; recursive partitioning analysis; skin toxicity; survival rate; survival time; visual disorder; vomiting; Aged; Aged, 80 and over; Antineoplastic Agents; Brain Neoplasms; Female; Humans; Melatonin; Middle Aged; Prevalence; Radiotherapy, Adjuvant; Risk Assessment; Risk Factors; Survival Analysis; Survival Rate; Treatment Outcome; United States",,"melatonin, 73-31-4; Antineoplastic Agents; Melatonin, 73-31-4",,"Cardiovascular Research, United States","Reiter, R.J., Pineal melatonin: Cell biology of its synthesis and of its physiological interactions (1991) Endocr Rev, 12, pp. 151-180; Reiter, R.J., Melatonin: Multi-faceted messenger to the masses (1994) Lab Med, 24, pp. 436-441; Blask, D.E., Sauer, L.A., Dauchy, R.T., Melatonin as a chronobiotic/anticancer agent: Cellular, biochemical, and molecular mechanisms of action and their implications for circadian-based cancer therapy (2002) Curr Top Med Chem, 2, pp. 113-132; Tan, D.X., Manchester, L.C., Hardeland, R., Melatonin: A hormone, a tissue factor, an autocoid, a paracoid, and an antioxidant vitamin (2003) J Pineal Res, 34, pp. 75-78; Di, W.L., Kadva, A., Johnston, A., Silman, R., Variable bioavailability of oral melatonin (1997) N Engl J Med, 336, pp. 1028-1029; Dollins, A.B., Zhdanova, I.V., Wurtman, R.J., Lynch, H.J., Deng, M.H., Effect of inducing nocturnal serum melatonin concentrations in daytime on sleep, mood, body temperature, and performance (1994) Proc Natl Acad Sci USA, 91, pp. 1824-1828; DeMuro, R.L., Nafziger, A.N., Blask, D.E., Menhinick, A.M., Bertino Jr., J.S., The absolute bioavailability of oral melatonin (0091-2700) (2000) J Clin Pharmacol, 42, pp. 781-784; Akagi, T., Ushinohama, K., Ikesue, S., Chronopharmacology of melatonin in mice to maximize the antitumor effect and minimize the rhythm disturbance effect (2004) J Pharmacol Exp Ther, 308, pp. 378-384; Bartsch, H., Bartsch, C., Effect of melatonin on experimental tumors under different photoperiods and times of administration (1981) J Neural Transm, 52, pp. 269-279; Blask, D.E., Barthold, H.J., Dauchy, R.T., Melatonin radiosensitizes tumors and radioprotects normal tissues: Time-of-day dependency (2000) Am Assoc Cancer Res, , Abstract 338; Lissoni, P., Barni, S., Ardizzoia, A., Tancini, G., Conti, A., Maestroni, G., A randomized study with the pineal hormone melatonin versus supportive care alone in patients with brain metastases due to solid neoplasms (1994) Cancer, 73, pp. 699-701; Lissoni, P., Meregalli, S., Nosetto, L., Increased survival time in brain glioblastomas by a radioneuroendocrine strategy with radiotherapy plus melatonin compared to radiotherapy alone (1996) Oncology, 53, pp. 43-46; Haus, E., Chronobiology of the mammalian response to ionizing radiation. Potential applications in oncology (2002) Chronobiol Int, 19, pp. 77-100; Rich, T.A., Shelton III, C.H., Kirichenko, A., Straume, M., Chronomodulated chemotherapy and irradiation: An idea whose time has come? (2002) Chronobiol Int, 19, pp. 191-205; Dixon, D.O., Simon, R., Sample size considerations for studies comparing survival curves using historical controls (1988) J Clin Epidemiol, 41, pp. 1209-1213; Crum, R.M., Anthony, J.C., Bassett, S.S., Folstein, M.F., Population-based norms for the Mini-Mental State Examination by age and educational level (1993) J Am Med Assoc, 269, pp. 2386-2391; Tangalos, E.G., Smith, G.E., Ivnik, R.J., The Mini-Mental State Examination in general medical practice: Clinical utility and acceptance (1996) Mayo Clin Proc, 71, pp. 829-837; Barni, S., Lissoni, P., Cazzaniga, M., A randomized study of low-dose subcutaneous interleukin-2 plus melatonin versus supportive care alone in metastatic colorectal cancer patients progressing under 5-fluorouracil and folates (1995) Oncology, 52, pp. 243-245; Brackowski, R., Zubelewicz, B., Romanowski, W., Preliminary study on modulation of the biological effects of tumor necrosis factor-alpha in advanced cancer patients by the pineal hormone melatonin (1994) J Biol Regul Homeost Agents, 8, pp. 77-880; Cerea, G., Vaghi, M., Ardizzoia, A., Biomodulation of cancer chemotherapy for metastatic colorectal cancer: A randomized study of weekly low-dose irinotecan alone versus irinotecan plus the oncostatic pineal hormone melatonin in metastatic colorectal cancer patients progressing on 5-fluorouracil-containing combinations (2003) Anticancer Res, 23, pp. 1951-1954; Lissoni, P., Is there a role for melatonin in supportive care? (2002) Support Care Cancer, 10, pp. 110-116; Lissoni, P., Barni, S., Ardizzoia, A., Randomized study with the pineal hormone melatonin versus supportive care alone in advanced nonsmall cell lung cancer resistant to a first-line chemotherapy containing cisplatin (1992) Oncology, 49, pp. 336-339; Lissoni, P., Barni, S., Fossati, V., A randomized study of neuroimmunotherapy with low-dose subcutaneous interleukin-2 plus melatonin compared to supportive care alone in patients with untreatable metastatic solid tumour (1995) Support Care Cancer, 3, pp. 194-197; Lissoni, P., Barni, S., Mandala, M., Decreased toxicity and increased efficacy of cancer chemotherapy using the pineal hormone melatonin in metastatic solid tumour patients with poor clinical status (1999) Eur J Cancer, 35, pp. 1688-1692; Lissoni, P., Barni, S., Tancini, G., A randomised study with subcutaneous low-dose interleukin 2 alone vs. interleukin 2 plus the pineal neurohormone melatonin in advanced solid neoplasms other than renal cancer and melanoma (1994) Br J Cancer, 69, pp. 196-199; Lissoni, P., Brivio, F., Barni, S., Neuroimmunotherapy of human cancer with interleukin-2 and the neurohormone melatonin: Its efficacy in preventing hypotension (1990) Anticancer Res, 10, pp. 1759-1761; Lissoni, P., Brivio, O., Brivio, F., Adjuvant therapy with the pineal hormone melatonin in patients with lymph node relapse due to malignant melanoma (1996) J Pineal Res, 21, pp. 239-242; Lissoni, P., Mandala, M., Brivio, F., Abrogation of the negative influence of opioids on IL-2 immunotherapy of renal cell cancer by melatonin (2000) Eur Urol, 38, pp. 115-118; Lissoni, P., Meregalli, S., Fossati, V., A randomized study of immunotherapy with low-dose subcutaneous interleukin-2 plus melatonin vs. chemotherapy with cisplatin and etoposide as first-line therapy for advanced non-small cell lung cancer (1994) Tumori, 80, pp. 464-467; Lissoni, P., Paolorossi, F., Ardizzoia, A., A randomized study of chemotherapy with cisplatin plus etoposide versus chemoendocrine therapy with cisplatin, etoposide and the pineal hormone melatonin as a first-line treatment of advanced non-small cell lung cancer patients in a poor clinical state (1997) J Pineal Res, 23, pp. 15-19; Lissoni, P., Pittalis, S., Ardizzoia, A., Prevention of cytokine-induced hypotension in cancer patients by the pineal hormone melatonin (1996) Support Care Cancer, pp. 313-316; Lissoni, P., Tancini, G., Barni, S., Treatment of cancer chemotherapy-induced toxicity with the pineal hormone melatonin (1997) Support Care Cancer, 5, pp. 126-129; Ghielmini, M., Pagani, O., de Jong, J., Double-blind randomized study on the myeloprotective effect of melatonin in combination with carboplatin and etoposide in advanced lung cancer (1999) Br J Cancer, 80, pp. 1058-1061; Sarma, A., Rodriguez, M.A., Cabanillas, F., A randomized trial of CHOP chemotherapy with or without melatonin in patients with favorable prognosis large B-cell lymphoma (2004) J Clin Oncol, 22, p. 8066; Di, W.-L., Kadva, A., Johnston, A., Silman, R., Variable bioavailability of oral melatonin (1997) N Engl J Med, 336, pp. 1028-1029; Meyers, C.A., Wefel, J.S., The use of the Mini-Mental State Examination to assess cognitive functioning in cancer trials: No ifs, ands, buts, or sensitivity (2003) J Clin Oncol, 21, pp. 3557-3558; Murray, K.J., Scott, C., Zachariah, B., Importance of the Mini-Mental Status Examination in the treatment of patients with brain metastases: A report from the Radiation Therapy Oncology Group protocol 91-04 (2000) Int J Radiat Oncol Biol Phys, 48, pp. 59-64","Berk, L.; Department of Radiation Oncology; H. Lee Moffitt Cancer Center; University of South Florida Tampa, FL, United States; email: Berklb@moffitt.usf.edu",,,,,,,,03603016,,IOBPD,10.1016/j.ijrobp.2007.01.012,"English","International Journal of Radiation Oncology Biology Physics",Article,Scopus "Zheng Q.-H., Gao M., Mock B.H., Wang S., Hara T., Nazih R., Miller M.A., Receveur T.J., Lopshire J.C., Groh W.J., Zipes D.P., Hutchins G.D., DeGrado T.R.","Synthesis and biodistribution of new radiolabeled high-affinity choline transporter inhibitors [11C]hemicholinium-3 and [18F]hemicholinium-3",2007,"Bioorganic and Medicinal Chemistry Letters",17,8,,2220,2224,,4,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-33947702669&partnerID=40&rel=R8.0.0","Department of Radiology, Indiana University School of Medicine, Indianapolis, IN 46202, United States; Krannert Institute of Cardiology, Indiana University School of Medicine, Indianapolis, IN 46202, United States","The high-affinity choline transporter (CHT1) system is an attractive target for the development of positron emission tomography (PET) biomarkers to probe brain, cardiac, and cancer diseases. An efficient and convenient synthesis of new radiolabeled CHT1 inhibitors [11C]hemicholinium-3 and [18F]hemicholinium-3 by solid-phase extraction (SPE) technique using a cation-exchange CM Sep-Pak cartridge has been well developed. The preliminary evaluation of both tracers through biodistribution studies in 9L-glioma rats has been performed, and the uptakes in the heart and tumor were observed, while very low brain uptake was seen. © 2007 Elsevier Ltd. All rights reserved.","[11C]hemicholinium-3 ([11C]HC-3); [18F]hemicholinium-3 ([18F]HC-3); Biodistribution; High-affinity choline transporter (CHT1); Positron emission tomography (PET)","choline derivative; hemicholinium 3 carbon 11; hemicholinium 3 fluorine 18; radiopharmaceutical agent; animal model; animal tissue; article; brain; cation exchange; choline uptake; drug distribution; drug synthesis; evaluation; glioma; heart; isotope labeling; nonhuman; rat; solid phase extraction; Animals; Brain; Carbon Radioisotopes; Cation Transport Proteins; Fluorine Radioisotopes; Glioma; Hemicholinium 3; Myocardium; Positron-Emission Tomography; Protein Binding; Radiopharmaceuticals; Rats; Rattus",,"Carbon Radioisotopes; Cation Transport Proteins; CHT1 protein, rat; Fluorine Radioisotopes; Hemicholinium 3, 312-45-8; Radiopharmaceuticals",,,"Smart, L.A., (1983) J. Med. Chem., 26, p. 104; Gilissen, C., de Groot, T., Bronfman, F., van Leuven, F., Verbruggen, A.M., Bormans, G.M., (2003) J. Nucl. 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Chromatogr., 19, p. 379; Barinaga, M., (1999) Science, 278, p. 1226; note","Zheng, Q.-H.; Department of Radiology; Indiana University School of Medicine Indianapolis, IN 46202, United States; email: qzheng@iupui.edu",,,,,,,,0960894X,,BMCLE,10.1016/j.bmcl.2007.01.105,"English","Bioorganic and Medicinal Chemistry Letters",Article,Scopus "Loder R.T., Huffman G., Toney E., Wurtz L.D., Fallon R.","Abnormal rib number in childhood malignancy: Implications for the scoliosis surgeon",2007,"Spine",32,8,,904,910,,1,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-34247189659&partnerID=40&rel=R8.0.0","James Whitcomb Riley Children's Hospital, Indianapolis, IN, United States; Department of Orthopaedic Surgery, Indiana University School of Medicine, Indianapolis, IN, United States; Department of Pediatrics, Division of Hematology/Oncology, Indiana University School of Medicine, Indianapolis, IN, United States; Department of Orthopaedic Surgery, Pennsylvania State University, Hershey, PA, United States; James Whitcomb Riley Hospital for Children, 702 Barnhill Drive, Indianapolis, IN 46202, United States","STUDY DESIGN. Retrospective review. OBJECTIVE. To determine if rib anomalies are present in pediatric malignancies in the United States. SUMMARY OF BACKGROUND DATA. Scoliosis surgeons view radiographs of the entire spine, counting the number of ribs. A European study noted that rib anomalies were more common in certain malignancies. We wished to determine if this is also true in the United States. If so, the potential for screening, early detection of malignancy, and a better understanding of tumor biology is possible. METHODS. A retrospective review of 218 children with malignancy and a control group of 200 children with polytrauma or suspected child abuse was performed. Chest radiographs were reviewed to determine the number of ribs, and the presence of rib anomalies. 24 ribs was considered normal, <24 or >24 was considered abnormal. P < 0.05 was considered significant. RESULTS. The average age was 6.8 ± 5.5 years and number of ribs was 23.8 ± 0.6. Rib number was normal in 86.8%. There were significant differences between the malignancy and control groups in age (control, 5.7 ± 5.1 years; malignancy, 7.8 ± 5.7 years, P = 0.00007), rib number (control, 23.9 ± 0.5; malignancy, 23.7 ± 0.7, P = 0.001), and normal/abnormal rib counts (control, 92% normal; malignancy, 82% normal, P = 0.003). In the malignant group, 50% had a lymphoproliferative malignancy, 33% a solid tumor, and 17.0% a neural tumor. Neural malignancies had a higher incidence of rib abnormalities compared with lymphoproliferative or solid malignancies (P = 0.01). Relative to the control group, those with a neural and lymphoproliferative malignancy were 6.23 (95% CI, 2.7-14.5) and 2.0 (95% CI, 1.0-4.1) times more likely to have an abnormal rib count. CONCLUSIONS. Homeobox genes, important in vertebral and rib sequencing, are abnormally expressed in many different malignancies. This association is a question of great interest. What is the potential for rib number being used as a predictor of childhood malignancy? Can these findings be expanded to adults? These questions require further research. The association noted in this study is interesting but should not yet be used to alarm parents regarding an increased risk of malignancy in their children. © 2007 Lippincott Williams & Wilkins, Inc.","Child; Malignancy; Rib number","article; cancer risk; childhood cancer; controlled study; female; human; lymphoproliferative disease; major clinical study; male; nerve tumor; priority journal; retrospective study; rib malformation; school child; solid tumor; spine radiography; thorax radiography; United States; Adolescent; Brain Neoplasms; Child; Child, Preschool; Female; Genes, Homeobox; Humans; Incidence; Infant; Leukemia, Lymphocytic, Acute; Male; Neoplasms; Neuroblastoma; Prevalence; Retrospective Studies; Ribs; Sarcoma; Sarcoma, Ewing's; Scoliosis; Soft Tissue Neoplasms; Wilms Tumor",,,,,"Anbazhagan, A., Raman, V., Homeobox genes: Molecular link between congenital anomalies and cancer (1997) Eur J Cancer, 33, pp. 635-637; Méhes, K., Signer, E., Plüss, H.J., Increased prevalence of minor anomalies in childhood malignancy (1985) Eur J Pediatr, 144, pp. 243-249; Schumacher, R., Mai, A., Gutjahr, P., Association of rib anomalies and malignancy in childhood (1992) Eur J Pediatr, 151, pp. 432-434; Danseco, E.R., Miller, T.R., Spicer, R.S., Incidence and cost of 1987-1994 childhood injuries: Demographic breakdowns (2000) Pediatrics, 105, pp. e27; Kilborn, T.N., Teh, J., Goodman, T.R., Paediatric manifestations of Langerhans cell histiocytosis: A review of the clinical and radiological findings (2003) Clin Radiol, 58, pp. 269-278; Egeler, R.M., D'Angio, G.J., Langerhans cell histiocytosis (1995) J Pediatr, 127, pp. 1-11; Herzog, K.M., Tubbs, R.R., Langerhans cell histiocytosis (1998) Adv Anat Pathol, 5, pp. 347-358; Arceci, R.J., The histiocytoses: The fall of the Tower of Babel (1999) Eur J Cancer, 35, pp. 747-769; Narod, S.A., Hawkins, M.M., Robertson, C.M., Congenital anomalies and childhood cancer in Great Britain (1997) Am J Hum Genet, 60, pp. 474-485; Burke, A.C., Nelson, C.E., Morgan, B.A., Hox genes and the evolution of vertebrate axial morphology (1995) Development, 121, pp. 333-346; Carapuco, M., Nóvoa, A., Bobola, N., Hox genes specify vertebral types in the presomitic mesoderm (2005) Genes Dev, 19, pp. 2116-2121; Wallin, J., Wilting, J., Koseki, H., The role of Pax-1 in axial skeleton development (1994) Development, 120, pp. 1109-1121; Johnson, D.R., O'Higgins, P.O., Is there a link between changes in the vertebral 'hox code' and the shape of vertebrae? 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Stuart, E.T., Kioussi, C., Aguzzi, A., Pax5 expression correlates with the increasing malignancy in human astrocytomas (1994) Clin Cancer Res, 1, pp. 207-214; Kozmik, K., Sure, U., Rüedi, D., Deregulated expression of PAX5 in medulloblastoma (1995) Proc Natl Acad Sci USA, 92, pp. 5709-5713; Geerts, D., Schilderink, N., Jorritsma, G., The role of the MEIS homeobox genes in neuroblastoma (2003) Cancer Lett, 197, pp. 87-92; Pelletier, J., Bruening, W., Li, F.P., WT1 mutations contribute to abnormal genital system development and hereditary Wilms' tumor (1991) Nature, 353, pp. 431-434; Dressler, G.R., Douglas, E.C., Pax-2 is a DNA-binding protein expressed in embryonic kidney and Wilm's tumor (1992) Proc Natl Acad Sci USA, 89, pp. 1179-1183; Poleev, A., Fickenscher, H., Mundlos, S., PAX8, a human paired box gene: Isolation and expression in developing thyroid, kidney, and Wilm's tumor (1992) Development, 116, pp. 611-623; Cillo, C., Barba, P., Freschi, G., HOX gene expression in normal and neoplastic human kidney (1992) Int J Cancer, 51, pp. 892-897; Tiberio, C., Barba, P., Magli, M.C., HOX gene expression in human smallcell lung cancers xenografted into nude mice (1994) Int J Cancer, 58, pp. 608-615; De Vita, G., Barba, P., Odartchenko, N., Expression of homeoboxcontaining genes in primary and metastatic colorectal cancer (1993) Eur J Cancer, 29, pp. 887-893; Vider, B.Z., Zimber, A., Hirsch, D., Human colorectal carcinogenesis is associated with deregulation of homebox gene expression (1997) Biochem Biophys Res Commun, 22, pp. 742-748","Loder, R.T.; James Whitcomb Riley Hospital for Children; 702 Barnhill Drive Indianapolis, IN 46202, United States; email: rloder@iupui.edu",,,,,,,,03622436,,SPIND,10.1097/01.brs.0000259834.28893.97,"English","Spine",Article,Scopus "Patel A.A., Gupta D., Seligson D., Hattab E.M., Balis U.J., Ulbright T.M., Kohane I.S., Berman J.J., Gilbertson J.R., Dry S., Schirripa O., Yu H., Becich M.J., Parwani A.V.","Availability and quality of paraffin blocks identified in pathology archives: A multi-institutional study by the Shared Pathology Informatics Network (SPIN)",2007,"BMC Cancer",7,, 37,,,,4,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-33847776571&partnerID=40&rel=R8.0.0","Department of Pathology, Center for Pathology Informatics, University of Pittsburgh, Pittsburgh, PA, United States; Department of Pathology, University of California, Los Angeles, CA, United States; Department of Pathology, Indiana University, Indianapolis, IN, United States; Department of Pathology, Harvard University, Boston, MA, United States; Cancer Diagnosis Program, National Cancer Institute, National Institutes of Health, Bethesda, MD, United States","Background: Shared Pathology Informatics Network (SPIN) is a tissue resource initiative that utilizes clinical reports of the vast amount of paraffin-embedded tissues routinely stored by medical centers. SPIN has an informatics component (sending tissue-related queries to multiple institutions via the internet) and a service component (providing histopathologically annotated tissue specimens for medical research). This paper examines if tissue blocks, identified by localized computer searches at participating institutions, can be retrieved in adequate quantity and quality to support medical researchers. Methods: Four centers evaluated pathology reports (1990-2005) for common and rare tumors to determine the percentage of cases where suitable tissue blocks with tumor were available. Each site generated a list of 100 common tumor cases (25 cases each of breast adenocarcinoma, colonic adenocarcinoma, lung squamous carcinoma, and prostate adenocarcinoma) and 100 rare tumor cases (25 cases each of adrenal cortical carcinoma, gastro-intestinal stromal tumor [GIST], adenoid cystic carcinoma, and mycosis fungoides) using a combination of Tumor Registry, laboratory information system (LIS) and/or SPIN-related tools. Pathologists identified the slides/blocks with tumor and noted first 3 slides with largest tumor and availability of the corresponding block. Results: Common tumors cases (n = 400), the institutional retrieval rates (all blocks) were 83% (A), 95% (B), 80% (C), and 98% (D). Retrieval rate (tumor blocks) from all centers for common tumors was 73% with mean largest tumor size of 1.49 cm; retrieval (tumor blocks) was highest-lung (84%) and lowest-prostate (54%). Rare tumors cases (n = 400), each institution's retrieval rates (all blocks) were 78% (A), 73% (B), 67% (C), and 84% (D). Retrieval rate (tumor blocks) from all centers for rare tumors was 66% with mean largest tumor size of 1.56 cm; retrieval (tumor blocks) was highest for GIST (72%) and lowest for adenoid cystic carcinoma (58%). Conclusion: A ssessment shows availability and quality of archival tissue blocks that are retrievable and associated electronic data that can be of value for researchers. This study serves to compliment the data from which uniform use of the SPIN query tools by all four centers will be measured to assure and highlight the usefulness of archival material for obtaining tumor tissues for research. © 2007 Patel et al; licensee BioMed Central Ltd.",,"access to information; adenoid cystic carcinoma; article; brain tumor; breast adenocarcinoma; cancer registry; cancer research; colon adenocarcinoma; computer program; controlled study; gastrointestinal stromal tumor; histopathology; hospital information system; human; human tissue; information dissemination; information retrieval; information system; Internet; lung squamous cell carcinoma; mycosis fungoides; prostate adenocarcinoma; qualitative analysis; quantitative analysis; tumor volume; health care facility; medical informatics; neoplasm; organization and management; pathology; statistics; United States; utilization review; paraffin; Humans; Medical Informatics; Neoplasms; Paraffin Embedding; Pathology, Clinical; Tissue Banks; United States",,,,,"Abati, A., Liotta, L.A., Looking forward in diagnostic pathology: The molecular superhighway (1996) Cancer, 78 (1), pp. 1-3. , 10.1002/(SICI)1097-0142(19960701)78:1<1::AID-CNCR1>3.0.CO;2-S 8646703; Fetsch, P.A., Simone, N.L., Bryant-Greenwood, P.K., Marincola, F.M., Filie, A.C., Petricoin, E.F., Liotta, L.A., Abati, A., Proteomic evaluation of archival cytologic material using SELDI affinity mass spectrometry: Potential for diagnostic applications (2002) Am J Clin Pathol, 118 (6), pp. 870-876. , 10.1309/EJKL-7328-KFPR-56WA 12472280; http://grants.nih.gov/grants/guide/rfa-files/RFA-CA-01-006.html, Shared Pathology Informatics Network: Release Date: March 27, 2000, RFA: CA-01-006, National Cancer InstituteBecich, M.J., The role of the pathologist as tissue refiner and data miner: The impact of functional genomics on the modern pathology laboratory and the critical roles of pathology informatics and bioinformatics (2000) Mol Diagn, 5 (4), pp. 287-299. , 10.1054/modi.2000.20431 11172493; http://www.cancerdiagnosis.nci.nih.gov/spin/, Shared Pathology Informatics Network websiteMarshall, E., Panel proposes tighter rules for tissue studies (1998) Science, 282 (5397), pp. 2165-2166. , 10.1126/science.282.5397.2165a 9890818; Mizuno, T., Nagamura, H., Iwamoto, K.S., Ito, T., Fukuhara, T., Tokunaga, M., Tokuoka, S., Seyama, T., RNA from decades-old archival tissue blocks for retrospective studies (1998) Diagn Mol Pathol, 7 (4), pp. 202-208. , 10.1097/00019606-199808000-00004 9917130; Qualman, S.J., France, M., Grizzle, W.E., LiVolsi, V.A., Moskaluk, C.A., Ramirez, N.C., Washington, M.K., Establishing a tumour bank: Banking, informatics and ethics (2004) Br J Cancer, 90 (6), pp. 1115-1119. , 10.1038/sj.bjc.6601678 15026787; Cooperberg, M.R., Broering, J.M., Litwin, M.S., Lubeck, D.P., Mehta, S.S., Henning, J.M., Carroll, P.R., The contemporary management of prostate cancer in the United States: Lessons from the cancer of the prostate strategic urologic research endeavor (CapSURE), a national disease registry (2004) J Urol, 171 (4), pp. 1393-1401. , 10.1097/01.ju.0000107247.81471.06 15017184; Lubeck, D.P., Litwin, M.S., Henning, J.M., Stier, D.M., Mazonson, P., Fisk, R., Carroll, P.R., The CaPSURE database: A methodology for clinical practice and research in prostate cancer. CaPSURE Research Panel. Cancer of the Prostate Strategic Urologic Research Endeavor (1996) Urology, 48 (5), pp. 773-777. , 10.1016/S0090-4295(96)00226-9 8911524; Grizzle, W., Grody, W.W., Noll, W.W., Sobel, M.E., Stass, S.A., Trainer, T., Travers, H., Woodruff, K., Recommended policies for uses of human tissue in research, education, and quality control. Ad Hoc Committee on Stored Tissue, College of American Pathologists (1999) Arch Pathol Lab Med, 123 (4), pp. 296-300. , 10320140; Grizzle, W.E., Aamodt, R., Clausen, K., LiVolsi, V., Pretlow, T.G., Qualman, S., Providing human tissues for research: How to establish a program (1998) Arch Pathol Lab Med, 122 (12), pp. 1065-1076. , 9870854; Grizzle, W.E., Woodruff, K.H., Trainer, T.D., The pathologist's role in the use of human tissues in research--legal, ethical, and other issues (1996) Arch Pathol Lab Med, 120 (10), pp. 909-912. , 12046602; Wertz, D.C., Archived specimens: A platform for discussion (1999) Community Genet, 2 (2-3), pp. 51-60. , 10.1159/000016187 11787507; Becich, M.J., Gilbertson, J.R., Gupta, D., Patel, A., Grzybicki, D.M., Raab, S.S., Pathology and patient safety: The critical role of pathology informatics in error reduction and quality initiatives (2004) Clin Lab Med, 24 (4), pp. 913-943. , vi 10.1016/j.cll.2004.05.019 15555749; Melamed, J., Datta, M.W., Becich, M.J., Orenstein, J.M., Dhir, R., Silver, S., Fidelia-Lambert, M., Berman, J.J., The cooperative prostate cancer tissue resource: A specimen and data resource for cancer researchers (2004) Clin Cancer Res, 10 (14), pp. 4614-4621. , 10.1158/1078-0432.CCR-04-0240 15269132; Patel, A.A., Kajdacsy-Balla, A., Berman, J.J., Bosland, M., Datta, M.W., Dhir, R., Gilbertson, J., Becich, M.J., The development of common data elements for a multi-institute prostate cancer tissue bank: The Cooperative Prostate Cancer Tissue Resource (CPCTR) experience (2005) BMC Cancer, 5, p. 108. , 1236914 16111498 10.1186/1471-2407-5-108; Glass, A.G., Donis-Keller, H., Mies, C., Russo, J., Zehnbauer, B., Taube, S., Aamodt, R., The Cooperative Breast Cancer Tissue Resource: Archival tissue for the investigation of tumor markers (2001) Clin Cancer Res, 7 (7), pp. 1843-1849. , 11448894; http://acsb.ucsf.edu/, AIDS and Cancer Specimen ResourcePatel, A.A., Gilbertson, J.R., Parwani, A.V., Dhir, R., Datta, M.W., Gupta, R., Berman, J.J., Becich, M.J., An informatics model for tissue banks - Lessons learned from the Cooperative Prostate Cancer Tissue Resource (2006) BMC Cancer, 6 (1), p. 120. , 1484486 16677389 10.1186/1471-2407-6-120; Beckwith, B.A., Mahaadevan, R., Balis, U.J., Kuo, F., Development and evaluation of an open source software tool for deidentification of pathology reports (2006) BMC Med Inform Decis Mak, 6, p. 12. , 1421388 16515714 10.1186/1472-6947-6-12; Gupta, D., Saul, M., Gilbertson, J., Evaluation of a deidentification (De-Id) software engine to share pathology reports and clinical documents for research (2004) Am J Clin Pathol, 121 (2), pp. 176-186. , 10.1309/E6K3-3GBP-E5C2-7FYU 14983930 14983930; McDonald, C.J., Dexter, P., Schadow, G., Chueh, H.C., Abernathy, G., Hook, J., Blevins, L., Berman, J.J., SPIN query tools for de-identified research on a humongous database (2005) AMIA Annu Symp Proc, pp. 515-519. , 16779093; Mitchell, K.J., Becich, M.J., Berman, J.J., Chapman, W.W., Gilbertson, J., Gupta, D., Harrison, J., Crowley, R.S., Implementation and evaluation of a negation tagger in a pipeline-based system for information extract from pathology reports (2004) Medinfo, 11 (PART 1), pp. 663-667; Mitchell, K.J., Crowley, R.S., Gupta, D., Gilbertson, J., A knowledge-based approach to information extraction from surgical pathology reports (2003) AMIA Annu Symp Proc, p. 937. , 1479971 14728442; Namini, A.H., Berkowicz, D.A., Kohane, I.S., Chueh, H., A submission model for use in the indexing, searching, and retrieval of distributed pathology case and tissue specimens (2004) Medinfo, 11 (PART 2), pp. 1264-1267. , 15361017; Schadow, G., McDonald, C.J., Extracting structured information from free text pathology reports (2003) AMIA Annu Symp Proc, pp. 584-588. , 1480213 14728240; Gilbertson, J.R., Gupta, R., Nie, Y., Patel, A.A., Becich, M.J., Automated clinical annotation of tissue bank specimens (2004) Medinfo, 11 (PART 1), pp. 607-610. , 15360884; Holzbach, A.M., Chueh, H., Porter, A.J., Kohane, I.S., Berkowicz, D., A query engine for distributed medical databases (2004) Medinfo, 11, p. 1519","Parwani, A.V.; Department of Pathology; Center for Pathology Informatics; University of Pittsburgh Pittsburgh, PA, United States; email: parwaniav@upmc.edu",,,,,,,,14712407,,BCMAC,10.1186/1471-2407-7-37,"English","BMC Cancer",Article,Scopus "Xu J., Peng H., Zhang J.-T.","Human multidrug transporter ABCG2, a target for sensitizing drug resistance in cancer chemotherapy",2007,"Current Medicinal Chemistry",14,6,,689,701,,3,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-33947580644&partnerID=40&rel=R8.0.0","Department of Pharmacology and Toxicology, Indiana University Cancer Center, Indiana University School of Medicine, 1044 W. Walnut St., Indianapolis, IN 46202, United States","Human ABCG2, a member of the ATP-binding cassette transporter superfamily which transports a wide variety of substrates, is highly expressed in placental syncytiotrophoblasts, in the canalicular membranes of liver, in the apical membrane of the small intestine epithelium, and at the luminal surface of the endothelial cells of human brain micro vessels. This strategic tissue localization indicates that ABCG2 plays an important role in absorption, distribution, and elimination of xenobiotics and drugs. High ABCG2 expression has also been detected in many hematological malignancies and solid tumors, indicating that ABCG2 is likely responsible also for the multidrug resistance in cancer chemotherapy. Indeed, ABCG2 can actively transport structurally diverse conjugated- or unconjugated-organic molecules and various anticancer drugs. Many chemo-sensitizing agents have been discovered, which can be developed for increasing drug adsorption and reversing drug resistance in cancer chemotherapy by inhibiting ABCG2 function or expression. This review summarizes current knowledge on ABCG2, its relevance to multidrug resistance and drug disposition, and its evergrowing numbers of substrates and inhibitors. © 2007 Bentham Science Publishers Ltd.","ABC transporter; ABCG2; Chemo-sensitization; Drug resistance; Inhibitors; MDR; Oligomerization; Substrates","9 aminocamptothecin; antineoplastic agent; biochanin A; biricodar; breast cancer resistance protein; camptothecin; cimetidine; cyclosporin; daunorubicin; diethylstilbestrol; doxorubicin; elacridar; fibrinogen receptor antagonist; flavopiridol; fumitremorgin C; gefitinib; idarubicin; imatinib; irinotecan; isoquercitrin; me 3229; me 3277; methotrexate; mitoxantrone; multidrug resistance protein 1; rubitecan; tamoxifen; topotecan; unindexed drug; verapamil; acute granulocytic leukemia; antineoplastic activity; biliary excretion; bioavailability; blood placenta barrier; brain blood vessel; cancer; cancer chemotherapy; clinical trial; drug absorption; drug bioavailability; drug clearance; drug disposition; drug distribution; drug elimination; drug inhibition; drug metabolism; drug penetration; drug potentiation; drug resistance; drug sensitization; drug structure; drug targeting; drug transport; drug uptake; human; liver membrane; multidrug resistance; nonhuman; placental transfer; protein expression; protein function; protein structure; review; small intestine mucosa; structure activity relation; syncytiotrophoblast; tissue distribution; Animals; Antineoplastic Agents; ATP-Binding Cassette Transporters; Drug Resistance, Neoplasm; Humans; Neoplasm Proteins; Neoplasms",,"biochanin A, 491-80-5; biricodar, 174254-13-8; camptothecin, 7689-03-4; cimetidine, 51481-61-9, 70059-30-2; cyclosporin, 79217-60-0; daunorubicin, 12707-28-7, 20830-81-3, 23541-50-6; diethylstilbestrol, 30498-85-2, 56-53-1; doxorubicin, 23214-92-8, 25316-40-9; elacridar, 143664-11-3; flavopiridol, 131740-09-5, 146426-40-6; fumitremorgin C, 118974-02-0; gefitinib, 184475-35-2, 184475-55-6, 184475-56-7; idarubicin, 57852-57-0, 58957-92-9; imatinib, 152459-95-5, 220127-57-1; irinotecan, 100286-90-6; isoquercitrin, 21637-25-2, 482-35-9; methotrexate, 15475-56-6, 59-05-2, 7413-34-5; mitoxantrone, 65271-80-9, 70476-82-3; rubitecan, 91421-42-0; tamoxifen, 10540-29-1; topotecan, 119413-54-6, 123948-87-8; verapamil, 152-11-4, 52-53-9; ABCG2 protein, human; Antineoplastic Agents; ATP-Binding Cassette Transporters; Neoplasm Proteins","gf 120918; gleevec; me 3229; me 3277; zd 1839",,"Doyle, L.A., Yang, W., Abruzzo, L.V., Krogmann, T., Gao, Y., Rishi, A.K., Ross, D.D., (1998) Proc. 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Walnut St. Indianapolis, IN 46202, United States; email: jianzhan@iupui.edu",,,,,,,,09298673,,CMCHE,10.2174/092986707780059580,"English","Current Medicinal Chemistry",Review,Scopus "Mathew R.M., Vandenberghe R., Garcia-Merino A., Yamamoto T., Landolfi J.C., Rosenfeld M.R., Rossi J.E., Thiessen B., Dropcho E.J., Dalmau J.","Orchiectomy for suspected microscopic tumor in patients with anti-Ma2-associated encephalitis",2007,"Neurology",68,12,,900,905,,7,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-34147134976&partnerID=40&rel=R8.0.0","Department of Neurology, Division Neuro-oncology, University of Pennsylvania, Philadelphia; Department of Neurology, University Hospital Gasthuisberg, Leuven, Belgium; Department of Neurology, Clínica Puerta de Hierro, Madrid, Spain; Department of Neurology, University of Tokyo Hospital, Japan; New Jersey Neuroscience Institute, JFK Medical Center, Edison; Division of Medical Oncology, British Columbia Cancer Agency, Vancouver, Canada; Department of Neurology, Indiana University Medical Center, Indianapolis, United States; Division Neuro-oncology, Department of Neurology, University of Pennsylvania, 3 W. Gates, 3400 Spruce Street, Philadelphia, PA 19104, United States","OBJECTIVE: To report the presence of microscopic neoplasms of the testis in men with anti-Ma2-associated encephalitis (Ma2-encephalitis) and to discuss the clinical implications. METHODS: Orchiectomy specimens were examined using immunohistochemistry with Ma2 and Oct4 antibodies. RESULTS: Among 25 patients with Ma2-encephalitis younger than 50 years, 19 had germ-cell tumors, and 6 had no evidence of cancer. These 6 patients underwent orchiectomy because they fulfilled five criteria: 1) demonstration of anti-Ma2 antibodies in association with MRI or clinical features compatible with Ma2-encephalitis, 2) life-threatening or progressive neurologic deficits, 3) age < 50 years, 4) absence of other tumors, and 5) new testicular enlargement or risk factors for germ-cell tumors, mainly cryptorchidism or ultrasound evidence of testicular microcalcifications. All orchiectomy specimens showed intratubular-germ cell neoplasms unclassified type (IGCNU) and other abnormalities including microcalcifications, atrophy, fibrosis, inflammatory infiltrates, or hypospermatogenesis. Ma2 was expressed by neoplastic cells in three of three patients examined. Even though most patients had severe neurologic deficits at the time of orchiectomy (median progression of symptoms, 10 months), 4 had partial improvement and prolonged stabilization (8 to 84 months, median 22.5 months) and two did not improve after the procedure. CONCLUSIONS: In young men with Ma2-encephalitis, 1) the disorder should be attributed to a germ-cell neoplasm of the testis unless another Ma2-expressing tumor is found, 2) negative tumor markers, ultrasound, body CT, or PET do not exclude an intratubular germ-cell neoplasm of the testis, and 3) if no tumor is found, the presence of the five indicated criteria should prompt consideration of orchiectomy. ©2007AAN Enterprises, Inc.",,"antibody; ma2 antibody; oct4 antibody; article; calcification; clinical article; clinical feature; cryptorchism; echography; encephalitis; fibrosis; genital system disease; germ cell tumor; human; human tissue; hypospermatogenesis; immunohistochemistry; inflammatory infiltrate; male; neurologic disease; nuclear magnetic resonance imaging; orchiectomy; priority journal; risk factor; testicular enlargement; testis atrophy; testis cancer; testis tumor; tumor cell; Adult; Antigens, Neoplasm; Autoantibodies; Brain; Diagnosis, Differential; Early Diagnosis; Humans; Limbic Encephalitis; Magnetic Resonance Imaging; Male; Neoplasms, Germ Cell and Embryonal; Nerve Tissue Proteins; Neural Pathways; Orchiectomy; Predictive Value of Tests; Testicular Neoplasms; Tumor Markers, Biological",,"Antigens, Neoplasm; Autoantibodies; Ma2 antigen; Nerve Tissue Proteins; Tumor Markers, Biological",,,"Graus, F., Dalmau, J., Rene, R., Anti-Hu antibodies in patients with small-cell lung cancer: Association with complete response to therapy and improved survival (1997) J Clin Oncol, 15, pp. 2866-2872; Darnell, R.B., Posner, J.B., Paraneoplastic syndromes involving the nervous system (2003) N Engl J Med, 349, pp. 1543-1554; Younes-Mhenni, S., Janier, M.F., Cinotti, L., FDG-PET improves tumour detection in patients with paraneoplastic neurological syndromes (2004) Brain, 127, pp. 2331-2338; Dalmau, J., Graus, F., Villarejo, A., Clinical analysis of anti-Ma2-associated encephalitis (2004) Brain, 127, pp. 1831-1844; Montironi, R., Intratubular germ cell neoplasia of the testis: Testicular intraepithelial neoplasia (2002) Eur Urol, 41, pp. 651-654; Mathew RM, Yamamoto T, Nakamura K, Dropcho E, Tsuji S, Dalmau J. Orchiectomy for suspected microscopic tumor in patients with paraneoplastic anti-Ma2 encephalitis. 58th annual meeting of the AAN; San Diego, CA; April 5, 2006. Abstract and video clips available at: http://www.abstracts2view.com/aan/ view.php?nu=AAN06L_PL01.001; http://www.marathonmultimedia.com/aan_library/ master2.php?ud=56136Landolfi, J.C., Nadkarni, M., Paraneoplastic limbic encephalitis and possible narcolepsy in a patient with testicular cancer: Case study (2003) Neurooncol, 5, pp. 214-216; Rosenfeld, M.R., Eichen, J.G., Wade, D.F., Posner, J.B., Dalmau, J., Molecular and clinical diversity in paraneoplastic immunity to Ma proteins (2001) Ann Neurol, 50, pp. 339-348; Furneaux, H.M., Rosenblum, M.K., Dalmau, J., Selective expression of Purkinje-cell antigens in tumor tissue from patients with paraneoplastic cerebellar degeneration (1990) N Engl J Med, 322, pp. 1844-1851; Cattoretti, G., Pileri, S., Parravicini, C., Antigen unmasking on formalin-fixed, paraffin-embedded tissue sections (1993) J Pathol, 171, pp. 83-98; Voltz, R., Gultekin, S.H., Rosenfeld, M.R., A serologic marker of paraneoplastic limbic and brain-stem encephalitis in patients with testicular cancer (1999) N Engl J Med, 340, pp. 1788-1795; Waragai, M., Chiba, A., Uchibori, A., Fukushima, T., Anno, M., Tanaka, K., Anti-Ma2 associated paraneoplastic neurological syndrome presenting as encephalitis and progressive muscular atrophy (2006) J Neurol Neurosurg Psychiatry, 77, pp. 111-113; Blumenthal, D.T., Salzman, K.L., Digre, K.B., Jensen, R.L., Dunson, W.A., Dalmau, J., Early pathologic findings and long-term improvement in anti-Ma2-associated encephalitis (2006) Neurology, 67, pp. 146-149; Bosl, G.J., Motzer, R.J., Testicular germ-cell cancer (1997) N Engl J Med, 337, pp. 242-253; Hattab, E.M., Tu, P.H., Wilson, J.D., Cheng, L., OCT4 immunohistochemistry is superior to placental alkaline phosphatase (PLAP) in the diagnosis of central nervous system germinoma (2005) Am J Surg Pathol, 29, pp. 368-371; Jones, T.D., Ulbright, T.M., Eble, J.N., Cheng, L., OCT4: A sensitive and specific biomarker for intratubular germ cell neoplasia of the testis (2004) Clin Cancer Res, 10, pp. 8544-8547; Jones, T.D., Ulbright, T.M., Eble, J.N., Baldridge, L.A., Cheng, L., OCT4 staining in testicular tumors: A sensitive and specific marker for seminoma and embryonal carcinoma (2004) Am J Surg Pathol, 28, pp. 935-940; Linke, J., Loy, V., Dieckmann, K.P., Prevalence of testicular intraepithelial neoplasia in healthy males (2005) J Urol, 173, pp. 1577-1579; Harland, S.J., Cook, P.A., Fossa, S.D., Intratubular germ cell neoplasia of the contralateral testis in testicular cancer: Defining a high risk group (1998) J Urol, 160, pp. 1353-1357; Derogee, M., Bevers, R.F., Prins, H.J., Jonges, T.G., Elbers, F.H., Boon, T.A., Testicular microlithiasis, a premalignant condition: Prevalence, histopathologic findings, and relation to testicular tumor (2001) Urology, 57, pp. 1133-1137; Vegni-Talluri, M., Bigliardi, E., Vanni, M.G., Tota, G., Testicular microliths: Their origin and structure (1980) J Urol, 124, pp. 105-107; Kim, B., Winter III, T.C., Ryu, J.A., Testicular microlithiasis: Clinical significance and review of the literature (2003) Eur Radiol, 13, pp. 2567-2576; Miller, R.L., Wissman, R., White, S., Ragosin, R., Testicular microlithiasis: A benign condition with a malignant association (1996) J Clin Ultrasound, 24, pp. 197-202; Bryniarski, K., Szczepanik, M., Maresz, K., Ptak, M., Ptak, W., Subpopulations of mouse testicular macrophages and their immunoregulatory function (2004) Am J Reprod Immunol, 52, pp. 27-35; Sundstrom, J., Verajnkorva, E., Salminen, E., Pelliniemi, L.J., Pollanen, P., Experimental testicular teratoma promotes formation of humoral immune responses in the host testis (1999) J Reprod Immunol, 42, pp. 107-126; Castle, J., Sakonju, A., Dalmau, J., Newman-Toker, D.E., Anti-Ma2-associated encephalitis with normal FDG-PET: A case of pseudo-Whipple's Disease (2006) Nat Clin Pract Neurol, 10, pp. 566-572; Dieckmann, K.P., Loy, V., False-negative biopsies for the diagnosis of testicular intraepithelial neoplasia (TIN)-an update (2003) Eur Urol, 43, pp. 516-521; Dieckmann, K.P., Pottek, T., Heinemann, V., Hopker, W.W., Loy, V., Four testicular biopsies failing to detect a case of testicular intraepithelial neoplasia (2004) Acta Oncol, 43, pp. 212-214; Bonita, R., Beaglehole, R., Modification of Rankin Scale: Recovery of motor function after stroke (1988) Stroke, 19, pp. 1497-1500","Dalmau, J.; Division Neuro-oncology; Department of Neurology; University of Pennsylvania; 3 W. Gates, 3400 Spruce Street Philadelphia, PA 19104, United States; email: josep.dalmau@uphs.upenn.edu",,,,,,,,00283878,,NEURA,10.1212/01.wnl.0000252379.81933.80,"English","Neurology",Article,Scopus "Ahles T.A., Saykin A.J.","Candidate mechanisms for chemotherapy-induced cognitive changes",2007,"Nature Reviews Cancer",7,3,,192,201,,14,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-33847195328&partnerID=40&rel=R8.0.0","Department of Psychiatry and Behavioural Sciences, Memorial Sloan-Kettering Cancer Center, New York, NY, United States; Department of Psychiatry (Neuropsychology Program), Norris Cotton Cancer Center, Dartmouth-Hitchcock Medical Center, Lebanon, NH, United States; New Hampshire Hospital, Concord, NH, United States; Department of Radiology, Indiana University, School of Medicine, Indianapolis, IN, United States","The mechanism(s) for chemotherapy-induced cognitive changes are largely unknown; however, several candidate mechanisms have been identified. We suggest that shared genetic risk factors for the development of cancer and cognitive problems, including low-efficiency efflux pumps, deficits in DNA-repair mechanisms and/or a deregulated immune response, coupled with the effect of chemotherapy on these systems, might contribute to cognitive decline in patients after chemotherapy. Furthermore, the genetically modulated reduction of capacity for neural repair and neurotransmitter activity, as well as reduced antioxidant capacity associated with treatment-induced reduction in oestrogen and testosterone levels, might interact with these mechanisms and/or have independent effects on cognitive function. © 2007 Nature Publishing Group.",,"estrogen; progesterone; antioxidant activity; cancer chemotherapy; cognition; DNA repair; gene control; genetic risk; human; nerve regeneration; neurotransmission; priority journal; review; risk factor; Animals; Antineoplastic Agents; Brain; Cognition Disorders; Genetic Predisposition to Disease; Humans; Neoplasms; Risk Factors",,"progesterone, 57-83-0; Antineoplastic Agents",,,"Silberfarb, P.M., Chemotherapy and cognitive defects in cancer patients (1983) Annu. Rev. 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These investigators developed an animal model of chemotherapy-induced cognitive deficits and showed deficits in memory and learning tasks in mice treated with chemotherapy that were similar to deficits seen in breast cancer survivors","Ahles, T.A.; Department of Psychiatry and Behavioural Sciences; Memorial Sloan-Kettering Cancer Center New York, NY, United States; email: ahlest@mskcc.org",,,,,,,,1474175X,,NRCAC,10.1038/nrc2073,"English","Nature Reviews Cancer",Review,Scopus "Fishel M.L., Vasko M.R., Kelley M.R.","DNA repair in neurons: So if they don't divide what's to repair?",2007,"Mutation Research - Fundamental and Molecular Mechanisms of Mutagenesis",614,1-2,,24,36,,13,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-33845518305&partnerID=40&rel=R8.0.0","Department of Pediatrics, (Section of Hematology/Oncology), Herman B Wells Center for Pediatric Research, Indiana University School of Medicine, 1044 W. Walnut, Indianapolis, IN 46202, United States; Department of Pharmacology and Toxicology, Indiana University School of Medicine, 1044 W. Walnut St, Indianapolis, IN 46202, United States; Department of Biochemistry and Molecular Biology, Indiana University School of Medicine, 1044 W. Walnut, Indianapolis, IN 46202, United States","Neuronal DNA repair remains one of the most exciting areas for investigation, particularly as a means to compare the DNA repair response in mitotic (cancer) vs. post-mitotic (neuronal) cells. In addition, the role of DNA repair in neuronal cell survival and response to aging and environmental insults is of particular interest. DNA damage caused by reactive oxygen species (ROS) such as generated by mitochondrial respiration includes altered bases, abasic sites, and single- and double-strand breaks which can be prevented by the DNA base excision repair (BER) pathway. Oxidative stress accumulates in the DNA of the human brain over time especially in the mitochondrial DNA (mtDNA) and is proposed to play a critical role in aging and in the pathogenesis of several neurological disorders including Parkinson's disease, ALS, and Alzheimer's diseases. Because DNA damage accumulates in the mtDNA more than nuclear DNA, there is increased interest in DNA repair pathways and the consequence of DNA damage in the mitochondria of neurons. The type of damage that is most likely to occur in neuronal cells is oxidative DNA damage which is primarily removed by the BER pathway. Following the notion that the bulk of neuronal DNA damage is acquired by oxidative DNA damage and ROS, the BER pathway is a likely area of focus for neuronal studies of DNA repair. BER variations in brain aging and pathology in various brain regions and tissues are presented. Therefore, the BER pathway is discussed in greater detail in this review than other repair pathways. Other repair pathways including direct reversal, nucleotide excision repair (NER), mismatch repair (MMR), homologous recombination and non-homologous end joining are also discussed. Finally, there is a growing interest in the role that DNA repair pathways play in the clinical arena as they relate to the neurotoxicity and neuropathy associated with cancer treatments. Among the numerous side effects of cancer treatments, major clinical effects include neurocognitive dysfunction and peripheral neuropathy. These symptoms occur frequently and have not been effectively studied at the cellular or molecular level. Studies of DNA repair may help our understanding of how those cells that are not dividing could succumb to neurotoxicity with the clinical manifestations discussed in the following article. © 2006 Elsevier B.V. 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Neuroradiol., 25, pp. 1575-1582; Schagen, S.B., Hamburger, H.L., Muller, M.J., Boogerd, W., van Dam, F.S., Neurophysiological evaluation of late effects of adjuvant high-dose chemotherapy on cognitive function (2001) J. Neurooncol., 51, pp. 159-165; Schagen, S.B., Muller, M.J., Boogerd, W., Van Dam, F.S., Cognitive dysfunction and chemotherapy: neuropsychological findings in perspective (2002) Clin. Breast Cancer, 3 (SUPPL. 3), pp. S100-S108; Schagen, S.B., Muller, M.J., Boogerd, W., Rosenbrand, R.M., van Rhijn, D., Rodenhuis, S., van Dam, F.S., Late effects of adjuvant chemotherapy on cognitive function: a follow-up study in breast cancer patients (2002) Ann. Oncol., 13, pp. 1387-1397; Ness, K.K., Bhatia, S., Baker, K.S., Francisco, L., Carter, A., Forman, S.J., Robison, L.L., Gurney, J.G., Performance limitations and participation restrictions among childhood cancer survivors treated with hematopoietic stem cell transplantation: the bone marrow transplant survivor study (2005) Arch. Pediatr. Adolesc. Med., 159, pp. 706-713; Scharer, O.D., Chemistry and biology of DNA repair (2003) Angew Chem. Int. Ed. Engl., 42, pp. 2946-2974; Izumi, T., Wiederhold, L.R., Roy, G., Roy, R., Jaiswal, A., Bhakat, K.K., Mitra, S., Hazra, T.K., Mammalian DNA base excision repair proteins: their interactions and role in repair of oxidative DNA damage (2003) Toxicology, 193, pp. 43-65","Kelley, M.R.; Department of Pediatrics; (Section of Hematology/Oncology); Herman B Wells Center for Pediatric Research, Indiana University School of Medicine; 1044 W. Walnut Indianapolis, IN 46202, United States; email: mkelley@iupui.edu",,,,,,,,00275107,,MRFME,10.1016/j.mrfmmm.2006.06.007,"English","Mutation Research - Fundamental and Molecular Mechanisms of Mutagenesis",Article,Scopus "Cheng L., Sung M.-T., Cossu-Rocca P., Jones T.D., MacLennan G.T., De Jong J., Lopez-Beltran A., Montironi R., Looijenga L.H.J.","OCT4: Biological functions and clinical applications marker of germ cell neoplasia",2007,"Journal of Pathology",211,1,,1,9,,9,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-33846228391&partnerID=40&rel=R8.0.0","Department of Pathology and Laboratory Medicine, Indiana University School of Medicine, 350 West 11th Street, Indianapolis, IN 46202, United States; Department of Urology, Indiana University School of Medicine, 350 West 11th Street, Indianapolis, IN 46202, United States; Department of Pathology, Chang Gung Memorial Hospital-Kaohsiung Medical Centre, Chang Gung University College of Medicine, Kaohsiung, Taiwan; Dipartimento di Patologia, Universitá di Sassari, Sassari, Italy; Department of Pathology, Case Western Reserve University, Cleveland, OH, United States; Department of Pathology, Josephine Nefkens Institute Erasmus Medical Centre, University Medical Centre Rotterdam, Rotterdam, Netherlands; Department of Pathology, Cordoba University, Cordoba, Spain; Institute of Pathological Anatomy and Histopathology, School of Medicine, Polytechnic University of the Marche Region (Ancona), Ancona, Italy","Germ cell tumours (GCTs) are a heterogeneous group of neoplasms, which develop in the gonads as well as in extragonadal sites, that share morphological patterns and an over-all good prognosis, owing to their responsiveness to current surgical, chemotherapeutic, and radiotherapeutic measures. GCTs demonstrate extremely interesting biological features because of their close relationships with normal embryonal development as demonstrated by the pluripotentiality of some undifferentiated GCT variants. The similarities between GCTs and normal germ cell development have made it possible to identify possible pathogenetic pathways in neoplastic transformation and progression of GCTs. Genotypic and immunophenotypic profiles of these tumours are also useful in establishing and narrowing the differential diagnosis in cases of suspected GCTs. Recently, OCT4 (also known as OCT3 or POU5F1), a transcription factor that has been recognized as fundamental in the maintenance of pluripotency in embryonic stem cells and primordial germ cells, has been proposed as a useful marker for GCTs that exhibit features of pluripotentiality, specifically seminoma/dysgerminoma/ germinoma and embryonal carcinoma. The development of commercially available OCT4-specific antibodies suitable for immunohistochemistry on paraffin-embedded specimens has generated increasing numbers of reports of OCT4 expression in a wide variety of gonadal and extragonadal GCTs. OCT4 immunostaining has been shown to be a sensitive and specific marker for seminomatous/(dys)germinomatous tumours and in embryonal carcinoma variants of non-seminomatous GCTs, whether in primary gonadal or extragonadal sites or in metastatic lesions. Therefore, OCT4 immunohistochemistry is an additional helpful marker both in the differential diagnosis of specific histological subtypes of GCTs and in establishing a germ cell origin for some metastatic tumours of uncertain primary. OCT4 expression has also been reported in pre-invasive conditions such as intratubular germ cell neoplasia, unclassified (IGCNU) and the germ cell component of gonadoblastoma. Additionally, OCT4 immunostaining shows promise as a useful tool in managing patients known to be at high risk for the development of invasive GCTs. Copyright © 2006 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.","Embryonal carcinoma; Germ cell tumuor; Oct3/4; POU5F1; Seminoma; Stem cell biomarkers; Testis","octamer transcription factor 4; tumor marker; cancer risk; carcinogenesis; cryptorchism; diagnostic accuracy; diagnostic value; dysgerminoma; embryonal carcinoma; embryonic stem cell; gene expression; germ cell tumor; gonadoblastoma; histopathology; human; immunohistochemistry; immunoreactivity; infertility; malignant transformation; nonhuman; ovary tumor; pluripotent stem cell; primordial germ cell; priority journal; protein analysis; protein expression; protein function; review; risk assessment; risk factor; seminoma; testis tumor; tumor biopsy; Brain Neoplasms; Diagnosis, Differential; Female; Humans; Lymphatic Metastasis; Male; Neoplasms, Germ Cell and Embryonal; Octamer Transcription Factor-3; Ovarian Neoplasms; Testicular Neoplasms; Tumor Markers, Biological",,"Octamer Transcription Factor-3; Tumor Markers, Biological",,,"Nichols, J., Zernike, B., Anastassiadis, K., Niwa, H., Klewe-Nebenius, D., Chambers, I., Formation of pluripotent stem cells in the mammalian embryo depends on the POU transcription factor Oct4 (1998) Cell, 95, pp. 379-391; Donovan, P.J., High Oct-ane fuel powers the stem cell (2001) Nat Genet, 29, pp. 246-247; Ovitt, C.E., Scholer, H.R., The molecular biology of Oct-4 in the early mouse embryo (1998) Mol Hum Reprod, 4, pp. 1021-1031; Pesce, M., Scholer, H.R., Oct-4: Gatekeeper in the beginnings of mammalian development (2001) Stem Cells, 19, pp. 271-278; Ben-Shushan, E., Sharir, H., Pikarsky, E., Bergman, Y., A dynamic balance between ARP-1/COUP-TFII, EAR-3/COUP-TFI, and retinoic acid receptor: Retinoid X receptor heterodimers regulates Oct-3/4 expression in embryonal carcinoma cells (1995) Mol Cell Biol, 15, pp. 1034-1048; Gidekel, S., Bergman, Y., A unique developmental pattern of Oct-3/4 DNA methylation is controlled by a cis-demodification element (2002) J Biol Chem, 277, pp. 34521-34530; Hattori, N., Nishino, K., Ko, Y.G., Hattori, N., Ohgane, J., Tanaka, S., Epigenetic control of mouse Oct-4 gene expression in embryonic stem cells and trophoblast stem cells (2004) J Biol Chem, 279, pp. 17063-17069; Deb-Rinker, P., Ly, D., Jezierski, A., Sikorska, M., Walker, P.R., Sequential DNA methylation of the Nanog and Oct-4 upstream regions in human NT2 cells during neuronal differentiation (2005) J Biol Chem, 280, pp. 6257-6260; Gidekel, S., Pizov, G., Bergman, Y., Pikarsky, E., Oct-3/4 is a dose-dependent oncogenic fate determinant (2003) Cancer Cell, 4, pp. 361-370; Kehler, J., Tolkunova, E., Koschorz, B., Pesce, M., Gentile, L., Boiani, M., Oct4 is required for primordial germ cell survival (2004) EMBO Rep, 5, pp. 1078-1083; Boiani, M., Eckardt, S., Scholer, H.R., McLaughlin, K.J., Oct4 distribution and level in mouse clones: Consequences for pluripotency (2002) Genes Dev, 16, pp. 1209-1219; Niwa, H., Miyazaki, J., Smith, A.G., Quantitative expression of Oct-3/4 defines differentiation, dedifferentiation or self-renewal of ES cells (2000) Nat Genet, 24, pp. 372-376; Hay, D.C., Sutherland, L., Clark, J., Burdon, T., Oct-4 knockdown induces similar patterns of endoderm and trophoblast differentiation markers in human and mouse embryonic stem cells (2004) Stem Cells, 22, pp. 225-235; Velkey, J.M., O'Shea, K.S., Oct4 RNA interference induces trophectoderm differentiation in mouse embryonic stem cells (2003) Genesis, 37, pp. 18-24; van Berlo, R.J., Oosterhuis, J.W., Schrijnemakers, E., Schoots, C.J., de Jong, B., Darnjanov, I., Yolk-sac carcinoma develops spontaneously as a late occurrence in slow-growing teratoid tumors produced from transplanted 7-day mouse embryos (1990) Int J Cancer, 45, pp. 153-155; Kraft, H.J., Mosselman, S., Smits, H.A., Hohenstein, P., Pick, E., Chen, Q., Oct-4 regulates alternative platelet-derived growth factor alpha receptor gene promoter in human embryonal carcinoma cells (1996) J Biol Chem, 271, pp. 12873-12878; Palumbo, C., van Roozendaal, K., Gillis, A.J., van Gurp, R.H., de Munnik, H., Oosterhuis, J.W., Expression of the PDGF alpha-receptor 1.5 kb transcript, OCT-4, and c-KIT in human normal and malignant tissues. Implications for the early diagnosis of testicular germ cell tumours and for our understanding of regulatory mechanisms (2002) J Pathol, 196, pp. 467-477; Looijenga, L.H., Stoop, H., de Leeuw, H.P., de Gouveia Brazao, C.A., Gillis, A.J., van Roozendaal, K.E., POU5F1 (OCT3/4) identifies cells with pluripotent potential in human germ cell tumors (2003) Cancer Res, 63, pp. 2244-2250; Jones, T.D., Ulbright, T.M., Eble, J.N., Baldridge, L.A., Cheng, L., OCT4 staining in testicular tumors: A sensitive and specific marker for seminoma and embryonal carcinoma (2004) Am J Surg Pathol, 28, pp. 935-940; De Jong, J., Stoop, H., Dohle, G.R., Bangma, C.H., Kliffen, M., van Esser, J.W., Diagnostic value of OCT3/4 for pre-invasive and invasive testicular germ cell tumours (2005) J Pathol, 206, pp. 242-249; Reuter, V.E., Origins and molecular biology of testicular germ cell tumors (2005) Mod Pathol, 18 (SUPPL. 2), pp. S51-S60; Rajpert-De Meyts, E., Hanstein, R., Jorgensen, N., Graem, N., Vogt, P.H., Skakkebaek, N.E., Developmental expression of POU5F1 (OCT-3/4) in normal and dysgenetic human gonads (2004) Hum Reprod, 19, pp. 1338-1344; Jones, T.D., Ulbright, T.M., Eble, J.N., Cheng, L., OCT4: A sensitive and specific biomarker for intratubular germ cell neoplasia of the testis (2004) Clin Cancer Res, 10, pp. 8544-8547; Gaskell, T.L., Esnal, A., Robinson, L.L., Anderson, R.A., Saunders, P.T., Immunohistochemical profiling of germ cells within the human fetal testis: Identification of three subpopulations (2004) Biol Reprod, 71, pp. 2012-2021; Honecker, F., Stoop, H., de Krijger, R.R., Chris Lau, Y.F., Bokemeyer, C., Looijenga, L.H., Pathobiological implications of the expression of markers of testicular carcinoma in situ by fetal germ cells (2004) J Pathol, 203, pp. 849-857; Hughes, I.A., Houk, C., Ahmed, S.F., Lee, P.A., Consensus statement on management of intersex disorders (2006) Arch Dis Child, 91, pp. 554-563; Cools, M., van Aerde, K., Kersemaekers, A.M., Boter, M., Drop, S.L., Wolffenbuttel, K.P., Morphological and immunohistochemical differences between gonadal maturation delay and early germ cell neoplasia in patients with undervirilisation syndromes (2005) J Clin Endocrinol Metab, 90, pp. 5295-5303; Cools, M., Drop, S.L., Wolffenbuttel, K.P., Oosterhuis, J.W., Looijenga, L.H., Germ cell tumors in the intersex gonad: Old paths, new directions, moving frontiers (2006) Endocr Rev, 27, pp. 468-484; Cools, M., Stoop, H., Kersemaekers, A.M., Drop, S.L., Wolffenbuttel, K.P., Bourguinon, J.P., Gonadoblastoma arising in undifferentiated gonadal tissue within dysgenetic gonads (2006) J Clin Endocrinol Metab, 91, pp. 2404-2413; Jones, T.D., MacLennan, G.T., Bonnin, J.M., Varsegi, M.F., Blair, J.E., Cheng, L., Screening for intratubular germ cell neoplasia of the testis using OCT4 immunohistochemistry (2006) Am J Surg Pathol, 30, pp. 1427-1431; Montironi, R., Intratubular germ cell neoplasia of the testis: Testicular intraepithelial neoplasia (2002) Eur Urol, 41, pp. 651-654; Cheng, L., Thomas, A., Roth, L.M., Zheng, W., Michael, H., Karim, F.W., OCT4: A novel biomarker for dysgerminoma of the ovary (2004) Am J Surg Pathol, 28, pp. 1341-1346; Kersemaekers, A.M., Honecker, F., Stoop, H., Cools, M., Molier, M., Wolffenbuttel, K., Identification of germ cells at risk for neoplastic transformation in gonadoblastoma: An immunohistochemical study for OCT3/4 and TSPY (2005) Hum Pathol, 36, pp. 512-521; Stoop, H., Honecker, F., Cools, M., de Krijger, R., Bokemeyer, C., Looijenga, L.H., Differentiation and development of human female germ cells during prenatal gonadogenesis: An immunohistochemical study (2005) Hum Reprod, 20, pp. 1466-1476; Hattab, E.M., Tu, P.H., Wilson, J.D., Cheng, L., OCT4 immunohistochemistry is superior to placental alkaline phosphatase (PLAP) in the diagnosis of central nervous system germinoma (2005) Am J Surg Pathol, 29, pp. 368-371; Sung, M.T., MacLennan, G.T., Cheng, L., Retroperitoneal seminoma in limited biopsies: Morphologic criteria and immunohistochemical findings in 30 cases (2006) Am J Surg Pathol, 30, pp. 766-773; Cheng, L., Establishing a germ cell origin for metastatic tumors using OCT4 immunohistochemistry (2004) Cancer, 101, pp. 2006-2010; Barnea, E., Bergman, Y., Synergy of SF1 and RAR in activation of Oct-3/4 promoter (2000) J Biol Chem, 275, pp. 6608-6619; Berney, D.M., Shamash, J., Pieroni, K., Oliver, R.T., Loss of CD30 expression in metastatic embryonal carcinoma: The effects of chemotherapy? (2001) Histopathology, 39, pp. 382-385; Sung, M.T., Jones, T.D., Beck, S.D., Foster, R.S., Cheng, L., OCT4 is superior to CD30 in the diagnosis of metastatic embryonal carcinomas after chemotherapy (2006) Hum Pathol, 37, pp. 662-667; Hoei-Hansen, C.E., Rajpert-De Meyts, E., Daugaard, G., Skakkebaek, N.E., Carcinoma in situ testis, the progenitor of testicular germ cell tumours: A clinical review (2005) Ann Oncol, 16, pp. 863-868; De Gouveia Brazao, C.A., Pierik, F.H., Oosterhuis, J.W., Dohle, G.R., Looijenga, L.H., Weber, R.F., Bilateral testicular microlithiasis predicts the presence of the precursor of testicular germ cell tumors in subfertile men (2004) J Urol, 171, pp. 158-160; Dieckmann, K.P., Skakkebaek, N.E., Carcinoma in situ of the testis: Review of biological and clinical features (1999) Int J Cancer, 83, pp. 815-822; Pauls, K., Franke, F.E., Buttner, R., Zhou, H., Gonadoblastoma: Evidence for a stepwise progression to dysgerminoma in a dysgenetic ovary (2005) Virchows Arch, 447, pp. 603-609","Cheng, L.; Department of Pathology and Laboratory Medicine; Indiana University School of Medicine; 350 West 11th Street Indianapolis, IN 46202, United States; email: lcheng@upui.edu",,,,,,,,00223417,,JPTLA,10.1002/path.2105,"English","Journal of Pathology",Review,Scopus "Pan C.-X., Zhang H., Lara Jr. P.N., Cheng L.","Small-cell carcinoma of the urinary bladder: Diagnosis and management",2006,"Expert Review of Anticancer Therapy",6,12,,1707,1713,,1,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-33846068222&partnerID=40&rel=R8.0.0","University of California at Davis, Department of Internal Medicine, Division of Hematology/Oncology, 4501 X Street, Sacramento, CA 95817, United States; Department of Pathology and Laboratory Medicine, Indiana University School of Medicine, 350 West 11th Street, Indianapolis, IN 46202, United States","Small-cell carcinoma of the urinary bladder (SCCUB) accounts for less than 1% of all cancers arising in the urinary bladder. Current diagnosis and management of SCCUB are often patterned after small-cell lung cancer (SCLC). However, SCCUB therapy is different from that for SCLC. For example, many patients with SCCUB undergo local resection, which is rarely performed in SCLC. As in SCLC, platinum-etoposide combination chemotherapy is employed as the main systemic treatment option for SCCUB. Chemotherapy is usually combined with other therapeutic modalities, especially in patients whose disease is limited to the locoregional area. Owing to the rarity of this malignancy, no prospective study has been performed that establishes the efficacy and duration of chemotherapy or the relative efficacy of platinum-etoposide versus other chemotherapeutic regimens. This article provides a comprehensive review of the current status of SCCUB diagnosis and management, as well as some unique insights into this rare tumor. © 2006 Future Drugs Ltd.","Chemotherapy; Radiation therapy; Small cell carcinoma of the urinary bladder; Small cell lung cancer; Targeted therapy","antineoplastic agent; carboplatin; CD56 antigen; chromogranin; cisplatin; cyclophosphamide; cytokeratin 20; cytokeratin 7; doxorubicin; etoposide; fluorodeoxyglucose f 18; fluorouracil; gastrin releasing peptide; gemcitabine; ifosfamide; irinotecan; methotrexate; neuron specific enolase; paclitaxel; platinum complex; serotonin; somatomedin C; synaptophysin; taxane derivative; topotecan; vasoactive intestinal polypeptide; vinblastine; bladder biopsy; bladder carcinogenesis; bladder carcinoma; brain metastasis; cancer adjuvant therapy; cancer combination chemotherapy; cancer palliative therapy; cancer radiotherapy; cancer regression; cancer staging; cancer survival; clinical feature; cystectomy; cystoscopy; diagnostic value; disease marker; drug efficacy; drug response; drug substitution; drug withdrawal; human; immunohistochemistry; positron emission tomography; prognosis; repeated drug dose; review; skull irradiation; small cell carcinoma; systemic therapy; treatment duration; tumor differentiation; unspecified side effect; Aged; Antineoplastic Combined Chemotherapy Protocols; Carcinoma, Small Cell; Cell Lineage; Chemotherapy, Adjuvant; Chromosome Aberrations; Combined Modality Therapy; Cystectomy; Female; Hematuria; Humans; Keratin-20; Keratin-7; Male; Middle Aged; Neoplasm Invasiveness; Neoplasm Proteins; Neoplasm Staging; Palliative Care; Radiotherapy, Adjuvant; Risk Factors; Smoking; Survival Rate; Tumor Markers, Biological; Urinary Bladder Neoplasms",,"carboplatin, 41575-94-4; cisplatin, 15663-27-1, 26035-31-4, 96081-74-2; cyclophosphamide, 50-18-0; doxorubicin, 23214-92-8, 25316-40-9; etoposide, 33419-42-0; fluorodeoxyglucose f 18, 63503-12-8; fluorouracil, 51-21-8; gastrin releasing peptide, 74815-57-9, 80043-53-4; gemcitabine, 103882-84-4; ifosfamide, 3778-73-2; irinotecan, 100286-90-6; methotrexate, 15475-56-6, 59-05-2, 7413-34-5; paclitaxel, 33069-62-4; serotonin, 50-67-9; somatomedin C, 67763-96-6; topotecan, 119413-54-6, 123948-87-8; vasoactive intestinal polypeptide, 37221-79-7; vinblastine, 865-21-4; Keratin-20; Keratin-7; Neoplasm Proteins; Tumor Markers, Biological",,,"Cramer, S.F., Aikawa, M., Cebelin, M., Neurosecretory granules in small cell invasive carcinoma of the urinary bladder (1981) Cancer, 47, pp. 724-730; Blomjous, C.E., Vos, W., De Voogt, H.J., Van der Valk, P., Meijer, C.J., Small cell carcinoma of the urinary bladder. 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Lung Cancer, 6, pp. 355-360","Pan, C.-X.; University of California at Davis; Department of Internal Medicine; Division of Hematology/Oncology; 4501 X Street Sacramento, CA 95817, United States; email: cxpan@ucdavis.edu",,,,,,,,14737140,,ERATB,10.1586/14737140.6.12.1707,"English","Expert Review of Anticancer Therapy",Review,Scopus "Hara T., Bansal A., DeGrado T.R.","Choline transporter as a novel target for molecular imaging of cancer",2006,"Molecular Imaging",5,4,,498,509,,5,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-33846430535&partnerID=40&rel=R8.0.0","Department of Radiology, Indiana University School of Medicine, Indianapolis, IN; 1345 West 16th Street, Indianapolis, IN 46202-9028","Abnormalities of choline processing in cancer cells have been used as a basis for imaging of cancer with positron emission tomography and magnetic resonance spectroscopy. In this study, the transport mechanism for choline was investigated in cultured PC-3 prostate cancer cells. Furthermore, tritiated hemicholinium 3 (HC-3), a well-known inhibitor of choline transport, was studied as a prototypic molecular imaging probe in PC-3 cells and 9L glioma-bearing rats. [3H]Choline uptake by PC-3 cells was found to have both facultative and nonfacilitative components. Facultative transport was characterized by partial sodium dependence and intermediate affinity (K M = 9.7 ± 0.8 μM). HC-3 inhibited choline with a K I of 10.5± 2.2 μM. Ouabain (1 mM) caused a 94% reduction in choline uptake. At physiologic choline concentration, phosphocholine was the rapid and predominant metabolic fate. The binding of [3H]HC-3 to PC-3 cells was rapid and specific (competitively blocked with unlabeled HC-3). Biodistribution of [3H]HC-3 in 9L glioma-bearing rats showed the ranking of uptake to be kidney > lung > tumor > liver > skeletal muscle ≈ blood > brain. In comparison with [14C]choline, [ 3H]HC-3 showed over twofold higher tumor uptake and favorable uptake ratios of tumor to blood, tumor to muscle, tumor to lung, and tumor to liver. The data demonstrate the quantitative importance of an intermediate-affinity, partially sodium-dependent choline transport system on choline processing in PC-3 cancer cells. The biodistribution properties of [3H]HC-3 in tumor-bearing rats encourage the development of molecular imaging probes based on choline transporter binding ligands. © 2006 BC Decker Inc.",,"Disease control; Enzyme inhibition; Magnetic resonance spectroscopy; Positron emission tomography; Transport properties; Tumors; Binding ligands; Choline; Facultative transport; Transport mechanism; Medical imaging; carbon; carrier protein; choline; choline transporter; CHT1 protein, human; hemicholinium 3; nerve protein; plasma membrane neurotransmitter transporter; Slc6a8 protein, rat; tritium; animal; article; Fischer 344 rat; glioma; human; kinetics; male; metabolism; neoplasm; prostate tumor; rat; scintiscanning; tumor cell line; Animals; Carbon Radioisotopes; Cell Line, Tumor; Choline; Glioma; Hemicholinium 3; Humans; Kinetics; Male; Membrane Transport Proteins; Neoplasms; Nerve Tissue Proteins; Plasma Membrane Neurotransmitter Transport Proteins; Prostatic Neoplasms; Rats; Rats, Inbred F344; Tritium",,"carbon, 7440-44-0; carrier protein, 80700-39-6; choline, 123-41-1, 13232-47-8, 1927-06-6, 4858-96-2, 62-49-7, 67-48-1; hemicholinium 3, 16478-59-4; tritium, 10028-17-8; Carbon Radioisotopes; choline transporter; Choline, 62-49-7; CHT1 protein, human; Hemicholinium 3, 312-45-8; Membrane Transport Proteins; Nerve Tissue Proteins; Plasma Membrane Neurotransmitter Transport Proteins; Slc6a8 protein, rat, 147652-48-0; Tritium, 10028-17-8",,,"Gillies, R.J., Morse, D.L., In vivo magnetic resonance spectroscopy in cancer (2005) Annu Rev Biomed Eng, 7, pp. 287-326; Hara, T., Kosaka, N., Shinoura, N., Kondo, T., PET imaging of brain tumor with [methyl-11C]choline (1997) J Nucl Med, 38, pp. 842-847; Molier-Hartmann, W., Herminghaus, S., Krings, T., Clinical application of proton magnetic resonance spectroscopy in the diagnosis of intracranial mass lesions (2002) Neuroradiology, 44, pp. 371-381; Kumar, R., Kumar, M., Jagannathan, N.R., Proton magnetic resonance spectroscopy with a body coil in the diagnosis of carcinoma prostate (2004) Urol Res, 32, pp. 36-40; 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The diagnosis of NBCCS was suspected based on the clinical examination, patient and family medical histories, and histopathological characteristics of the tumor. Radiotherapy was withheld. The diagnosis of NBCCS was confirmed by DNA testing, which revealed a novel mutation in the PTCH gene. This is the first report of an African-American child with MB diagnosed with NBCCS prior to radiotherapy. Although only a small number of patients with MB have NBCCS, the diagnosis must be considered because radiotherapy in such patients can lead to the formation of BCCs and other intracranial neoplasms within the irradiated field. This case emphasizes the importance of obtaining thorough family and patient medical histories and of carefully examining the patient and close relatives for signs of NBCCS to avoid the potentially devastating consequences of missing this diagnosis.","Desmoplastic medulloblastoma; Gorlin syndrome; Nevoid basal cell carcinoma syndrome; Pediatric neurosurgery; PTCH; Sonic hedgehog protein","protein Patched; African American; anamnesis; article; basal cell nevus syndrome; cancer radiotherapy; cancer susceptibility; case report; clinical feature; craniotomy; disease association; disease course; family history; follow up; gene mutation; histopathology; human; laminectomy; male; medulloblastoma; multiple cancer; nuclear magnetic resonance imaging; physical examination; preschool child; priority journal; treatment outcome; tumor diagnosis; tumor localization; African Americans; Basal Cell Nevus Syndrome; Brain Neoplasms; Cerebellar Neoplasms; Cerebral Ventricle Neoplasms; Child, Preschool; Cranial Fossa, Posterior; Humans; Magnetic Resonance Imaging; Male; Medulloblastoma; Mutation; Neoplasms, Multiple Primary; Receptors, Cell Surface",,"patched receptors; Receptors, Cell Surface",,,"Amlashi, S.F.A., Riffaud, L., Brassier, G., Morandi, X., Nevoid basal cell carcinoma syndrome: Relation with desmoplastic medulloblastoma in infancy. 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Case report (1997) J Neurosurg, 86, pp. 286-288; Oro, A.E., Higgins, K.M., Hu, Z., Bonifas, J.M., Epstein Jr., E.H., Scott, M.P., Basal cell carcinomas in mice overexpressing sonic hedgehog (1997) Science, 276, pp. 817-821; Ozturk, A., Oguz, K.K., Tumer, C., Balci, S., Neuroradiological findings in a mother and daughter with Gorlin syndrome (2003) Clin Dysmorphol, 12, pp. 145-146; Pramanik, P., Sharma, M.C., Mukhopadhyay, P., Singh, V.P., Sarkar, C., A comparative study of classical vs. desmoplastic medulloblastomas (2003) Neurol Ind, 51, pp. 27-34; Shanley, S., Ratcliffe, J., Hockey, A., Haan, E., Oley, C., Ravine, D., Nevoid basal cell carcinoma syndrome: Review of 118 affected individuals (1994) Am J Med Genet, 50, pp. 282-290; Stavale, J.N., Souza Cruz, J.R., Desmoplastic medulloblastoma: Histologic factors of prognosis (1993) Arq Neuro-Psiq, 51, pp. 487-490; Stavrou, T., Dubovsky, E.C., Reaman, G.H., Goldstein, A.M., Vezina, G., Intracranial calcifications in childhood medulloblastoma: Relation to nevoid basal cell carcinoma syndrome (2000) AJNR Am J Neuroradiol, 21, pp. 790-794; Takanashi, J., Fujii, K., Takano, H., Sugita, K., Kohno, Y., Empty sella syndrome in nevoid basal cell carcinoma syndrome (2000) Brain Dev, 22, pp. 272-274; Wicking, C., Shanley, S., Smyth, I., Gillies, S., Negus, K., Graham, S., Most germ-line mutations in the nevoid basal cell carcinoma syndrome lead to a premature termination of the PATCHED protein, and no genotype-phenotype correlations are evident (1997) Am J Hum Genet, 60, pp. 21-26; Young, J.L., Miller, R.W., Incidence of malignant tumors in US children (1975) J Pediatr, 86, pp. 254-258; Zedan, W., Robinson, P.A., High, A.S., A novel pleomorphism in the PTC gene allows easy identification of allelic loss in basal cell nevus syndrome lesions (2001) Diagn Mol Pathol, 10, pp. 41-45","Smith, J.L.; Division of Pediatric Neurosurgery; James Whitcomb Riley Hospital for Children; 702 Barnhill Drive Indianapolis, IN 46202, United States; email: jodlsmit@iupui.edu",,,,,,,,00223085,,JONSA,,"English","Journal of Neurosurgery",Article,Scopus "Cornetta K., Croop J., Dropcho E., Abonour R., Kieran M.W., Kreissman S., Reeves L., Erickson L.C., Williams D.A.","A pilot study of dose-intensified procarbazine, CCNU, vincristine for poor prognosis brain tumors utilizing fibronectin-assisted, retroviral-mediated modification of CD34+ peripheral blood cells with O6-methylguanine DNA methyltransferase",2006,"Cancer Gene Therapy",13,9,,886,895,,7,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-33747273605&partnerID=40&rel=R8.0.0","Department of Medical and Molecular Genetics, Indiana University School of Medicine, Indianapolis, IN, United States; Department of Medicine, Indiana University School of Medicine, Indianapolis, IN, United States; Department of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, IN, United States; Department of Pediatrics, Indiana University School of Medicine, Indianapolis, IN, United States; Department of Neurology, Indiana University School of Medicine, Indianapolis, IN, United States; Department of Pathology, Indiana University School of Medicine, Indianapolis, IN, United States; Department of Pediatric Oncology, Dana-Farber Cancer Institute, Children's Hospital, Boston, MA, United States; Department of Pediatrics, Duke University, Durham, NC, United States; Division of Experimental Hematology, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, OH, United States; Department of Pharmacology, Indiana University School of Medicine, Indianapolis, IN, United States; Department of Medical and Molecular Genetics, Indiana University School of Medicine, IB 130, 975 W Walnut Street, Indianapolis, IN 46202, United States","Administration of chemotherapy is often limited by myelosuppression. Expression of drug-resistance genes in hematopoietic cells has been proposed as a means to decrease the toxicity of cytotoxic agents. In this pilot study, we utilized a retroviral vector expressing methylguanine DNA methyltransferase (MGMT) to transduce hematopoietic progenitors, which were subsequently used in the setting of alkylator therapy (procarbazine, CCNU, vincristine (PCV)) for poor prognosis brain tumors. Granulocyte colony-stimulating factor (G-CSF)-mobilized peripheral blood progenitor cells were collected by apheresis and enriched for CD34+ expression. Nine subjects were infused with CD34+-enriched cells treated in a transduction procedure involving a 4-day exposure to cytokines with vector exposure on days 3 and 4. No major adverse event was related to the gene therapy procedure. Importantly, the engraftment kinetics of the treated product was similar to unmanipulated peripheral blood stem cells, suggesting that the ex vivo manipulation did not significantly reduce engrafting progenitor cell function. Gene-transduced cells were detected in all subjects. Although the level and duration was limited, patients receiving cells transduced using fibronectin 'preloaded' with virus supernatant appeared to show improved in vivo marking frequency. These findings demonstrate the feasibility and safety of utilizing MGMT-transduced CD34+ peripheral blood progenitor cells in the setting of chemotherapy. © 2006 Nature Publishing Group All rights reserved.","Brain tumors; Clinical trial; Methylguanine DNA methyltransferase; Retroviral gene transfer","alkylating agent; CD34 antigen; cytotoxic agent; fibronectin; granulocyte colony stimulating factor; lomustine; methylated DNA protein cysteine methyltransferase; procarbazine; retrovirus vector; vincristine; absence; adult; aged; apheresis; article; brain tumor; cancer combination chemotherapy; cell function; clinical article; clinical trial; dose response; drug safety; female; gene expression; gene transfer; genetic transduction; hematopoietic cell; histoplasmosis; human; human cell; lung diffusion capacity; lung fibrosis; lung function test; male; peripheral blood stem cell; pilot study; priority journal; pruritus; respiratory failure; side effect; stem cell; stem cell gene therapy; viral gene therapy; virus gene; Adolescent; Adult; Antigens, CD34; Antineoplastic Agents; Antineoplastic Combined Chemotherapy Protocols; Brain Neoplasms; Colony-Forming Units Assay; DNA Primers; Female; Fibronectins; Gene Therapy; Genetic Vectors; Granulocyte Colony-Stimulating Factor; Humans; Lomustine; Male; Middle Aged; O(6)-Methylguanine-DNA Methyltransferase; Peripheral Blood Stem Cell Transplantation; Pilot Projects; Polymerase Chain Reaction; Procarbazine; Retroviridae; Transduction, Genetic; Vincristine",,"fibronectin, 86088-83-7; lomustine, 13010-47-4; procarbazine, 366-70-1, 671-16-9; vincristine, 57-22-7; Antigens, CD34; Antineoplastic Agents; DNA Primers; Fibronectins; Granulocyte Colony-Stimulating Factor, 143011-72-7; Lomustine, 13010-47-4; O(6)-Methylguanine-DNA Methyltransferase, EC 2.1.1.63; Procarbazine, 671-16-9; Vincristine, 57-22-7",,"Amgen, Canada","Chu, E., DeVita, V.T., Principles of cancer management: Chemotherapy (2001) Cancer Principles and Practice of Oncology, pp. 289-305. , DeVita VT, Hellman S, Rosenberg SA (eds). Lippincott Williams and Wilkins: Philadelphia; Banerjee, D., Schweitzer, B.I., Volkenandt, M., Li, M.X., Waltham, M., Mineishi, S., Transfection with cDNA encoding Ser 31 or Ser 34 mutant human dihydrofolate reductase into Chinese hamster ovary and mouse marrow progenitor cells confers methotrexate resistance (1994) Gene, 139, pp. 269-274; Hock, R.A., Miller, A.D., Retrovirus-mediated transfer and expression of drug resistance genes in human haematopoietic progenitor cells (1986) Nature, 320, pp. 275-277; Sorrentino, B.P., Gene therapy to protect haematopoietic cells from cytotoxic cancer drugs (2002) Nat Rev Cancer, 2 (6), pp. 431-441; Banerjee, D., Bertino, J.R., Myeloprotection with drug-resistance genes (2002) Lancet Oncol, 3 (3), pp. 154-158; Hobin, D.A., Fairbairn, L.J., Genetic chemoprotection with mutant O6-alkylguanine-DNA-alkyltransferases (2002) Curr Gene Ther, 2 (1), pp. 1-8; Jansen, M., Sorg, U.R., Ragg, S., Flasshove, M., Seeber, S., Williams, D.A., Hematoprotection and enrichment of transduced cells in vivo after gene transfer of MGMT (P140K) into hematopoietic stem cells (2002) Cancer Gene Ther, 9 (9), pp. 737-746; Ragg, S., Xu-Welliver, M., Bailey, J., D'Souza, M., Cooper, R., Chandra, S., Direct reversal of DNA damage by mutant methyltransferase protein protects mice against dose-intensified chemotherapy and leads to in vivo selection of hematopoietic stem cells (2000) Cancer Res, 60 (18), pp. 5187-5195; Allay, J.A., Davis, B.M., Gerson, S.L., Human alkyltransferase-transduced murine myeloid progenitors are enriched in vivo by BCNU treatment of transplanted mice (1997) Exp Hematol, 25 (10), pp. 1069-1076; Williams, D.A., Smith, F.O., Progress in the use of gene transfer methods to treat genetic blood diseases (2000) Hum Gene Ther, 11 (15), pp. 2059-2066; Kohn, D.B., Sadelain, M., Dunbar, C., Bodine, D., Kiem, H.P., Candotti, F., American Society of Gene Therapy (ASGT) ad hoc subcommittee on retroviral-mediated gene transfer to hematopoietic stem cells (2003) Mol Ther: J Am Soc Gene Ther, 8 (2), pp. 180-187; Hesdorffer, C., Ayello, J., Ward, M., Kaubisch, A., Vahdat, L., Balmaceda, C., Phase I trial of retroviral-mediated transfer of the human MDR1 gene as marrow chemoprotection in patients undergoing high-dose chemotherapy and autologous stem-cell transplantation (1998) J Clin Oncol, 16 (1), pp. 165-172; Moscow, J.A., Huang, H., Carter, C., Hines, K., Zujewski, J., Cusack, G., Engraftment of MDR1 and NeoR gene-transduced hematopoietic cells after breast cancer chemotherapy (1999) Blood, 94 (1), pp. 52-61; Cowan, K.H., Moscow, J.A., Huang, H., Zujewski, J.A., O'Shaughnessy, J., Sorrentino, B., Paclitaxel chemotherapy after autologous stem-cell transplantation and engraftment of hematopoietic cells transduced with a retrovirus containing the multidrug resistance complementary DNA (MDR1) in metastatic breast cancer patients (1999) Clin Cancer Res, 5 (7), pp. 1619-1628; Devereux, S., Corney, C., Macdonald, C., Watts, M., Sullivan, A., Goldstone, A.H., Feasibility of multidrug resistance (MDR-1) gene transfer in patients undergoing high-dose therapy and peripheral blood stem cell transplantation for lymphoma (1998) Gene Ther, 5 (3), pp. 403-408; Abonour, R., Williams, D.A., Einhorn, L., Hall, K.M., Chen, J., Coffman, J., Efficient retrovirus-mediated transfer of the multidrug resistance 1 gene into autologous human long-term repopulating hematopoietic stem cells (2000) Nat Med, 6 (6), pp. 652-658; Pollok, K.E., In vivo protection of hematopoietic cells from alkylator-mediated DNA damage (2003) Curr Hematol Rep, 2 (4), pp. 341-347; Gerson, S.L., Clinical relevance of MGMT in the treatment of cancer (2002) J Clin Oncol, 20 (9), pp. 2388-2399; Jakacki, R.I., Siffert, J., Jamison, C., Velasquez, L., Allen, J.C., Dose-intensive, time-compressed procarbazine, CCNU, vincristine (PCV) with peripheral blood stem cell support and concurrent radiation in patients with newly diagnosed high-grade gliomas (1999) J Neuro-Oncol, 44 (1), pp. 77-83; Maze, R., Carney, J.P., Kelley, M.R., Glassner, B.J., Williams, D.A., Samson, L., Increasing DNA repair methyltransferase levels via bone marrow stem cell transduction rescues mice from the toxic effects of 1,3-bis(2-chloroethyl)-1- nitrosourea, a chemotherapeutic alkylating agent (1996) Proc Natl Acad Sci USA, 93 (1), pp. 206-210; Hawley, R.G., Lieu, F.H., Fong, A.Z., Hawley, T.S., Versatile retroviral vectors for potential use in gene therapy (1994) Gene Ther, 1 (2), pp. 136-138; Markowitz, D., Goff, S., Bank, A., Construction and use of a safe and efficient amphotropic packaging cell line (1988) Virology, 167 (2), pp. 400-406; Hanenberg, H., Xiao, X.L., Dilloo, D., Hashino, K., Kato, I., Williams, D.A., Colocalization of retrovirus and target cells on specific fibronectin fragments increases genetic transduction of mammalian cells (1996) Nat Med, 2, pp. 1-6; Hanenberg, H., Hashino, K., Konishi, H., Hock, R.A., Kato, I., Williams, D.A., Optimization of fibronectin-assisted retroviral gene transfer into human CD34+ hematopoietic cells (1997) Hum Gene Ther, 8 (18), pp. 2193-2206; Relander, T., Brun, A., Hawley, R.G., Karlsson, S., Richter, J., Retroviral transduction of human CD34+ cells on fibronectin fragment CH-296 is inhibited by high concentrations of vector containing medium (2001) J Gene Med, 3 (3), pp. 207-218; Chen, J., Reeves, L., Sanburn, N., Croop, J., Williams, D.A., Cornetta, K., Packaging cell line DNA contamination of vector supernatants: Implication for laboratory and clinical research (2001) Virology, 282 (1), pp. 186-197; Cornetta, K., Nguyen, N., Morgan, R.A., Muenchau, D.D., Hartley, J.W., Blaese, R.M., Infection of human cells with murine amphotropic replication-competent retroviruses (1993) Hum Gene Ther, 4 (5), pp. 579-588; Stewart, L.A., Chemotherapy in adult high-grade glioma: A systematic review and meta-analysis of individual patient data from 12 randomised trials (2002) Lancet, 359 (9311), pp. 1011-1018; Cairncross, G., MacDonald, D., Ludwin, S., Lee, D., Cascino, T., Buckner, J., Chemotherapy of anaplastic oligodendroglioma (1994) J Clin Oncol, 12, p. 2013; Wilson, C.A., Ng, T., Miller, A.E., Evaluation of recommendations for replication-competent retrovirus testing associated with use of retroviral vectors (1997) Hum Gene Ther, 8, pp. 869-874; Kiem, H.P., Andrews, R.G., Morris, J., Peterson, L., Heyward, S., Allen, J.M., Improved gene transfer into baboon marrow repopulating cells using recombinant human fibronectin fragment CH-296 in combination with interleukin-6, stem cell factor, FLT-3 ligand, and megakaryocyte growth and development factor (1998) Blood, 92 (6), pp. 1878-1886; Aiuti, A., Slavin, S., Aker, M., Ficara, F., Deola, S., Mortellaro, A., Correction of ADA-SCID by stem cell gene therapy combined with nonmyeloablative conditioning (2002) Science, 296, pp. 2410-2413; Williams, D.A., Maze, R., Kurpad, C., Pegg, A., Erickson, L.C., Protection of hematopoietic cells against combined O6-benzylguanine and chloroethylnitrosourea treatment by mutant forms of O6-methylguanine DNA methyltransferase (2000) Bone Marrow Transplant, 25 (2 SUPPL.), pp. S105-S109; Gerson, S.L., MGMT: Its role in cancer aetiology and cancer therapeutics (2004) Nat Rev Cancer, 4 (4), pp. 296-307; Davis, B.M., Reese, J.S., Koc, O.N., Lee, K., Schupp, J.E., Gerson, S.L., Selection for G156A 06-methylguanine DNA methyltransferase gene transduced hematopoietic progenitors and protection from lethality in mice treated with O6-benzylguanine and 1,3-bis(2-chloroethyl)-1-nitrosourea (1997) Cancer Res, 57, pp. 5093-5099; Koc, O.M., Reese, J.S., Davis, B.M., Liu, L., Majczenko, K.J., Gerson, S.L., DMGMT-transduced bone marrow infusion increases tolerance to 06-benzylguanine and 1,3-bis(2-chloroethyl)-1-nitrosourea and allows intensive therapy of 1,3-bis(2-chloroethyl)-1-nitrosourea-resistant human colon cancer xenografts (1999) Hum Gene Ther, 10, pp. 1021-1030; Maze, R., Kurpad, C., Pegg, A.E., Erickson, L.C., Williams, D.A., Retroviral mediated expression of the P140A but not P140A/G156A mutant form of O6-methylguanine DNA methyltransferase protects hematopoietic cells against O6-benzylguanine sensitization to chloroethylnitrosourea treatment (1999) J Pharmacol Exp Ther, 290, pp. 1467-1474; Ragg, S., Xu-Welliver, M., Bailey, J., D'Souza, M., Cooper, R., Chandra, S., Direct reversal of DNA damage by mutant methyltransferase protein protects mice against dose-intensified chemotherapy and leads to in vivo selection of hematopoietic stem cells (2000) Cancer Res, 60, pp. 5187-5195; Pollok, K., Hartwell, J., Braber, A., Cooper, R., Jansen, M., Ragg, S., Effective in vivo selection of human hematopoietic cells in a xenograft model using combined pharmacologic and genetic manipulations (2003) Hum Gene Ther, 14, pp. 1703-1714","Cornetta, K.; Department of Medical and Molecular Genetics; Indiana University School of Medicine; IB 130; 975 W Walnut Street Indianapolis, IN 46202, United States; email: kcornett@iupui.edu",,,,,,,,09291903,,CGTHE,10.1038/sj.cgt.7700963,"English","Cancer Gene Therapy",Article,Scopus "Lo S.S., Abdulrahman R., DesRosiers P.M., Fakiris A.J., Witt T.C., Worth R.M., Dittmer P.H., DesRosiers C.M., Frost S., Timmerman R.D.","The role of Gamma Knife Radiosurgery in the management of unresectable gross disease or gross residual disease after surgery in ependymoma",2006,"Journal of Neuro-Oncology",79,1,,51,56,,1,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-33745952557&partnerID=40&rel=R8.0.0","Department of Radiation Oncology, Indiana University Medical Center, 535 Barnhill Drive, Indianapolis, IN 46202, United States; Department of Neurosurgery, Indiana University Medical Center, 535 Barnhill Drive, Indianapolis, IN 46202, United States; Department of Radiation Oncology, Univ. of Texas Southwestern Medical School, Dallas, TX, United States; Indiana Lions Gamma Knife Center, Indianapolis, IN, United States","Purpose/Objective: To evaluate the efficacy and the toxicity of Gamma Knife (GK)-based stereotactic radiosurgery (SRS) in the management of gross disease in ependymoma. Materials and methods: Eight patients with 13 ependymomas were treated with GK-based SRS in our institution for gross disease. Five patients were treated for recurrent disease that developed after surgery and external beam radiotherapy (EBRT), two received SRS to the gross disease after surgery and EBRT, and one received SRS alone (in a 1.3 year old child). Median EBRT dose was 54.4 Gy (range 50-55.8 Gy). Median SRS dose was 14 Gy (range 12-20 Gy). Seven of eight (87.5%) patients had SRS to a single lesion and one of eight (12.5%) patients had treatment to six tumors in three different sessions. Results: The median follow up was 3 0.2 months (range 8-65.4 months). Out of the eight patients treated with SRS, six (75%) were alive, four (50%) were alive with no recurrence, two (25%) were alive with recurrence, and two (25%) died of recurrent disease. Both patients treated with SRS as a boost were alive and without recurrence. Out of the five patients who received SRS as salvage treatment, three (60%) were alive, two (40%) were alive without recurrence, two (40%) developed distant failure, and three (60%) had in-field control. Two patients who received SRS to their brainstem lesions developed symptoms related to radionecrosis and were successfully treated with steroid with good control of symptoms. Conclusions: GK-based SRS appears to be a feasible and safe treatment modality for patients with ependymoma with unresectable gross disease or gross residual disease after surgery. SRS provides reasonable local control but out-of-field tumor progression remains an issue. For patients who receive SRS as a boost, the local control appears to be excellent. © Springer Science+Business Media, Inc. 2006.","Ependymoma; Gross disease; Radiosurgery","cisplatin; cyclophosphamide; etoposide; oxygen; steroid; vincristine; adolescent; adult; article; brain stem tumor; brain surgery; cancer chemotherapy; cancer control; cancer mortality; cancer survival; child; clinical article; disease free survival; ependymoma; external beam radiotherapy; feasibility study; female; follow up; gamma knife radiosurgery; human; hyperbaric oxygen; Kaplan Meier method; male; nerve fiber; nuclear magnetic resonance imaging; overall survival; patient safety; radiation necrosis; recurrent cancer; retrospective study; salvage therapy; stereotaxic surgery; steroid therapy; surgical approach; surgical technique; symptomatology; treatment failure; treatment outcome; treatment response; tumor growth; Adolescent; Adult; Brain Neoplasms; Child; Child, Preschool; Ependymoma; Female; Humans; Infant; Male; Neoplasm Recurrence, Local; Neoplasm, Residual; Radiosurgery; Survival Analysis; Survival Rate; Treatment Outcome",,"cisplatin, 15663-27-1, 26035-31-4, 96081-74-2; cyclophosphamide, 50-18-0; etoposide, 33419-42-0; oxygen, 7782-44-7; vincristine, 57-22-7","B-model Leksell Gamma Knife Unit, Elekta, United States","Elekta, United States","Foreman, N.K., Love, S., Thorne, R., Intracranial ependymomas: Analysis of prognostic factors in a population-based series (1996) Pediatr Neurosurg, 24, pp. 119-125; Perilongo, G., Massimino, M., Sotti, G., Belfontali, T., Masiero, L., Rigobello, L., Garre, L., Madon, E., Analyses of prognostic factors in a retrospective review of 92 children with ependymoma: Italian Pediatric Neuro-oncology Group (1997) Med Pediatr Oncol, 29, pp. 79-85; Horn, B., Heideman, R., Geyer, R., Pollack, I., Packer, R., Goldwein, J., Tomita, T., Russo, C., A multi-institutional retrospective study of intracranial ependymoma in children: Identification of risk factors (1999) J Pediatr Hematol Oncol, 21, pp. 203-211; Sutton, L.N., Goldwein, J., Perilongo, G., Lang, B., Schut, L., Rorke, L., Packer, R., Prognostic factors in childhood ependymomas (1990) Pediatr Neurosurg, 16, pp. 57-65; Pollack, I.F., Gerszten, P.C., Martinez, A.J., Lo, K.H., Shultz, B., Albright, A.L., Janosky, J., Deutsch, M., Intracranial ependymomas of childhood: Long-term outcome and prognostic factors (1995) Neurosurg, 37, pp. 655-666; Rousseau, P., Habrand, J.L., Sarrazin, D., Kalifa, C., Terrier-Lacombe, M.J., Rekacewicz, C., Rey, A., Treatment of intracranial ependymomas of children: Review of a 15-year experience (1994) Int J Radiat Biol Phys, 28, pp. 381-386; Robertson, P.L., Zeltzer, P.M., Boyett, J.M., Rorke, L.B., Allen, J.C., Geyer, J.R., Stanley, P., Wisoff, J., Survival and prognostic factors following radiation therapy and chemotherapy for ependymomas in children: A report of the Children's Cancer Group (1998) J Neurosurg, 88, pp. 695-703; Needle, M.N., Goldwein, J.W., Grass, J., Cnaan, A., Bergman, I., Molloy, P., Sutton, L., Phillips, P.C., Adjuvant chemotherapy for the treatment of intracranial ependymoma of childhood (1997) Cancer, 80, pp. 341-347; Nazar, G.B., Hoffman, H.J., Becker, L.E., Jenkin, D., Humphreys, R.P., Hendrick, E.B., Infratentorial ependymomas in childhood: Prognostic factors and treatment (1990) J Neurosurg, 72, pp. 408-417; Healey, E.A., Barnes, P.D., Kupsky, W.J., Scott, R.M., Sallan, S.E., Black, P.M., Tarbell, N.J., The prognostic significance of postoperative residual tumor in ependymoma (1991) Neurosurgery, 28, pp. 666-671; Horn, B., Heideman, R., Geyer, R., Pollack, I., Packer, R., Goldwein, J., Tomita, T., Russo, C., A multi-institutional retrospective study of intracranial ependymoma in children: Identification of risk factors (1999) J Pediatr Hematol Oncol, 21, pp. 203-211; Sanford, R.A., Gajjar, A., Ependymomas (1997) Clin Neurosurg, 44, pp. 559-570; Merchant, T.E., Haida, T., Wang, M.H., Finlay, J.L., Leibel, S.A., Anaplastic ependymoma: Treatment of pediatric patients with or without craniospinal radiation therapy (1997) J Neurosurg, 86, pp. 943-949; Vanuytsel, L.J., Bessell, E.M., Ashley, S.E., Bloom, H.J., Brada, M., Intracranial ependymoma: Long-term results of a policy of surgery and radiotherapy (1992) Int J Radiat Oncol Biol Phys, 23, pp. 313-319; Marks, J.E., Adler, S.J., A comparative study of ependymomas by site of origin (1982) Int J Radiat Oncol Biol Phys, 8, pp. 37-43; Goldwein, J.W., Leahy, J.M., Packer, R.J., Sutton, L.N., Curran, W.J., Rorke, L.B., Schut, L., D'Angio, G.J., Intracranial ependymomas in children (1990) Int J Radiat Oncol Biol Phys, 19, pp. 1497-1502; Kovnar, E., Curran, W., Tomita: Hyperfractionated irradiation for childhood ependymoma: Improved local control in subtotally resected tumors (1998) Childs Nerv Syst, 14, p. 489. , (abstract); Merchant, T.E., Mulhern, R.K., Krasin, M.J., Kun, L.E., Williams, T., Li, C., Xiong, X., Sanford, R.A., Preliminary results from a phase II trial of conformal radiation therapy and evaluation of radiation-related CNS effects for pediatric patients with localized ependymoma (2004) J Clin Oncol, 22 (15), pp. 3156-3162; Aggarwal, R., Yeung, D., Kumar, P., Muhlbauer, M., Kun, L.E., Efficacy and feasibility of stereotactic radiosurgery in the primary management of unfavorable pediatric ependymoma (1997) Radiother Oncol, 43 (3), pp. 269-273; Mansur, D.B., Drzymala, R.E., Rich, K.M., Klein, E.E., Simpson, J.R., The efficacy of stereotactic radiosurgery in the management of intracranial ependymoma (2004) J Neurooncol, 66 (1-2), pp. 187-190; Hodgson, D.C., Goumnerova, L.C., Loeffler, J.S., Dutton, S., Black, P.M., Alexander III, E., Xu, R., Tarbell, N.J., Radiosurgery in the management of pediatric brain tumors (2001) Int J Radiat Oncol Biol Phys, 50 (4), pp. 929-935; Merchant, T.E., Current management of childhood ependymoma (2002) Oncology, 16 (5), pp. 629-642. , (Williston Park) 644; Hirato, M., Nakamura, M., Inoue, H.K., Ohye, C., Hirato, J., Shibazaki, T., Andou, Y., Gamma knife radiosurgery for the treatment of brainstem tumors (1995) Stereotact Funct Neurosurg, 64 (SUPPL. 1), pp. 32-41; Loeffler, J.S., Rossitch Jr., E., Siddon, R., Moore, M.R., Rockoff, M.A., Alexander III, E., Role of stereotactic radiosurgery with a linear accelerator in treatment of intracranial arteriovenous malformations and tumors in children (1990) Pediatrics, 85, pp. 774-782; Grabb, P.A., Lunsford, L.D., Albright, A.L., Kondziolka, D., Flickinger, J.C., Stereotactic radiosurgery for glial neoplasms of childhood (1996) Neurosurgery, 38 (4), pp. 696-701; Jawahar, A., Kondziolka, D., Flickinger, J.C., Lunsford, L.D., Adjuvant stereotactic radiosurgery for anaplastic ependymoma (1999) Stereotact Funct Neurosurg, 73 (1-4), pp. 23-30; Stafford, S.L., Pollock, B.E., Foote, R.L., Gorman, D.A., Nelson, D.F., Schomberg, P.J., Stereotactic radiosurgery for recurrent ependymoma (2000) Cancer, 88 (4), pp. 870-875","Lo, S.S.; Department of Radiation Oncology; Indiana University Medical Center; 535 Barnhill Drive Indianapolis, IN 46202, United States; email: slo@iupui.edu",,,,,,,,0167594X,,JNODD,10.1007/s11060-005-9112-y,"English","Journal of Neuro-Oncology",Article,Scopus "McGarvey C.K., Applegate K., Lee N.D., Sokol D.K.","False-positive metaiodobenzylguanidine scan for neuroblastoma in a child with opsoclonus-myoclonus syndrome treated with adrenocorticotropic hormone (ACTH)",2006,"Journal of Child Neurology",21,7,,606,610,,1,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-33748068452&partnerID=40&rel=R8.0.0","Department of Neurology, Riley Hospital for Children, Indiana University School of Medicine, Indianapolis, IN, United States; Department of Radiology, Riley Hospital for Children, Indiana University School of Medicine, Indianapolis, IN, United States; Department of Hematology/Oncology, Riley Hospital for Children, Indiana University School of Medicine, Indianapolis, IN, United States; 575 West Drive XE 040, Indianapolis, IN 46202, United States","We describe the case of a 2-year-old girl with opsoclonusmyoclonus syndrome treated with chronic adrenocorticotropic hormone (ACTH) in which a metaiodobenzylguanidine scan showed abnormal radiotracer uptake in the left adrenal gland region, interpreted as the site of an occult neuroblastoma. As this finding was not corroborated by previous or subsequent metaiodobenzylguanidine scans or by computed tomography (CT) or magnetic resonance imaging (MRI), we attribute the finding to being a false-positive result from adrenal hyperplasia owing to chronic use of ACTH and not to neuroblastoma. Metaiodobenzylguanidine scintigraphy is an extremely important nuclear medicine examination tool used for the evaluation and staging of pediatric neuroblastoma. We highlight the need for cautious interpretation of metaiodobenzylguanidine as a screening tool for neuroblastoma in patients treated with ACTH.",,"(3 iodobenzyl)guanidine i 125; (3 iodobenzyl)guanidine i 131; corticotropin; immunoglobulin; rituximab; adrenal hyperplasia; article; ataxia; brain scintiscanning; cancer scintiscanning; cancer screening; cancer staging; case report; chronic drug administration; computer assisted tomography; contrast enhancement; differential diagnosis; drug dose reduction; drug uptake; false positive result; female; human; hypertension; hypokalemia; myoclonus; neuroblastoma; nuclear magnetic resonance imaging; opsoclonus; preschool child; priority journal; 3-Iodobenzylguanidine; Adrenal Gland Neoplasms; Adrenocorticotropic Hormone; Child, Preschool; False Positive Reactions; Female; Hormones; Humans; Neuroblastoma; Opsoclonus-Myoclonus Syndrome; Radiopharmaceuticals",,"(3 iodobenzyl)guanidine i 125, 74075-13-1; (3 iodobenzyl)guanidine i 131, 77679-27-7; corticotropin, 11136-52-0, 9002-60-2, 9061-27-2; immunoglobulin, 9007-83-4; rituximab, 174722-31-7; 3-Iodobenzylguanidine, 77679-27-7; Adrenocorticotropic Hormone, 9002-60-2; Hormones; Radiopharmaceuticals",,,"Lott, I., Kinsbourne, M., Myoclonic encephalopathy of infants (1986) Adv Neurol, 43, pp. 127-136; Shapiro, B., Shulkin, B.L., Hutchinson, R.J., Locating neuroblastoma in the opsoclonus-myoclonus syndrome (1994) J Nucl Biol Med, 38, pp. 545-555; Bray, P.F., Ziter, F.A., Lahey, M.E., Myers, G.G., The coincidence of neuroblastoma and acute cerebellar encephalopathy (1969) Trans Am Neurol Assoc, 94, pp. 106-109; Baker, M.E., Kirks, D.R., Korobkin, M., The association of neuroblastoma and myoclonic encephalopathy: An imaging approach (1985) Pediatr Radiol, 15, pp. 184-190; Koh, P.S., Raffensperger, J.G., Berry, S., Long-term outcome in children with opsoclonus-myoclonus and ataxia and coincident neuroblastoma (1994) J Pediatr, 125, pp. 712-716; Wolff, M., Schoning, M., Niemann, G., Krageloh-Mann, I., Late detection of neuroblastoma in a patient with prolonged cerebellar ataxia without opsoclonus (2001) Neuropediatrics, 32, pp. 101-103; Gelfand, M.J., Elgazzar, A.H., Kriss, V.M., Iodine-123-MIBG SPECT versus planar imaging in children with neural crest tumors (1994) J Nucl Med, 35, pp. 1753-1757; Hoefnagel, C.A., Voute, P.A., de Kraker, J., Marcuse, H.R., Radionuclide diagnosis and therapy of neural crest tumors using iodine-131 metaiodobenzylguanidine (1987) J Nucl Med, 28, pp. 308-314; Feine, U., Muller-Schauenburg, W., Treuner, J., Klingebiel, T., Metaiodobenzylguanidine (MIBG) labeled with 123I/131I in neuroblastoma diagnosis and follow-up treatment with a review of the diagnostic results of the International Workshop of Pediatric Oncology held in Rome, September 1986 (1987) Med Pediatr Oncol, 15, pp. 181-187; Snyder, H.M., Evans, A.E., Raney, R.B., Pediatric oncology (1986) Campbell's Urology, pp. 2265-2276. , in Philadelphia, Saunders; Ziegelbaum, M.M., Kay, R., Rothner, A.D., Lorig, R., The association of neuroblastoma with myoclonic encephalopathy of infants: The use of magnetic resonance as an imaging modality (1988) J Urol, 139, pp. 81-82; Boltshauser, E., Deonna, T., Hirt, H.R., Myoclonic encephalopathy of infants or ""dancing eyes syndrome."" Report of 7 cases with long-term follow-up and review of the literature (cases with and without neuroblastoma) (1979) Helv Paediatr Acta, 34, pp. 119-133; Farrelly, C., Daneman, A., Chan, H.S., Martin, D.J., Occult neuroblastoma presenting with opsomyoclonus: Utility of computed tomography (1984) AJR Am J Roentgenol, 142, pp. 807-810; Lumbroso, J.D., Guermazi, F., Hartmann, O., Meta-iodobenzylguanidine (mIBG) scans in neuroblastoma: Sensitivity and specificity, a review of 115 scans (1988) Prog Clin Biol Res, 271, pp. 689-705; IVth International Workshop in Pediatric Oncology, ""The role of MIBG in therapy, diagnosis, and monitoring of neuroblastoma"" Rome, Italy, September 22 and 23, 1986 (1987) Proceedings. Med Pediatr Oncol, 15, pp. 226-228. , International Society of Pediatric Oncology, Italian Society of Radiology and Nuclear Medicine, Italian Society of Biology and Nuclear Medicine, and Associazione Genitori Oncologia Pediatrica; Leung, A., Shapiro, B., Hattner, R., Specificity of radioiodinated MIBG for neural crest tumors in childhood (1997) J Nucl Med, 38, pp. 1352-1357; Stewart, R.E., Grossman, D.M., Shulkin, B.L., Shapiro, B., Iodine-131 metaiodobenzylguanidine uptake in infantile myofibromatosis (1989) Clin Nucl Med, 14, pp. 344-346; Feggi, L., Degli Uberti, E., Pansini, G.C., Pitfalls in scintigraphic detection of neuroendocrine tumours (1992) Eur J Nucl Med, 19, pp. 214-218; Horne, T., Glaser, B., Krausz, Y., Unusual causes of I-131 metaiodobenzylguanidine uptake in non-neural crest tissue (1991) Clin Nucl Med, 16, pp. 239-242; Von Moll, L., McEwan, A.J., Shapiro, B., Iodine-131 MIBG scintigraphy of neuroendocrine tumors other than pheochromocytoma and neuroblastoma (1987) J Nucl Med, 28, pp. 979-988; Dessner, D.A., DiPietro, M.A., Shulkin, B.L., MIBG detection of hepatic neuroblastoma: Correlation with CT, US and surgical findings (1993) Pediatr Radiol, 23, pp. 276-280; Burt, M.G., Allen, B., Conaglen, J.V., False positive 131I-metaiodobenzylguanidine scan in the postoperative assessment of malignant phaeochromocytoma secondary to medullary hyperplasia (2002) N Z Med J, 115, p. 18; Boersma, H.H., Wensing, J.W., Kho, T.L., Compensatory uptake of I-123 MIBG in the contralateral adrenal gland after removal of a pheochromocytoma (2002) Clin Nucl Med, 27, pp. 113-116; Kusher, B.H., Neuroblastoma: A disease requiring a multitude of imaging studies (2004) J Nucl Med, 45, pp. 1172-1188; Olivier, P., Colarinha, P., Fettich, J., Guidelines for radioiodinated MBG scintigraphy in children (2003) Eur J Nucl Med Mol Imaging, 30, pp. 39-44; Liebling, M.S., Starc, T.J., McAlister, W.H., ACTH induced adrenal enlargement in infants treated for infantile spasms and acute cerebellar encephalopathy (1993) Pediatr Radiol, 23, pp. 454-456; Gumbinas, M., Gratz, E.S., Johnston, G.S., Schwartz, A.D., Positive gallium scan in the syndrome of opsoclonus-myoclonus treated with adrenocorticotropic hormone (1984) Cancer, 54, pp. 815-816","Sokol, D.K.575 West Drive XE 040 Indianapolis, IN 46202, United States; email: dksokol@iupui.edu",,,,,,,,08830738,,JOCNE,10.1177/08830738060210070801,"English","Journal of Child Neurology",Article,Scopus "Lo S.S., Henderson M.A., Fakiris A.J., Tinnel B.A.","Efaproxiral (RSR13) and whole brain radiation therapy for brain metastases",2006,"American Journal of Oncology Review",5,6,,381,383,,,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-33745896847&partnerID=40&rel=R8.0.0","Department of Radiation Oncology, Indiana University Medical Center, Indianapolis, IN, United States; Department of Radiation Oncology, Indiana University Medical Center, 535 Barnhill Drive, Indianapolis, IN 46202, United States",[No abstract available],,"carbogen; efaproxiral; nicotinamide; oxygen; brain metastasis; breast cancer; cancer radiotherapy; cancer survival; cause of death; clinical trial; drug half life; follow up; human; hypoxemia; Karnofsky Performance Status; lung cancer; medical literature; neuroimaging; nonhuman; note; oxygen therapy; quality of life; questionnaire; unspecified side effect",,"carbogen, 8063-77-2; efaproxiral, 131179-95-8, 170787-99-2; nicotinamide, 11032-50-1, 98-92-0; oxygen, 7782-44-7","rsr 13",,"Suh, J.H., Stea, B., Nabid, A., Phase III study of efaproxiral as an adjunct to whole-brain radiation therapy for brain metastases (2006) J Clin Oncol, 24, pp. 106-114; Hall, E.J., The oxygen effect and reoxygenation (2000) Radiobiology for the Radiologist. 5th Ed., pp. 91-111. , Philadelphia, Pa: Lippincott Williams & Wilkins; Rampling, R., Cruickshank, G., Lewis, A.D., Direct measurement of pO2 distribution and bioreductive enzymes in human malignant brain tumors (1994) Int J Radiat Oncol Biol Phys, 29, pp. 427-431; Varlotto, J., Stevenson, M.A., Anemia, tumor hypoxemia, and the cancer patient (2005) Int J Radiat Oncol Biol Phys, 63, pp. 25-36; Randad, R.S., Mahran, M.A., Mehanna, A.S., Allosteric modifiers of hemoglobin. 1. Design, synthesis, testing, and structure-allosteric activity relationship of novel hemoglobin oxygen affinity decreasing agents (1991) J Med Chem, 34, pp. 752-757; Safo, M.K., Moure, C.M., Burnett, J.C., High-resolution crystal structure of deoxy hemoglobin complexed with a potent allosteric effector (2001) Protein Sci, 10, pp. 951-957; Stryer, L., Portrait of an allosteric protein (1995) Biochemistry. 4th Ed., pp. 147-180. , New York, NY: WH Freeman and Company; Amorino, G.P., Lee, H., Holburn, G.E., Enhancement of tumor oxygenation and radiation response by the allosteric effector of hemoglobin, RSR13 (2001) Radiat Res, 156, pp. 294-300; Eichelbronner, O., Sielenkamper, A., D'Almeida, M., Effects of FI(O(2)) on hemodynamic responses and O(2) transport during RSR13-induced reduction in P(50) (1999) Am J Physiol, 277, pp. H290-H298; Rockwell, S., Kelley, M., RSR13, a synthetic allosteric modifier of hemoglobin, as an adjunct to radiotherapy: Preliminary studies with EMT6 cells and tumors and normal tissues in mice (1998) Radiat Oncol Investig, 6, pp. 199-208; Sarraf-Yazdi, S., Sheng, H., Grocott, H.P., Effects of RSR13, a synthetic allosteric modifier of hemoglobin, alone and in combination with dizocilpine, on outcome from transient focal cerebral ischemia in the rat (1999) Brain Res, 826, pp. 172-180; Grinberg, O.Y., Miyake, M., Hou, H., The dose-dependent effect of RSR13, a synthetic allosteric modifier of hemoglobin, on physiological parameters and brain tissue oxygenation in rats (2003) Adv Exp Med Biol, 530, pp. 287-296; Hou, H., Khan, N., O'Hara, J.A., Increased oxygenation of intracranial tumors by efaproxyn (efaproxiral), an allosteric hemoglobin modifier: In vivo EPR oximetry study (2005) Int J Radiat Oncol Biol Phys, 61, pp. 1503-1509; Hou, H., Khan, N., O'Hara, J.A., Effect of RSR13, an allosteric hemoglobin modifier, on oxygenation in murine tumors: An in vivo electron paramagnetic resonance oximetry and bold MRI study (2004) Int J Radiat Oncol Biol Phys, 59, pp. 834-843; Kavanagh, B.D., Khandelwal, S.R., Schmidt-Ullrich, R.K., A phase I study of RSR13, a radiation-enhancing hemoglobin modifier: Tolerance of repeated intravenous doses and correlation of pharmacokinetics with pharmacodynamics (2001) Int J Radiat Oncol Biol Phys, 49, pp. 1133-1139; Stea, B., Suh, J.H., Boyd, A.P., Whole-brain radiotherapy with or without efaproxiral for the treatment of brain metastases: Determinants of response and its prognostic value for subsequent survival (2006) Int J Radiat Oncol Biol Phys, 64, pp. 1023-1030; Nieder, C., Berberich, W., Schnabel, K., Tumor-related prognostic factors for remission of brain metastases after radiotherapy (1997) Int J Radiat Oncol Biol Phys, 39, pp. 25-30; Goodman, K.A., Sneed, P.K., McDermott, M.W., Relationship between pattern of enhancement and local control of brain metastases after radiosurgery (2001) Int J Radiat Oncol Biol Phys, 50, pp. 139-146; Andrews, D.W., Scott, C.B., Sperduto, P.W., Whole brain radiation therapy with or without stereotactic radiosurgery boost for patients with one to three brain metastases: Phase III results of the RTOG 9508 randomised trial (2004) Lancet, 363, pp. 1665-1672","Lo, S.S.; Department of Radiation Oncology; Indiana University Medical Center; 535 Barnhill Drive Indianapolis, IN 46202, United States; email: slo@iupui.edu",,,,,,,,15429520,,,,"English","American Journal of Oncology Review",Note,Scopus "Bedano P.M., Bonnin J., Einhorn L.H.","Metachronous intracranial germinoma in a patient with a previous primary mediastinal seminoma",2006,"Journal of Clinical Oncology",24,15,,2386,2387,,,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-33744817086&partnerID=40&rel=R8.0.0","Indiana University, School of Medicine, Indianapolis, IN, United States",[No abstract available],,"alpha fetoprotein; bleomycin; bromocriptine; chorionic gonadotropin; cisplatin; etoposide; ifosfamide; vinblastine; antineoplastic agent; adult; article; case report; combination chemotherapy; computer assisted tomography; fatigue; germ cell tumor; gynecomastia; headache; hormone substitution; human; intracranial tumor; laboratory test; libido disorder; lymph node metastasis; male; mediastinal seminoma; mediastinum tumor; multiple cycle treatment; nuclear magnetic resonance imaging; physical examination; polydipsia; polyuria; positron emission tomography; priority journal; prolactinoma; risk factor; seminoma; spinal cord metastasis; testis atrophy; tumor biopsy; tumor localization; visual impairment; brain tumor; multimodality cancer therapy; neurosurgery; radiotherapy; second cancer; tumor recurrence; Adult; Antineoplastic Combined Chemotherapy Protocols; Bleomycin; Brain Neoplasms; Cisplatin; Combined Modality Therapy; Etoposide; Germinoma; Humans; Ifosfamide; Male; Mediastinal Neoplasms; Neoplasm Recurrence, Local; Neoplasms, Second Primary; Neurosurgical Procedures; Radiotherapy; Seminoma; Vinblastine",,"bleomycin, 11056-06-7; bromocriptine, 25614-03-3; chorionic gonadotropin, 9002-61-3; cisplatin, 15663-27-1, 26035-31-4, 96081-74-2; etoposide, 33419-42-0; ifosfamide, 3778-73-2; vinblastine, 865-21-4; Bleomycin, 11056-06-7; Cisplatin, 15663-27-1; Etoposide, 33419-42-0; Ifosfamide, 3778-73-2; Vinblastine, 865-21-4",,,"Collins, D.H., Pugh, R.C.B., Classification and frequency of testicular tumors (1984) Br J Urol, 36, pp. 1-11; Nichols, C.R., Heerena, N.A., Einhorn, L.H., Klinefelter syndrome associated with mediastinal germ cell neoplasms (1987) J Clin Oncol, 5, pp. 1290-1294; Hainsworth, J.D., Greco, A., Extragonadal germ cell tumors and unrecognized germ cell tumors (1992) Semin Oncol, 19, p. 197; Glenn, O.A., Barkovich, A.J., Intracranial germ cell tumors: A comprehensive review of proposed embryologic derivation (1996) Pediatr Neurosurg, 24, pp. 242-251; Strother, D.R., Pollack, I.F., Fisher, P.G., Tumors of the central nervous system in Pizzo PA (2002) Principles and Practice of Pediatric Oncology, p. 798. , Poplack DG eds, ed 4, Philadelphia, PA, Lippincott, Williams, and Wilkins; van Leeuwen, F.E., Stiggelbout, A., van den Belt-Dusebout, R.N., Second cancer risk following testicular cancer: A follow up study of 1,909 patients (1993) J Clin Oncol, 11, p. 415; Trentini, G.P., Maiorana, A., De Benedittis, A., Metachronous seminoma of the pineal region and right testis (1985) Appl Pathol, 3, pp. 129-133; Miyamoto, H., Moriyama, M., Fukushima, S., Retroperitoneal tumor eleven years after initial treatment of testicular cancer (1994) Urology, 43, pp. 116-117; Peat, D.S., Trowell, J.E., Testicular seminoma in a patient with pineal germinoma (1994) J Clin Pathol, 47, pp. 771-772; Lokich, J., Metachronous gonadal and extragonadal primary germ cell tumors: Two case reports (1994) Cancer Invest, 12, pp. 406-408; Hupperets, P.S.G.J., Defesche, H.F., Bruijckere, L.M., The role of chemotherapy in intracranial germinoma: A case report (1999) Ann Oncol, 10, pp. 723-726; Daniel, C., Fizazi, K., Culine, S., Metachronous gonadal and extragonadal primaries, or late relapse of germ cell tumor? (2001) Urol Oncol, 6, pp. 49-52; Benesch, M., Schereibmayer, N., Manfred, R., Mediastinal yolk sac tumor ten years after treatment of intracranial germinoma (2003) Med Pediatr Oncol, 40, pp. 54-56; Hisashi, I., Yoshio, M., Hisato, T., Mediastinal growing teratoma syndrome after cisplatin-based chemotherapy and radiotherapy for intracranial germinoma (2004) J Thorac Cardiovasc Surg, 127, pp. 291-293","Bedano, P.M.; Indiana University; School of Medicine Indianapolis, IN, United States",,,,,,,,0732183X,,JCOND,10.1200/JCO.2005.02.1576,"English","Journal of Clinical Oncology",Article,Scopus "Lo S.S., Chang E.L., Sloan A.E.","Role of stereotactic radiosurgery and fractionated stereotactic radiotherapy in the management of intracranial ependymoma",2006,"Expert Review of Neurotherapeutics",6,4,,501,507,,2,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-33646786401&partnerID=40&rel=R8.0.0","Department of Radiation Oncology, Indiana Lions Gamma Knife Center, Indiana University Medical Center, 535 Barnhill Drive, RT 041, Indianapolis, IN 46202, United States; Department of Radiation Oncology, University of Texas MD Anderson Cancer Center, 1515 Holcombe Blvd, Houston, TX 77030, United States; Department of Neurosurgery, University of South Florida, Tampa, FL 33612, United States; Division of Neuro-Oncology, H. Lee Moffitt Cancer Center and Research Institute, 12902 Magnolia Drive, Tampa, FL 33612, United States","Ependymoma accounts for 5-10% of all childhood CNS tumors and less than 5% of intracranial tumors in adults. Ependymomas typically have a sharp tumor-brain parenchyma interface and this characteristic lends itself well to stereotactic radiation delivery. Data on the use of stereotactic radiosurgery (SRS) and fractionated stereotactic radiotherapy (FSRT) for ependymoma in various settings have emerged over the past 10 years. SRS has been used in recurrent disease and as a boost after external beam radiation therapy. FSRT has been used in pediatric brain tumors and can potentially limit the long-term toxicities associated with radiation therapy by reducing the amount of normal brain parenchyma treated. Long-term follow-up is needed to determine the long-term efficacy and toxicities associated with these treatment modalities. © 2006 Future Drugs Ltd.","Ependymoma; Stereotactic radiosurgery; Stereotactic radiotherapy","brain tumor; cancer radiotherapy; cancer recurrence; cancer surgery; cancer survival; ependymoma; facial nerve paralysis; follow up; gamma knife radiosurgery; human; radiation dose fractionation; radiation necrosis; review; seizure; stereotaxic surgery; treatment planning; Brain Neoplasms; Ependymoma; Humans; Radiosurgery",,,,,"Foreman, N.K., Love, S., Thorne, R., Intracranial ependymomas: Analysis of prognostic factors in a population-based series (1996) Pediatr. Neurosurg., 24, pp. 119-125; Horn, B., Heideman, R., Geyer, R., A multi-institutional retrospective study of intracranial ependymoma in children: Identification of risk factors (1999) J. Pediatr. Hematol. Oncol., 21, pp. 203-211; Pollack, I.F., Gerszten, P.C., Martinez, A.J., Intracranial ependymomas of childhood: Long-term outcome and prognostic factors (1995) Neurosurgery, 37, pp. 655-666; Rousseau, P., Habrand, J., Sarrazin, D., Treatment of intracranial ependymomas of children: Review of a 15-year experience (1994) Int. J. Radiat. Biol. Phys., 28, pp. 381-386; Robertson, P.L., Zeltzer, P.M., Boyett, J.M., Survival and prognostic factors following radiation therapy and chemotherapy for ependymomas in children: A report of the Children's Cancer Group (1998) J. Neurosurg., 88, pp. 695-703; Perilongo, G., Massimino, M., Sotti, G., Analyses of prognostic factors in a retrospective review of 92 children with ependymoma: Italian Pediatric Neurooncology Group (1997) Med. Pediatr. Oncol., 29, pp. 79-85; Needle, M.N., Goldwein, J.W., Grass, J., Adjuvant chemotherapy for the treatment of intracranial ependymoma of childhood (1997) Cancer, 80, pp. 341-347; Merchant, T.E., Current management of childhood ependymoma (2002) Oncology, 6 (5), pp. 629-642; Sutton, L.N., Goldwein, J., Perilongo, G., Prognostic factors in childhood ependymomas (1990) Pediatr. Neurosurg., 16, pp. 57-65; Nazar, G.B., Hoffman, H.J., Becker, L.E., Infratentorial ependymomas in childhood: Prognostic factors and treatment (1990) J. Neurosurg., 72, pp. 408-417; Duffner, P.K., Krischer, J.P., Sanford, R.A., Prognostic factors in infants and very young children with intracranial ependymomas (1998) Pediatr. Neurosurg., 28, pp. 215-222; Merchant, T.E., Jenkins, J.J., Burger, P.C., Influence of tumor grade on time to progression after irradiation for localized ependymoma in children (2002) Int. J. Radiat. Oncol. Biol. 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Phys., 25 (3), pp. 557-561; Aggarwal, R., Yeung, D., Kumar, P., Efficacy and feasibility of stereotactic radiosurgery in the primary management of unfavorable pediatric ependymoma (1997) Radiother. Oncol., 43 (3), pp. 269-273; Mansur, D.B., Drzymala, R.E., Rich, K.M., The efficacy of stereotactic radiosurgery in the management of intracranial ependymoma (2004) J. Neurooncol., 66 (1-2), pp. 187-190; Hodgson, D.C., Goumnerova, L.C., Loeffler, J.S., Radiosurgery in the management of pediatric brain tumors (2001) Int. J. Radiat. Oncol. Biol. Phys., 50 (4), pp. 929-935; Abdulrahman, R., Lo, S.S., DesRosiers, P.M., The role of γ knife radiosurgery in the management of unresectable gross disease or gross residual disease after surgery in ependymoma (2005) Int. J. Radiat. Oncol. Biol. Phys., 63 (1 SUPPL.), pp. S273; Hirato, M., Nakamura, M., Inoue, H.K., γ knife radiosurgery for the treatment of brainstem tumors (1995) Stereotact. Funct. 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Phys., 61 (2), pp. 374-379","Lo, S.S.; Department of Radiation Oncology; Indiana Lions Gamma Knife Center; Indiana University Medical Center; 535 Barnhill Drive, RT 041 Indianapolis, IN 46202, United States; email: slo@iupui.edu",,,,,,,,14737175,,ERNXA,10.1586/14737175.6.4.501,"English","Expert Review of Neurotherapeutics",Review,Scopus "Zaloga G.P.","Parenteral nutrition in adult inpatients with functioning gastrointestinal tracts: assessment of outcomes",2006,"Lancet",367,9516,,1101,1111,,17,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-33645738342&partnerID=40&rel=R8.0.0","Methodist Research Institute, Indiana University School of Medicine, 1812 North Capitol Avenue, IN 46202, United States","Malnutrition is a common comorbidity that places inpatients at risk of complications, infections, long length of stay, higher costs, and increased mortality. Thus, nutrition support has become an important therapeutic adjunctive to the care of these patients. For patients unable to feed themselves, nutrition can be delivered via the parenteral or enteral routes. The formulations used to deliver nutrients and the route of nutrient delivery, absorption, and processing differ substantially between parenteral and enteral nutrition. Over the past two decades, many randomised clinical trials have assessed the effects of parenteral versus enteral nutrition on outcomes (ie, complications, infections, length of stay, costs, mortality) in diverse inpatient populations. From a search of medical publications, studies were selected that assessed important clinical outcomes of parenteral versus enteral feeding or intravenous fluids in patients with trauma/burn injuries, surgery, cancer, pancreatic disease, inflammatory bowel disease, critical illness, liver failure, acute renal failure, and organ transplantation. Our goal was to determine the optimum route of feeding in these patient groups. The available evidence lends support to the use of enteral over parenteral feeding in inpatients with functioning gastrointestinal tracts. © 2006 Elsevier Ltd. All rights reserved.",,"brain injury; caloric intake; cancer; clinical trial; enteric feeding; enteritis; fluid therapy; gastrointestinal tract function; health care cost; human; injury; kidney failure; length of stay; liver failure; medical assessment; mortality; nonhuman; nutritional support; organ transplantation; outcome assessment; pancreas disease; parenteral nutrition; patient care; priority journal; review; adult; animal; controlled clinical trial; economics; hospitalization; nutritional requirement; postoperative period; randomized controlled trial; treatment outcome; Adult; Animals; Enteral Nutrition; Hospital Mortality; Hospitalization; Humans; Length of Stay; Nutritional Requirements; Parenteral Nutrition; Postoperative Period; Randomized Controlled Trials; Treatment Outcome",,,,,"Buzby, G., Mullen, J., Matthews, D., Hobbs, C., Rosato, E., Prognostic nutritional index in gastrointestinal surgery (1980) Am J Surg, 139, pp. 160-167; Detsky, A., Baker, J., O'Rourke, K., Predicting nutrition-associated complications for patients undergoing gastrointestinal surgery (1987) JPEN J Parenter Enteral Nutr, 11, pp. 440-446; Middleton, M., Nazarenko, G., Nivison-Smith, I., Smerdely, P., Prevalence of malnutrition and 12-month incidence of mortality in two Sydney teaching hospitals (2001) Intern Med J, 31, pp. 455-461; Robinson, G., Goldstein, M., Levine, G., Impact of nutritional status on DRG length of stay (1987) JPEN J Parenter Enteral Nutr, 11, pp. 49-52; Marik, P., Zaloga, G., Early enteral nutrition in acutely ill patients-a systematic review (2001) Crit Care Med, 29, pp. 2264-2270; AGA technical review on parenteral nutrition (2001) Gastroenterology, 121, pp. 970-1001. , American Gastroenterological Association clinical practice and practice economics committee; Zaloga, G., Siddiqui, R., Biologically active dietary peptides (2004) Mini Rev Med Chem, 4, pp. 815-821; Roberts, P., Zaloga, G., Dietary bioactive peptides (1994) New Horiz, 2, pp. 237-243; Furst, P., Stehle, P., Are intravenous amino acid solutions unbalanced? 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A randomized clinical trial (2000) Crit Care Med, 28, pp. 3606-3611; Basttistella, F., Widergren, J., Anderson, J., Siepler, J., Weber, J., MacColl, K., A prospective randomized trial of intravenous fat emulsion administration in trauma victims requiring total parenteral nutrition (1997) J Trauma, 43, pp. 52-60","Zaloga, G.P.; Methodist Research Institute; Indiana University School of Medicine; 1812 North Capitol Avenue IN 46202, United States; email: gzaloga@clarian.org",,,,,,,,01406736,,LANCA,10.1016/S0140-6736(06)68307-4,"English","Lancet",Review,Scopus "Wagner J.D.","Fluorodeoxyglucose positron emission tomography for melanoma staging: Refining the indications",2006,"Annals of Surgical Oncology",13,4,,444,446,,2,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-33644976599&partnerID=40&rel=R8.0.0","Department of Plastic Surgery, Indiana University School of Medicine, Indianapolis, IN, United States; Wagner and Associates Plastic and Reconstructive Surgery Consultants, 8040 Clearvista Parkway, Indianapolis, IN 46256, United States",[No abstract available],,"fluorodeoxyglucose f 18; technetium; advanced cancer; bone metastasis; bone scintiscanning; brain metastasis; cancer staging; computer assisted tomography; decision making; diagnostic accuracy; diagnostic error; drug specificity; drug uptake; early cancer; editorial; human; liver metastasis; lung metastasis; lymph node metastasis; melanoma; metastasis; nuclear magnetic resonance imaging; patient selection; positron emission tomography; preoperative evaluation; sentinel lymph node; spiral computer assisted tomography; Decision Making; Fluorodeoxyglucose F18; Humans; Melanoma; Neoplasm Staging; Preoperative Care; Radiopharmaceuticals; Skin Neoplasms; Tomography, Emission-Computed",,"fluorodeoxyglucose f 18, 63503-12-8; technetium, 7440-26-8; Fluorodeoxyglucose F18, 63503-12-8; Radiopharmaceuticals",,,"Gritters, L.S., Francis, I.R., Zasadny, D.R., Wahl, R.L., Initial assessment of positron emission tomography using 2-fluorine-18-fluoro-D-glucose in the imaging of malignant melanoma (1993) J Nucl Med, 34, pp. 1420-1427; 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Finkelstein, S.E., Carrasquillo, J.A., Hoffman, J.M., A prospective analysis of positron emission tomography and conventional imaging for detection of stage IV metastatic melanoma in patients undergoing metastasectomy (2004) Ann Surg Oncol, 11, pp. 731-738; Tyler, D.S., Onaitis, M., Kherani, A., Positron emission tomography scanning in malignant melanoma: Clinical utility in patients with stage III disease (2000) Cancer, 89, pp. 1019-1025; Swetter, S.M., Carroll, L.A., Johnson, D.L., Segall, G.M., Positron emission tomography is superior to computed tomography for metastatic detection in melanoma patients (2002) Ann Surg Oncol, 9, pp. 646-653; Holder, W.D., White, R.L., Zuger, J.H., Easton, E.J., Greene, F.L., Effectiveness of positron emission tomography for the detection of melanoma metastases (1998) Ann Surg, 227, pp. 764-771; Acland, K.M., Healy, C., Calonje, E., Comparison of positron emission tomography scanning and sentinel node biopsy for the detection of micrometastases of primary cutaneous melanoma (2001) J Clin Oncol, 19, pp. 2674-2678; Wagner, J.D., Schauwecker, D., Davidson, D., Inefficacy of F-18 fluorodeoxy-d-glucose positron emission tomography scans for initial evaluation in early-stage cutaneous melanoma (2005) Cancer, 104, pp. 570-579","Wagner, J.D.; Wagner and Associates Plastic and Reconstructive Surgery Consultants; 8040 Clearvista Parkway Indianapolis, IN 46256, United States; email: jdwagner@insightbb.com",,,,,,,,10689265,,ASONF,10.1245/ASO.2006.09.921,"English","Annals of Surgical Oncology",Editorial,Scopus "Kavanagh B.D., McGarry R.C., Timmerman R.D.","Extracranial radiosurgery (stereotactic body radiation therapy) for oligometastases",2006,"Seminars in Radiation Oncology",16,2,,77,84,,12,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-33645080417&partnerID=40&rel=R8.0.0","Department of Radiation Oncology, University of Colorado Comprehensive Cancer Center, Aurora, CO, United States; Department of Radiation Oncology, Indiana University School of Medicine, Indianapolis, IN, United States; Department of Radiation Oncology, University of Texas Southwestern Medical Center, Dallas, TX, United States; Department of Radiation Oncology, University of Texas Southwestern Medical Center, 5801 Forest Park Road, Dallas, TX 75390-9183, United States","Extracranial radiosurgery, also known as stereotactic body radiation therapy (SBRT), is an increasingly used method of treatment of limited cancer metastases located in a variety of organs/sites including the spine, lungs, liver, and other areas in the abdomen and pelvis. The techniques used to perform SBRT were initially modeled after intracranial radiosurgery, although considerable evolution in technique and conduct has occurred for extracranial applications. Unlike intracranial radiosurgery, SBRT requires characterization and accounting for inherent organ movement including breathing motion. Potent dose hypofractionation schedules have been used with SBRT such that the treatment is generally both ablative and convenient. Because the treatment is severely damaging to tissues within and about the target, the volume of adjacent normal tissue must be strictly minimized to avoid toxic late effects. Outcomes in various sites show very high rates of local control with toxicity mostly related to tubular tissues like the airways and bowels. With proper conduct though, SBRT can be an extremely effective treatment option for oligometastases. © 2006 Elsevier Inc. All rights reserved.",,"brain metastasis; dosimetry; fractionation; human; imaging; metastasis; non invasive procedure; palliative therapy; patient selection; priority journal; radiosurgery; review; technique; tissue injury; treatment outcome; treatment planning; whole body radiation; Clinical Trials; Dose Fractionation; Dose-Response Relationship, Radiation; Humans; Liver Neoplasms; Lung Neoplasms; Neoplasm Recurrence, Local; Patient Selection; Radiotherapy Dosage; Spinal Neoplasms; Stereotaxic Techniques; Whole-Body Irradiation",,,,,"Leksell, L., The stereotaxic method and radiosurgery of the brain (1951) Acta Chir Scand, 102, pp. 316-319; Flickinger, J.C., Kondziolka, D., Lunsford, L.D., Clinical applications of stereotactic radiosurgery (1998) Cancer Treat Res, 93, pp. 283-297; Larson, D.A., Gutin, P.H., Leibel, S.A., Stereotaxic irradiation of brain tumors (1990) Cancer, 65, pp. 792-799; Loeffler, J.S., Shrieve, D.C., Wen, P.Y., Radiosurgery for Intracranial Malignancies (1995) Semin Radiat Oncol, 5, pp. 225-234; Kondziolka, D., Patel, A., Lunsford, L.D., Stereotactic radiosurgery plus whole brain radiotherapy versus radiotherapy alone for patients with multiple brain metastases (1999) Int J Radiat Oncol Biol Phys, 45, pp. 427-434; Andrews, D.W., Scott, C.B., Sperduto, P.W., Whole brain radiation therapy with or without stereotactic radiosurgery boost for patients with one to three brain metastases: Phase III results of the RTOG 9508 randomised trial (2004) Lancet, 363, pp. 1665-1672; Rosenthal, D.I., Glatstein, E., We've got a treatment, but what's the disease? (1996) Or a Brief History of Hypofractionation and Its Relationship to Stereotactic Radiosurgery. Oncologist, 1, pp. 1-7; Goffman, T.E., Glatstein, E., Hypofractionation redux? (2004) J Clin Oncol, 22, pp. 589-591; Potters, L., Steinberg, M., Rose, C., American Society for Therapeutic Radiology and Oncology; American College of Radiology. American Society for Therapeutic Radiology and Oncology and American College of Radiology practice guideline for the performance of stereotactic body radiation therapy (2004) Int J Radiat Oncol Biol Phys, 60, pp. 1026-1032; Kini, V.R., Vedam, S.S., Keall, P.J., Patient training in respiratory-gated radiotherapy (2003) Med Dosim, 28, pp. 7-11; Vedam, S.S., Keall, P.J., Kini, V.R., Determining parameters for respiration-gated radiotherapy (2001) Med Phys, 28, pp. 2139-2146; Hara, R., Itami, J., Aruga, T., Development of stereotactic irradiation system of body tumors under respiratory gating (2001) Nippon Igaku Hoshasen Gakkai Zasshi, 62, pp. 156-160; Wang, L.T., Solberg, T.D., Medin, P.M., Infrared patient positioning for stereotactic radiosurgery of extracranial tumors (2001) Comput Biol Med, 31 (2), pp. 101-111; Shirato, H., Shimizu, S., Tadashi, S., Real time tumour-tracking radiotherapy (1999) Lancet, 353, pp. 1331-1332; Kitamura, K., Shirato, H., Seppenwoolde, Y., Tumor location, cirrhosis, and surgical history contribute to tumor movement in the liver, as measured during stereotactic irradiation using a real-time tumor-tracking radiotherapy system (2003) Int J Radiat Oncol Biol Phys, 56, pp. 221-228; Sharp, G.C., Jiang, S.B., Shimizu, S., Prediction of respiratory tumour motion for real-time image-guided radiotherapy (2004) Phys Med Biol, 49, pp. 425-440; Schweikard, A., Shiomi, H., Adler, J., Respiration tracking in radiosurgery (2004) Med Phys, 31, pp. 2738-2741; Yin, F., Kim, J.G., Haughton, C., Extracranial radiosurgery: Immobilizing liver motion in dogs using high-frequency jet ventilation and total intravenous anesthesia (2001) Int J Radiat Oncol Biol Phys, 49, pp. 211-216; O'Dell, W.G., Schell, M.C., Reynolds, D., Dose broadening due to target position variability during fractionated breath-held radiation therapy (2002) Med Phys, 29, pp. 1430-1437; Murphy, M.J., Martin, D., Whyte, R., The effectiveness of breath-holding to stabilize lung and pancreas tumors during radiosurgery (2002) Int J Radiat Oncol Biol Phys, 53, pp. 475-482; Kimura, T., Hirokawa, Y., Murakami, Y., Reproducibility of organ position using voluntary breath-hold method with spirometer for extracranial stereotactic radiotherapy (2004) Int J Radiat Oncol Biol Phys, 60, pp. 1307-1313; Lax, I., Blomgren, H., Naslund, I., Stereotactic radiotherapy of malignancies in the abdomen: Methodological aspects (1994) Acta Oncol, 33, pp. 677-683; Lohr, F., Debus, J., Frank, C., Noninvasive patient fixation for extracranial stereotactic radiotherapy (1999) Int J Radiat Oncol Biol Phys, 45, pp. 521-527; Wulf, J., Hadinger, U., Oppitz, U., Stereotactic radiotherapy of extracranial targets: CT-simulation and accuracy of treatment in the stereotactic body frame (2000) Radiother Oncol, 57, pp. 225-236; Herfarth, K.K., Debus, J., Lohr, F., Extracranial stereotactic radiation therapy: Set-up accuracy of patients treated for liver metastases (2000) Int J Radiat Oncol Biol Phys, 46, pp. 329-335; Nagata, Y., Negoro, Y., Aoki, T., Three-dimensional conformal radiotherapy for extracranial tumors using a stereotactic body frame (2001) Igaku Butsuri, 21, pp. 28-34; Negoro, Y., Nagata, Y., Aoki, T., The effectiveness of an immobilization device in conformal radiotherapy for lung tumor: Reduction of respiratory tumor movement and evaluation of the daily setup accuracy (2001) Int J Radiat Oncol Biol Phys, 50, pp. 889-898; Papiez, L., Timmerman, R., Desrosiers, C., Extracranial stereotactic radioablation: Physical principles (2003) Acta Oncol, 42, pp. 882-894; Wolbarst, A.B., Chin, L.M., Svensson, G.K., Optimization of radiation therapy: Integral-response of a model biological system (1982) Int J Radiat Oncol Biol Phys, 8, pp. 1761-1769; Yeas, R.J., Kalend, A., Local stem cell depletion model for radiation myelitis (1988) Int J Radiat Oncol Biol Phys, 14, pp. 1247-1259; Pastorino, U., Buyse, M., Friedel, G., Long-term results of lung metastasectomy: Prognositic analyses based on 5206 cases (1997) J Thorac Cardiovasc Surg, 113, pp. 37-49; Fong, Y., Cohen, A.M., Forter, J.G., Liver resection for colorectal metastases (1997) J Clin Oncol, 15, pp. 938-946; Singletary, A.E., Walsh, G., Vauthey, J.N., A role for curative surgery in the treatment of selected patients with metastatic breast cancer (2003) Oncologist, 8, pp. 241-251; Fornier, M., Norton, L., Dose-dense adjuvant chemotherapy for primary breast cancer (2005) Breast Cancer Res, 7, pp. 64-69; Blomgren, H., Lax, I., Naslund, I., Stereotactic high dose radiation therapy of extracranial tumors using an accelerator (1995) Acta Oncol, 34, pp. 861-870; Blomgren, J., Lax, I., Goranson, H., Radiosurgery for tumors in the body: Clinical experience using a new method (1998) J Radiosurg, 1, pp. 63-74; Herfarth, K.K., Debus, J., Lohr, F., Stereotactic single-dose radiation therapy of liver tumors: Results of a phase I/II trial (2001) J Clin Oncol, 19, pp. 164-170; Herfarth, K.K., Hof, H., Bahner, M.L., Assessment of focal liver reaction by multiphasic CT after stereotactic single-dose radiotherapy of liver tumors (2003) Int J Radiat Oncol Biol Phys, 57, pp. 444-451; Krix, M., Plathow, C., Essig, M., Monitoring of liver metastases after stereotactic radiotherapy using low-MI contrast-enhanced ultrasound-Initial results (2005) Eur Radiol, 15, pp. 677-684; Wulf, J., Hadinger, U., Oppitz, U., Stereotactic radiotherapy of targets in lung and liver (2001) Strahlenther Onkol, 177, pp. 645-655; Schefter, T.E., Kavanagh, B.D., Timmerman, R.D., A phase I trial of stereotactic body radiation therapy (SBRT) for liver metastases (2005) Int J Radiat Oncol Biol Phys, 62, pp. 1371-1378; Jackson, A., Ten Haken, R.K., Robertson, J.M., Analysis of clinical complication data for radiation hepatitis using a parallel architecture model (1995) Int J Radiat Oncol Biol Phys, 31, pp. 883-891; Song, D.Y., Blomgren, H., Stereotactic body radiation therapy for lung tumors (2005) Stereotactic Body Radiation Therapy, pp. 99-107. , B.K. Kavanagh R.D. Timmerman Lippincott Philadelphia, PA; Uematsu, M., Shioda, A., Tahara, K., Focal, high dose, and fractionated modified stereotactic radiation therapy for lung carcinoma patients: A preliminary experience (1998) Cancer, 82, pp. 1062-1070; Nagata, Y., Negoro, Y., Aoki, T., Clinical outcomes of 3D conformal hypofractionated single high-dose radiotherapy for one or two lung tumors using a stereotactic body frame (2002) Int J Radiat Oncol Biol Phys, 52, pp. 1041-1046; Timmerman, R., Papiez, L., McGarry, R., Extracranial stereotactic radioablation: Results of a phase I study in medically inoperable stage I non-small cell lung cancer (2003) Chest, 124, pp. 1946-1955; Onishi, H., Araki, T., Shirato, H., Stereotactic hypofractionated high-dose irradiation for stage I nonsmall cell lung carcinoma: Clinical outcomes in 245 subjects in a Japanese multiinstitutional study (2004) Cancer, 101, pp. 1623-1631; Wulf, J., Haedinger, U., Oppitz, U., Stereotactic radiotherapy for primary lung cancer and pulmonary metastases: A noninvasive treatment approach in medically inoperable patients (2004) Int J Radiat Oncol Biol Phys, 60, pp. 186-196","Timmerman, R.D.; Department of Radiation Oncology; University of Texas Southwestern Medical Center; 5801 Forest Park Road Dallas, TX 75390-9183, United States; email: robert.timmerman@utsouthwestern.edu",,,,,,,,10534296,,SRONE,10.1016/j.semradonc.2005.12.003,"English","Seminars in Radiation Oncology",Review,Scopus "Kesler K.A., Hammoud Z.T., Helft P.R., Rieger K.M., Pritz M.B., Brown J.W.","Long-term survival after excision of a solitary esophageal cancer brain metastasis",2006,"Journal of Thoracic and Cardiovascular Surgery",131,2,,497,498,,1,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-31044455173&partnerID=40&rel=R8.0.0","Indiana University School of Medicine, Department of Surgery, Thoracic Division, Indianapolis, IN, United States; Indiana University School of Medicine, Department of Medicine, Medical Oncology Division, Indianapolis, IN, United States; Indiana University, School of Medicine, Department of Neurosurgery, Indianapolis, IN, United States; Indiana University, Dept. of Surgery, Thoracic Division, Barnhill Dr EM #212, Indianapolis, IN 46202, United States",[No abstract available],,"cisplatin; fluorouracil; folinic acid; adult; article; brain metastasis; cancer staging; cancer surgery; cancer survival; case report; computer assisted tomography; craniotomy; echography; esophageal adenocarcinoma; esophagogastrostomy; esophagoscopy; esophagus biopsy; esophagus cancer; gamma radiation; hemiparesis; histopathology; human; human tissue; male; nuclear magnetic resonance imaging; priority journal; Adenocarcinoma; Brain Neoplasms; Esophageal Neoplasms; Humans; Male; Middle Aged",,"cisplatin, 15663-27-1, 26035-31-4, 96081-74-2; fluorouracil, 51-21-8; folinic acid, 58-05-9, 68538-85-2",,,"Weinberg, J.S., Suki, D., Hanbali, F., Metastasis of esophageal carcinoma to the brain (2002) Cancer, 94, pp. 759-764; Khuntia, D., Sajja, R., Chidel, M.A., Factors associated with improved survival in patients with brain metastases from esophageal cancer: A retrospective review (2003) Technol Cancer Res Treat, 2, pp. 267-272; Mao, Y.S., Suntharalingam, M., Krasna, M.J., Management of late distant metastases after trimodality therapy for esophageal cancer (2003) Ann Thorac Surg, 76, pp. 1742-1743; Kesler, K.A., Helft, P.R., Werner, E.A., A retrospective analysis of locally advanced esophageal cancer patients treated with neoadjuvant chemoradiation therapy followed by surgery or surgery alone (2005) Ann Thorac Surg, 79, pp. 1116-1121","Kesler, K.A.; Indiana University; Dept. of Surgery; Thoracic Division; Barnhill Dr EM #212 Indianapolis, IN 46202, United States; email: kkesler@iupui.edu",,,,,,,,00225223,,JTCSA,10.1016/j.jtcvs.2005.09.041,"English","Journal of Thoracic and Cardiovascular Surgery",Article,Scopus "Boeglin M.L., Wessels D., Henshel D.","An investigation of the relationship between air emissions of volatile organic compounds and the incidence of cancer in Indiana counties",2006,"Environmental Research",100,2,,242,254,,4,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-31544441612&partnerID=40&rel=R8.0.0","Environmental Science Research Center, School of Public and Environmental Affairs, Indiana University, 1315 E. Tenth Street, Bloomington, IN 47405, United States","Cancer is a health endpoint influenced by a multitude of factors, including genetic history, individual behavior, and environmental insults. The ubiquity of toxicants in the environment has raised questions about the extent of their role in causing cancer in humans. More specifically, it is desirable to understand the cancer incidence due to airborne toxicants in anthropogenic pollution. One particular class of such pollutants is volatile organic compounds (VOCs). This paper reports an epidemiological investigation of the incidence of cancer in the 92 counties of Indiana. We evaluated the relationship between the amount of VOCs released in each county, as reported by the Toxic Release Inventory, and the county-by-county incidence of various types of cancer, especially those of less common organ systems not directly associated with the absorption or distribution of toxicants. Our evaluation considered chlorinated versus nonchlorinated emissions as well as stack versus fugitive emissions. We evaluated three models: linear, quadratic, and polynomial. Of these, the quadratic model appeared to be the best predictor (highest r2) for most endpoints for which there was a positive correlation. However, the linear model was the most sensitive (lowest P-value) for skin, melanoma, and endocrine-related cancers, including female genital system cancers. Our results indicate a relationship between emissions of VOCs and the incidence of some types of cancers. Most notable were strong correlations between VOC emissions and cancers of the brain, nervous system, endocrine system, and skin. © 2005 Elsevier Inc. All rights reserved.","Air emissions; Cancer incidence; Indiana; VOC; Volatile organic compounds","volatile agent; atmospheric pollution; cancer; disease incidence; volatile organic compound; airborne particle; article; cancer incidence; chlorination; environmental factor; gynecologic cancer; human; melanoma; priority journal; skin cancer; United States; Air Pollutants; Carcinogens; Female; Humans; Incidence; Indiana; Inhalation Exposure; Male; Models, Statistical; Neoplasms; Organic Chemicals; Indiana; North America; United States",,"Air Pollutants; Carcinogens; Organic Chemicals",,,"Cancer Facts & Figures (2001) Am. Cancer Soc. (Atlanta), , ACS; Bahrami, A.R., Distribution of volatile organic compounds in ambient air in Tehran (2001) Arch. Environ. Health, 56, pp. 380-383; Berry, M., Bove, F., Birth weight reduction associated with residence near a hazardous waste landfill (1997) Environ. Health Perspect., 105, pp. 856-861; Bertacchi, M., Capuano, F., Fornaciari, S., Franzoni, C., Poluzzi, V., Renna, E., Vivi, B., Meglioli, E., Control of the air quality and research of smelling substances in landfills (1997) Environmental Impact, Aftercare and Remediation of Landfills, pp. 155-169; Bilello, K.S., Murin, S., Matthay, R.A., Epidemiology, etiology, and prevention of lung cancer (2002) Clin. Chest Med., 23, pp. 1-25; Chen, S.J., Wang, J.L., Chen, J.H., Huang, R.N., Possible involvement of glutathione and p53 in trichloroethylene- and perchloroethylene-induced lipid peroxidation and apoptosis in human lung cancer cells (2002) Free Radical Biol. Med., 33, pp. 464-472; Clewell, H.J., Gentry, P.R., Gearhart, J.M., Allen, B.C., Andersen, M.E., Considering pharmacokinetic and mechanistic information in cancer risk assessments for environmental contaminants: Examples with vinyl chloride and trichloroethylene (1995) Chemosphere, 31, pp. 2561-2578; Colome, S.D., Kade, N.Y., Jaques, P., Kleinman, M., Indoor-outdoor air pollution relations: Particulate matter less than 10 μm in aerodynamic diameter (PM10) in homes of asthmatics (1992) Atmos. Environ. a, 26, pp. 2173-2178; Dockery, D.W., Epidemiologic study design for investigating respiratory health effects of complex air pollution mixtures (1993) Environ. Health Perspect., 101 (SUPPL. 4), pp. 187-191; Eaton, D.L., Klaassen, C.D., Chapter 2: Principles of toxicology (2001) Casarett & Doull's Toxicology: The Basic Science of Poisons, , C.D. Classen sixth ed McGraw-Hill New York; Goldberg, M.S., Al-Homsi, N., Goulet, L., Riberdy, H., Incidence of cancer among persons living near a municipal solid waste landfill site in Montreal, Quebec (1995) Arch. Environ. Health, 50, pp. 416-424; Gordon, S.M., Szidon, J.P., Krotoszynski, B.K., Gibbons, R.D., O'Neill, H.J., Volatile organic compounds in exhaled air from patients with lung cancer (1985) Clin. Chem., 31, pp. 1278-1282; Hauptmann, M., Berhane, K., Langholz, B., Lubin, J., Using splines to analyse latency in the Colorado Plateau uranium miners cohort (2001) J. Epidemiol. Biostat., 6, pp. 417-424; Hopenhayn-Rich, C., Stump, M.L., Browning, S.R., Regional assessment of atrazine exposure and incidence of breast and ovarian cancers in Kentucky (2002) Arch. Environ. Contam. Toxicol., 42, pp. 127-136; (2001) Incidence Rate by Primary Site and Sex: Cases Diagnosed in Indiana, by County, , http://www.IN.gov/isdh/dataandstats/cancerinc/cancer_inc_index.htm, Indiana Department of Health, IN, USA; Jo, W.K., Park, K.H., Commuter exposure to volatile organic compounds under different driving conditions (1999) Atmos. Environ., 33, pp. 409-417; Jo, W.K., Song, K.B., Exposure to volatile organic compounds for individuals with occupations associated with potential exposure to motor vehicle exhaust and/or gasoline vapor emissions (2001) Sci. Total Environ., 269, pp. 25-37; Khyshiktyev, B.S., Khyshiktueva, N.A., Ivanov, V.N., Darenskaia, S.D., Novikov, S.V., Diagnostic value of investigating exhaled air condensate in lung cancer (in Russian) (1994) Vopr. Onkol., 40, pp. 161-164; Lee, S.C., Chiu, M.Y., Ho, K.F., Zou, S.C., Wang, X., Volatile organic compounds in urban atmosphere of Hong Kong (2002) Chemosphere, 48, pp. 375-382; Mohamed, M.F., Kang, D., Aneja, V.P., Volatile organic compounds in some urban locations in United States (2002) Chemosphere, 47, pp. 863-882; Moller, L., Schuetzle, D., Autrup, H., Future research needs associated with the assessment of potential human health risks from exposure to toxic ambient air pollutants (1994) Environ. Health Perspect., 102 (SUPPL. 4), pp. 193-210; Moore, M.M., Harrington-Brock, K., Mutagenicity of trichloroethylene and its metabolites: Implications for the risk assessment of trichloroethylene (2000) Environ. Health Perspect., 108, pp. 215-224; (1992) Cancer Statistics Review: 1973-1989, , Publication No. 92-2789. Division of Cancer Prevention and Control, NCI, Bethesda, MD, USA; O'Neill, H.J., Gordon, S.M., O'Neill, M.H., Gibbons, R.D., Szidon, J.P., A computerized classification technique for screening for the presence of breath biomarkers in lung cancer (1988) Clin. Chem., 34, pp. 1613-1618; Payne-Sturges, D.C., Burke, T.A., Breysse, P., Diener-West, M., Buckley, T.J., Personal exposure meets risk assessment: A comparison of measured and modeled exposures and risks in an urban community (2004) Environ. Health Perspect., 112, pp. 589-598; Phillips, M., Gleeson, K., Hughes, J.M.B., Greenberg, J., Cataneo, R.N., Baker, L., Volatile organic compounds in breath as markers of lung cancer: A cross-sectional study (1999) Lancet, 353, pp. 1930-1933; Preti, G., Labows, J.N., Kostelc, J.G., Aldinger, S., Daniele, R., Analysis of lung air from patients with bronchogenic carcinoma and controls using gas chromatography mass spectrometry (1988) J. Chromatogr., 432, pp. 1-11; Quackenboss, J.J., Lebowitz, M.D., Crutchfield, C.D., Indoor-outdoor relationships for particulate matter: Exposure classifications and health effects (1989) Environ. Int., 15, pp. 353-360; Reynolds, P., Von Behren, J., Gunier, R.B., Goldberg, D.E., Hertz, A., Smith, D.F., Childhood cancer incidence rates and hazardous air pollutants in California: An exploratory analysis (2003) Environ. Health Perspect., 111, pp. 663-668; Rose, G., Environmental factors and disease: The man-made environment (1987) Br. Med. J., 294, pp. 963-965; Shy, C.M., Epidemiologic studies of neurotoxic, reproductive, and carcinogenic effects of complex mixtures (1993) Environ. Health Perspect., 101 (SUPPL. 4), pp. 183-186; Steenland, K., Palu, S., Cohort mortality study of 57,000 painters and other union members: A 15 year update (1999) Occup. Environ. Med., 56, pp. 315-321; (2001) TRI Explorer, Version 3.2, , http://www.epa.gov/triexplorer/reports.htm, Office of Environmental Information, US Environmental Protection Agency, Washington, DC; (2002) National Air Toxics Assessment, , http://www.epa.gov/ttn/atw/nata/, US Environmental Protection Agency, Washington, DC; Wallace, L., Comparison of risks from outdoor and indoor exposure to toxic chemicals (1991) Environ. Health Perspect., 95, pp. 7-13","Henshel, D.; Environmental Science Research Center; School of Public and Environmental Affairs; Indiana University; 1315 E. Tenth Street Bloomington, IN 47405, United States; email: dhenshel@indiana.edu",,,,,,,,00139351,,ENVRA,10.1016/j.envres.2005.04.004,"English","Environmental Research",Article,Scopus "Kurup A., Lin C.-W., Murry D.J., Dobrolecki L., Estes D., Yiannoutsos C.T., Mariano L., Sidor C., Hickey R., Hanna N.","Recombinant human angiostatin (rhAngiostatin) in combination with paclitaxel and carboplatin in patients with advanced non-small-cell lung cancer: A phase II study from Indiana University",2006,"Annals of Oncology",17,1,,97,103,,9,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-29844452745&partnerID=40&rel=R8.0.0","Indiana University School of Medicine, Indianapolis, IN, United States; Indiana University, 535 Barnhill Drive, Indianapolis, IN 46202, United States; University of Iowa, College of Pharmacy, Iowa City, IA, United States; EntreMed, Inc., Rockville, MD, United States","Background: Recombinant human angiostatin (rhAngiostatin) functions as a potent inhibitor of angiogenesis. This study combined rhAngiostatin with a standard chemotherapy regimen in patients with advanced non-small-cell lung cancer (NSCLC). Patients and methods: Eligible patients had chemotherapy-naïve stage IIIB (with pleural effusion) or IV NSCLC, performance status (PS) 0 or 1, no history of bleeding, brain metastasis or requirements for anti-coagulation. Patients received carboplatin (AUC 5) intravenously and paclitaxel (175 mg/m2) intravenously day 1 + subcutaneous rhAngiostatin at either 15 mg or 60 mg twice daily. Cycles were repeated every 3 weeks, for up to six cycles. Patients without progression after completing at least four cycles were continued on maintenance rhAngiostatin until disease progression. Results: Patient characteristics (n = 24) were: 16 males, median age 66 years (range 45-78), 54% PS 1, 83.3% stage IV and 62.5% adenocarcinoma. Grade 3/4 toxicities included: fatigue 47.8%, neutropenia 39.1%, dyspnea 39.1%, vascular 26.1% and infection 17.4%. The overall response rate was 39.1%, 39.1% stable disease and 21.7% progressive disease. Median time to progression was 144 days, and 1-year survival was 45.8%. Conclusions: rhAngiostatin in combination with paclitaxel and carboplatin is feasible and results in a high disease control rate in patients with advanced NSCLC. © 2005 European Society for Medical Oncology.","Angiogenesis; Carboplatin; Lung cancer; Paclitaxel; RhAngiostatin","angiostatin; carboplatin; paclitaxel; recombinant human angiostatin; unclassified drug; adult; advanced cancer; aged; anemia; arthralgia; article; cancer combination chemotherapy; cancer growth; cancer staging; cancer survival; cerebrovascular accident; clinical protocol; clinical trial; controlled clinical trial; controlled study; drug clearance; drug efficacy; drug exposure; dyspnea; fatigue; female; heart atrium fibrillation; human; infection; lung adenocarcinoma; lung embolism; lung non small cell cancer; major clinical study; male; myalgia; nausea; neuropathy; neutropenia; phase 2 clinical trial; pleura effusion; priority journal; prognosis; randomized controlled trial; skin toxicity; transient ischemic attack; vascular disease; vomiting; Aged; Angiostatins; Antineoplastic Combined Chemotherapy Protocols; Brain Neoplasms; Carboplatin; Carcinoma, Non-Small-Cell Lung; Disease Progression; Disease-Free Survival; Feasibility Studies; Female; Humans; Lung Neoplasms; Male; Maximum Tolerated Dose; Middle Aged; Neoplasm Staging; Paclitaxel; Proteomics; Recombinant Proteins; Survival Rate; Time Factors",,"angiostatin, 172642-30-7, 86090-08-6; carboplatin, 41575-94-4; paclitaxel, 33069-62-4; Angiostatins, 86090-08-6; Carboplatin, 41575-94-4; Paclitaxel, 33069-62-4; Recombinant Proteins",,,"Chemotherapy in non-small cell lung cancer: A meta-analysis using updated data on individual patients from 52 randomized clinical trials (1995) BMJ, 311, pp. 899-909. , Non-small Cell Lung Cancer Collaborative Group; Marine, P., Pampallona, S., Preatoni, F., Chemotherapy vs supportive care in advanced non-small cell lung cancer: Results of a meta-analysis of the literature (1994) Chest, 106, pp. 861-865; Stephens, R., Fairlamb, N., Gower, N., The big lung trial (BLT): Determining the value of cisplatin-based chemotherapy for all patients with non-small cell lung cancer (NSCLC). Preliminary results in the supportive care setting (2002) Proc Am Soc Clin Oncol, 21, pp. 291a; Kelly, K., Crowley, J., Bunn, P., Randomized phase III trial of paclitaxel plus carboplatin versus vinorelbine plus cisplatin in the treatment of patients with advanced non-small cell lung cancer: A Southwest Oncology Group trial (2001) J Clin Oncol, 19, pp. 3210-3218; Schiller, J.H., Harrington, D., Belani, C.P., Comparison of four chemotherapy regimens for advanced non-small-cell lung cancer (2002) N Engl J Med, 346, pp. 92-98; Kerbel, R., Folkman, J., Clinical translation of angiogenesis inhibitors (2002) Nat Rev Cancer, 2, pp. 727-739; Folkman, J., Tumor angiogenesis: Therapeutic implications (1971) N Engl J Med, 285, pp. 1182-1186; Grunstein, J., Roberts, W.G., Mathieu-Costello, O., Tumor-derived expression of vascular endothelial growth factor is a critical factor in tumor expansion and vascular function (1999) Cancer Res, 59, pp. 1592-1598; Brekken, R.A., Overholser, J.P., Stastny, V.A., Selective inhibition of vascular endothelial growth factor (VEGF) receptor 2 (KDR/FIk-1) activity by a monoclonal anti-VEGF antibody blocks tumor growth in mice (2000) Cancer Res, 60, pp. 5117-5124; Ferrara, N., Gerber, H.P., LeCouter, J., The biology of VEGF and its receptors (2003) Nat Med, 9, pp. 669-676; Viloria-Petit, A., Miquerol, L., Yu, J.L., Contrasting effects of VEGF gene disruption in embryonic stem cell-derived versus oncogene-induced tumors (2003) EMBO J, 22, pp. 4091-4102; Denekamp, J., Vascular attack as a therapeutic strategy for cancer (1990) Cancer Metastasis Rev, 3, pp. 267-282; Ferrar, N., Alitalo, K., Clinical applications of angiogenic growth factors and their inhibitors (1999) Nat Med, 5, p. 1359; Hurwitz, H., Fehrenbacher, L., Novotny, W., Bevacizumab plus irinotecan, fluorouracil, and leucovorin for metastatic colorectal cancer (2004) N Engl J Med, 350, pp. 2335-2342; Yang, J.C., Haworth, L., Sherry, R.M., A randomized trial of Bevacizumab, an antivascular endothelial growth factor antibody, for metastatic renal cancer (2003) N Engl J Med, 349, p. 427; Bergers, G., Song, S., Meyer-Morse, N., Bergsland, E., Benefits of targeting both pericytes and endothelial cells in the tumor vasculature with kinase inhibitors (2003) J Clin Invest, 111, p. 1287; Morgan, B., Thomas, A.L., Drevs, J., Dyanmic contrast enhanced magnetic resonance imaging as a biomarker for the pharmacological response of PTK787/ZK 222584, an inhibitor of the vascular endothelial growth factor receptor tyrosine kinases, in patients with advanced colorectal cancer and liver metastases: Results from two phase I studies (2063) J Clin Oncol, 21, p. 3955; Holash, J., Davis, S., Papadopoulos, N., VEGF-Trap: A VEGF blocker with potent anti-tumor effects (2002) Proc Natl Acad Sci USA, 99, p. 11393; Kuo, C.J., Farnebo, F., Yu, E.Y., Comparative evaluation of antitumor activity of antiangiogenic proteins delivered by gene transfer (2001) Proc Natl Acad Sci USA, 98, p. 4605; O'Reilly, M.S., Holmgren, L., Shing, Y., Angiostatin: A novel angiogenesis inhibitor that mediates the suppression of metastases by a Lewis lung carcinoma (1994) Cell, 79, pp. 315-328; O'Reilly, M.S., The preclinical evaluation of angiogenesis inhibitors (1997) Invest New Drugs, 15, p. 5; O'Reilly, M.S., Boehm, T., Shing, Y., Endostatin: An endogenous inhibitor of angiogenesis and tumor growth (1997) Cell, 88, p. 277; MacDonald, N.J., Murad, A.C., Fogler, W.E., The tumor-suppressing activity of angiostatin protein resides within kringles 1 to 3 (1999) Biochem Biophys Res Commun, 264, pp. 469-477; DeMoraes, E.D., Fogler, W.E., Grant, D., Recombinant human angiostatin (rhA): A Phase I clinical trial assessing safety, pharmacokinetics (PK) and pharmacodynamics (PD) (2001) Proc Am Soc Clin Oncol, 20, pp. 3a; Sim, B.K., O'Reilly, M.S., Liang, H., A recombinant human angiostatin protein inhibits experimental primary and metastatic cancer (1997) Cancer Res, 57, pp. 1329-1334; Drixler, T.A., Rinkes, I.H., Ritchie, E.D., Continous administration of angiostatin inhibits accelerated growth of colorectal liver metastases after partial hepatectomy (2000) Cancer Res, 60, pp. 1761-1765; Velde, E.A., Vogten, J.M., Gebbink, M.F., Enhanced antitumor efficacy by combining conventional chemotherapy with angiostatin or endostatin in a liver metastasis model (2002) Br J Surg, 89, pp. 1302-1309; Maucer, H.J., Hanna, N.N., Beckett, M.A., Combined effects of angiostatin and ionizing radiation in antitumor therapy (1998) Nature, 394, pp. 287-291; Beerepoot, L.V., Witteveen, E.O., Groenewegen, G., Recombinant human angiostatin by twice-daily subcutaneous injection in advanced cancer: A pharmacokinetic and long-term safety study (2003) Clin Cancer Res, 9, pp. 4025-4033; Miller, A.B., Hogestraeten, B., Staquet, M., Reporting results of cancer treatment (1981) Cancer, 47, pp. 207-214; Ezekowitz, R.A., Mulliken, J.B., Folkman, J., Interferon alfa-2a therapy for life-threatening hemangiomas of infancy (1992) N Engl J Med, 326, pp. 1456-1463; Sandler, A.B., Gray, R., Brahmer, J., Randomized phase II/III trial of paclitaxel (P) plus carboplatin (C) with or without bevacizumab (NSC #704865) in patients with advanced non-squamous non-small cell lung cancer (NSCLC) (2005), An Eastern Cooperative Oncology Group (ECOG) Trial - E4599. ASCO Meetings 1 June 4Hurwitz, H.I., Fehrenbacher, L., Hainsworth, J.D., Bevacizumab in combination with fluorouracil and leucovorin: An active regimen for first-line metastatic colorectal cancer (2005) J Clin Oncol, 23, pp. 3502-3508; Johnson, D.H., Fehrenbacher, L., Novotny, W.F., Randomized phase II trial comparing bevacizumab plus carboplatin and paclitaxel with carboplatin and paclitaxel alone in previously untreated locally advanced or metastatic non-small-cell lung cancer (2004) J Clin Oncol, 22, pp. 2184-2191; Issaq, H.J., Veenstra, T.D., Conrads, T.P., The SELDI-TOF MS approach to proteomics: Protein profiling and biomarker identification (2002) Biochem Biophys Res Commun, 292, pp. 587-592","Hanna, N.H.; Indiana University; 535 Barnhill Drive Indianapolis, IN 46202, United States; email: nhanna@iupui.edu",,,,,,,,09237534,,ANONE,10.1093/annonc/mdj055,"English","Annals of Oncology",Article,Scopus "MacDonald T.J., Arenson E.B., Ater J., Sposto R., Bevan H.E., Bruner J., Deutsch M., Kurczynski E., Luerssen T., McGuire-Cullen P., O'Brien R., Shah N., Steinbok P., Strain J., Thomson J., Holmes E., Vezina G., Yates A., Phillips P., Packer R.","Phase II study of high-dose chemotherapy before radiation in children with newly diagnosed high-grade astrocytoma: Final analysis of Children's Cancer Group Study 9933",2005,"Cancer",104,12,,2862,2871,,5,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-29144459136&partnerID=40&rel=R8.0.0","Department of Hematology-Oncology, Children's National Medical Center, Washington, DC, United States; Department of Hematology/Oncology, Presbyterian/St. Lukes Medical Center, Englewood, CO, United States; Department of Hematology/Oncology, M. D. Anderson Cancer Center, Houston, TX, United States; Department of Hematology-Oncology, Childrens Hospital Los Angeles, Los Angeles, CA, United States; Department of Hematology-Oncology, Childrens Hospital - King's Daughters, Norfolk, VA, United States; Department of Pathology, M. D. Anderson Cancer Center, Houston, TX, United States; Department of Radiation Oncology, Children's Hospital of Pittsburgh, Pittsburgh, PA, United States; Department of Hematology/Oncology, West Virginia University HSC-Charleston, Charleston, WV, United States; Department of Surgery, Indiana University, Riley Childrens Hospital, Indianapolis, IN, United States; Department of Nursing, Presbyterian/St. Lukes Medical Center, Denver, CO, United States; Department of Hematology/Oncology, Primary Children's Medical Center, Salt Lake City, UT, United States; Department of Hematology/Oncology, Geisinger Medical Center, Danville, PA, United States; Department of Surgery, British Columbia's Children's Hospital, Vancouver, BC, Canada; Department of Radiology, Children's Hospital, Denver, CO, United States; Department of Radiation Oncology, Primary Children's Medical Center, Salt Lake City, UT, United States; Department of Statistics, Children's Oncology Group, Operations Center, Arcadia, CA, United States; Department of Radiology, Children's National Medical Center, Washington, DC, United States; Department of Pathology, Columbus Children's Hospital, Columbus, OH, United States; Department of Neurology, Childrens Hospital of Philadelphia, Philadelphia, PA, United States; Department of Neurology, Children's Hospital Medical Center, Washington, DC, United States; Children's National Medical Center, Hematology-Oncology, 111 Michigan Avenue NW, Washington, DC 20010, United States","BACKGROUND. High-grade astrocytomas (HGA) carry a dismal prognosis and compose nearly 20% of all childhood brain tumors. The role of high-dose chemotherapy (HDCT) in the treatment of HGA remains unclear. METHODS. In a nationwide study, The Children's Cancer Group (CCG) prospectively evaluated 102 children with HGA and postoperative residual disease for efficacy and toxicity of four courses of HDCT before radiotherapy (RT). Patients were randomly assigned to one of three couplets of drugs: carboplatin/etoposide (Regimen A), ifosfamide/etoposide (Regimen B), or cyclophosphamide/etoposide (Regimen C). After HDCT, all patients were to receive local RT followed by lomustine and vincristine. Twenty-six patients were excluded after central neuroradiographic review (n = 8) or pathology review (n = 18). RESULTS. Of 76 evaluable patients (median age, 11.95 yrs; range, 3-20 yrs), 30 patients relapsed during HDCT, and 11 others did not complete HDCT because of toxicity. Nonhematologic serious toxicities were common (29%), and 21% of patients did not receive RT. Objective response rates were not associated with amount of residual disease and did not statistically differ between regimens: 27% (Regimen A), 8% (Regimen B), and 29% (Regimen C). Overall survival (OS) was 24% ± 5% at 5 years and did not differ between groups. Median time to an event was longest for Regimen A (283 days compared with 83 and 91 days for Regimens B and C, respectively). The five-year, event-free survival (EFS) rate for all patients was 8% ± 3% and 14% ± 7% for Regimen A (P = 0.07). CONCLUSIONS. OS and EFS were not affected by histologic grade. Patients who responded to HDCT had a nominally higher survival rate (P = 0.03 for trend). The authors conclude that these commonly used HDCT regimens provide no additional clinical benefit to conventional treatment in HGA, regardless of the amount of measurable residual tumor. © 2005 American Cancer Society.","Children; phase II study; High-dose chemotherapy; High-grade astrocytoma","carboplatin; carmustine; corticosteroid; cyclophosphamide; cytarabine; etoposide; granulocyte colony stimulating factor; ifosfamide; lomustine; mesna; prednisone; thiotepa; vincristine; adolescent; adult; allergy; astrocytoma; ataxia; cancer chemotherapy; cancer grading; cancer radiotherapy; cancer survival; central nervous system disease; childhood cancer; clinical trial; controlled clinical trial; controlled study; drug efficacy; drug megadose; electrolyte disturbance; female; glioblastoma; hematuria; human; infection; major clinical study; male; minimal residual disease; muscle weakness; nausea and vomiting; neuroradiology; peripheral neuropathy; phase 2 clinical trial; preschool child; priority journal; prognosis; prospective study; randomized controlled trial; review; school child; seizure; Adolescent; Adult; Antineoplastic Combined Chemotherapy Protocols; Brain Stem Neoplasms; Child; Child, Preschool; Combined Modality Therapy; Disease-Free Survival; Dose-Response Relationship, Drug; Drug Administration Schedule; Female; Glioblastoma; Humans; Male; Neoadjuvant Therapy; Neoplasm Staging; Probability; Prognosis; Prospective Studies; Radiotherapy, High-Energy; Reference Values; Risk Assessment; Spinal Cord Neoplasms; Survival Analysis; Time Factors; Treatment Outcome",,"carboplatin, 41575-94-4; carmustine, 154-93-8; cyclophosphamide, 50-18-0; cytarabine, 147-94-4, 69-74-9; etoposide, 33419-42-0; ifosfamide, 3778-73-2; lomustine, 13010-47-4; mesna, 19767-45-4, 3375-50-6; prednisone, 53-03-2; thiotepa, 52-24-4; vincristine, 57-22-7","vp 16",,"Rilliet, B., Vernet, O., Gliomas in children: A review (2000) Childs Nerv Syst, 16, pp. 735-741; Wisoff, J.H., Boyett, J.M., Berger, M.S., Current neurosurgical management and the impact of the extent of resection in the treatment of malignant gliomas of childhood: A report of the Children's Cancer Group trial no. 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Direct integration of fMRI and PET data (2000) J Neuroradiol, 27, pp. 157-163; Pollack, I.F., Hamilton, R.L., Burnham, J., Impact of proliferation index on outcome in childhood malignant gliomas: Results in a multi-institutional cohort (2002) Neurosurgery, 50, pp. 1238-1244; Ho, D.M., Wong, T.T., Hsu, C.Y., MIB-1 labeling index in nonpilocytic astrocytoma of childhood: A study of 101 cases (1998) Cancer, 82, pp. 2459-2466; Pollack, I.F., Boyett, J.M., Yates, A.J., The influence of central review on outcome associations in childhood malignant gliomas: Results from the CCG-945 experience (2003) Neuro-oncol, 5, pp. 197-207; Bobola, M.S., Berger, M.S., Ellenbogen, R.G., O6-Methylguanine-DNA methyltransferase in pediatric primary brain tumors: Relation to patient and tumor characteristics (2001) Clin Cancer Res, 7, pp. 613-619; Esteller, M., Garcia-Foncillas, J., Andion, E., Inactivation of the DNA-repair gene MGMT and the clinical response of gliomas to alkylating agents (2000) N Engl J Med, 343, pp. 1350-1354; Silber, J.R., Blank, A., Bobola, M.S., O6-methylguanine-DNA methyltransferase-deficient phenotype in human gliomas: Frequency and time to tumor progression after alkylating agent-based chemotherapy (1999) Clin Cancer Res, 5, pp. 807-814; Hongeng, S., Brent, T.P., Sanford, R.A., O6-Methylguanine-DNA methyltransferase protein levels in pediatric brain tumors (1997) Clin Cancer Res, 3, pp. 2459-2463","MacDonald, T.J.; Children's National Medical Center; Hematology-Oncology; 111 Michigan Avenue NW Washington, DC 20010, United States; email: tmacdona@cnmc.org",,,,,,,,0008543X,,CANCA,10.1002/cncr.21593,"English","Cancer",Review,Scopus "Sun M., Graham J.S., Hegedus B., Marga F., Zhang Y., Forgacs G., Grandbois M.","Multiple membrane tethers probed by atomic force microscopy",2005,"Biophysical Journal",89,6,,4320,4329,,17,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-28444450194&partnerID=40&rel=R8.0.0","Department of Physics, University of Missouri, Columbia, MO, United States; Département de Pharmacologie, Université de Sherbrooke, Sherbrooke, Que., Canada; National Institute of Neurosurgery, Budapest, Hungary; Department of Physics, University of Indiana, Bloomington, IN, United States; Department of Biology, University of Missouri, Columbia, MO, United States","Using the atomic force microscope to locally probe the cell membrane, we observed the formation of multiple tethers (thin nanotubes, each requiring a similar pulling force) as reproducible features within force profiles recorded on individual cells. Forces obtained with Chinese hamster ovary cells, a malignant human brain tumor cell line, and human endothelial cells (EA hy926) were found to be 28 ± 10 pN, 29 ± 9 pN, and 29 ± 10 pN, respectively, independent of the nature of attachment to the cantilever. The rather large variation of the tether pulling forces measured at several locations on individual cells points to the existence of heterogeneity in the membrane properties of a morphologically homogeneous cell. Measurement of the summary lengths of the simultaneously extracted tethers provides a measure of the size of the available membrane reservoir through which co-existing tethers are associated. As expected, partial disruption of the actin cytoskeleton and removal of the hyaluronan backbone of the glycocalyx were observed to result in a marked decrease (30-50%) in the magnitude and a significant sharpening of the force distribution indicating reduced heterogeneity of membrane properties. Taken together, our results demonstrate the ability of the plasma membrane to locally produce multiple interdependent tethers-a process that could play an important role in the mechanical association of cells with their environment. © 2005 by the Biophysical Society.",,"actin; hyaluronic acid; nanotube; animal cell; article; atomic force microscopy; cancer cell culture; cell membrane; cell size; cell structure; CHO cell; controlled study; cytoskeleton; endothelium cell; force; glycocalyx; human; human cell; nonhuman; reproducibility; structure analysis; Animals; Brain Neoplasms; Cell Membrane; Cell Surface Extensions; Cells, Cultured; CHO Cells; Cricetinae; Cricetulus; Endothelial Cells; Humans; Mechanotransduction, Cellular; Membrane Fluidity; Microscopy, Atomic Force; Physical Stimulation; Animalia; Cricetulus griseus",,"hyaluronic acid, 31799-91-4, 9004-61-9, 9067-32-7",,,"Sheetz, M.P., Cellular plasma membrane domains (1995) Mol. Membr. 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J., 86, pp. 2714-2726","Grandbois, M.; Département de Pharmacologie; Université de Sherbrooke Sherbrooke, Que., Canada; email: michel.grandbois@usherbrooke.ca",,,,,,,,00063495,,BIOJA,10.1529/biophysj.104.058180,"English","Biophysical Journal",Article,Scopus "Liu W.-C., Feldman S.C., Schulder M., Kalnin A.J., Holodny A.I., Zimmerman A., Sinensky R., Rao S.","The effect of tumour type and distance on activation in the motor cortex",2005,"Neuroradiology",47,11,,813,819,,1,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-28044463156&partnerID=40&rel=R8.0.0","Department of Radiology, University of Medicine and Dentistry of New Jersey, 150 Bergen Street, Newark, NJ 07103, United States; Department of Neurosurgery, University of Medicine and Dentistry of New Jersey, 150 Bergen Street, Newark, NJ 07103, United States; Department of Radiology, Indiana University, School of Medicine, Indianapolis, IN, United States; Department of Radiology, Memorial-Sloan Kettering Cancer Center, New York, NY, United States","Functional MRI has been widely used to identify the eloquent cortex in neurosurgical/radiosurgical planning and treatment of CNS neoplasms and malformations. In this study we examined the effect of CNS tumours on the blood oxygenation level-dependent (BOLD) activation maps in the primary and supplementary motor cortex. A total of 33 tumour patients and five healthy right-handed adults were enrolled in the study. Patients were divided into four groups based on tumour type and distance from primary motor cortex: (1) intra-axial, near, (2) extra-axial, near, (3) intra-axial, far and (4) extra-axial, far. The intra-axial groups consisted of patients with astrocytomas, glioblastomas and metastatic tumours of mixed histology; all the extra-axial tumours were meningiomas. The motor task was a bilateral, self-paced, finger-tapping paradigm. Anatomical and functional data were acquired with a 1.5 T GE Echospeed scanner. Maps of the motor areas were derived from the BOLD images, using SPM99 software. For each subject we first determined the activation volume in the primary motor area and the supplementary motor area (SMA) and then calculated the percentage difference between the hemispheres. Two factors influenced the activation volumes: tumour type (p <0.04) and distance from the eloquent cortex (P <0.06). Patients in group 1 (intra-axial, near) had the smallest activation area in the primary motor cortex, the greatest percentage difference in the activation volume between the hemispheres, and the largest activation volume in the SMA. Patients in group 4 (extra-axial, far) had the largest activation volume in the primary motor cortex, the least percentage difference in volume between the hemispheres, and the smallest activation volume in the SMA. There was no significant change in the volume of the SMA in any group, compared with controls, suggesting that, although there is a gradual decrease in SMA volume with distance from the primary motor area, the effect on motor reorganisation is minimal. All the tumour patients showed a net loss in total activation volumes (both hemispheres plus SMA) compared with controls. The effect of the tumours on interhemispheric volume differences was: group 1>group 3>group 2>group 4. Within the intra-axial tumours, there was no significant effect of tumour type on the results. We conclude that BOLD-imaged activation volume is affected at least by the interplay of two factors: tumour type and distance from the motor cortex. Further, all tumours may be expected to cause some loss of activation volumes in motor areas. We suggest that, with proper precautions and planning, BOLD functional magnetic resonance imaging (fMRI) maps can be useful in minimising damage to the functional areas. © Springer-Verlag 2005.","Activation volume; fMRI; Primary motor area; Supplementary motor area; Tumour","adult; article; astrocytoma; blood oxygenation; brain cancer; brain malformation; brain mapping; brain metastasis; clinical article; computer program; controlled study; female; functional magnetic resonance imaging; glioblastoma; human; image analysis; male; meningioma; motor cortex; priority journal; task performance; Adult; Aged; Brain Neoplasms; Female; Humans; Image Processing, Computer-Assisted; Linear Models; Magnetic Resonance Imaging; Male; Middle Aged; Motor Cortex",,,"1.5 T GE Echospeed, General Electric; SPM99","General Electric","Ogawa, S., Lee, T., Kay, A., Brain magnetic resonance imaging with contrast dependent on blood oxygenation (1990) Proc. Natl. Acad. Sci. U.S.A., 87, pp. 9868-9872. , 2124706; Kwong, K.K., Belliveau, J.W., Chesler, D.A., Dynamic magnetic resonance imaging of human brain activity during primary sensory stimulation (1992) Proc. Natl. Acad Sci. U.S.A., 89, pp. 5675-5679. , 1608978; Roberts, T.P., Rowley, H.A., Mapping of the sensorimotor cortex: Functional MR and magnetic source imaging (1997) AJNR Am. J. Neuroradiol., 18, pp. 871-880. , 9159364; Baumann, S.B., Noll, D.C., Kondziolka, D.S., Comparison of functional magnetic resonance imaging with positron emission tomography and magnetoencephalography to identify the motor cortex in a patient with an arteriovenous malformation (1995) J. Image Guidance Surg., 1, pp. 191-197; Engel, S.A., Rumelhart, D.E., Wandell, B.A., fMRI of human visual cortex (1994) Nature, 369, p. 525. , 10.1038/369525a0; Turner, R., Jezzard, P., Wen, H., Functional mapping of the human visual cortex at 4 and 1.5 Tesla using deoxygenation contrast EPI (1993) Magn. Reson. Med., 29, pp. 277-279. , 8429797; Binder, J., Rao, S., Hammeke, T., Functional magnetic resonance imaging of human auditory cortex (1994) Ann. Neurol., 35, pp. 662-672. , 10.1002/ana.410350606; Dhankhar, A., Wexler, B.E., Fulbright, R.K., Functional magnetic resonance imaging assessment of the human brain auditory cortex response to increasing word presentation rates (1997) J. Neurophysiol., 77, pp. 476-483; Liu, W.-C., Mosier, K., Kalnin, A.J., BOLD fMRI activation induced by vagus nerve stimulation in seizure patients (2003) J. Neurol. Neurosurg. Psychiatry, 74, pp. 965-978. , 10.1136/jnnp.74.6.811; Schulder, M., Maldjian, J.A., Liu, W.-C., Functional image-guided surgery of intracranial tumors located in or near the sensorimotor cortex (1998) J. 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Brain Mapp., 2, pp. 189-210. , 10.1002/hbm.460020402; Krings, T., Topper, R., Willmes, K., Activation in primary and secondary motor areas in patients with CNS neoplasms and weakness (2002) Neurology, 58, pp. 381-390. , 11839836; Fried, I., Katz, A., McCarthy, G., Functional organization of human supplementary motor cortex studied by electrical stimulation (1991) J. Neurosci., 11, pp. 3656-3666. , 1941101; Schreiber, A., Hubbe, U., Ziyeh, S., The influence of gliomas and nonglial space-occupying lesions on blood-oxygen-level-dependent contrast enhancement (2000) AJNR Am. J. Neuroradiol., 21, pp. 1055-1063. , 10871013; Gorbach, A., Heiss, J., Kopylev, L., Intraoperative infrared imaging of brain tumors (2004) J. Neurosurg., 101, pp. 960-969. , 15599965; Roux, F.E., Ranjeva, J.P., Boulanouar, K., Motor functional MRI for presurgical evaluation of cerebral tumors (1997) Stereotact Funct Neurosurg, 68, pp. 106-111. , 9711703; Carpentier, A.C., Constable, R.T., Schlosser, M.J., Patterns of functional magnetic resonance imaging activation in association with structural lesions in the rolandic region: A classification system (2001) J. Neurosurg., 94, pp. 946-954. , 11409524; Baciu, M., Bas, J.L., Segebarth, C., Presurgical fMRI evaluation of cerebral reorganization and motor deficit in patients with tumors and vascular malformations (2003) Eur. J. Radiol., 46, pp. 139-146; Wunderlich, G., Knorr, U., Herzog, H., Precentral glioma location determines the displacement of cortical hand representation (1998) Neurosurgery, 42, pp. 18-26. , 10.1097/00006123-199801000-00005; Ulmer, J., Hacein-Bey, L., Mathews, V., Lesion-induced pseudo-dominance at functional magnetic resonance imaging: Implications for preoperative assessments (2004) Neurosurgery, 55, pp. 569-579. , 10.1227/01.NEU.0000134384.94749.B2","Liu, W.-C.; Department of Radiology; University of Medicine and Dentistry of New Jersey; 150 Bergen Street Newark, NJ 07103, United States; email: wliu@umdnj.edu",,,,,,,,00283940,,NRDYA,10.1007/s00234-005-1428-y,"English","Neuroradiology",Article,Scopus "Holstege C.P., Mitchell K., Barlotta K., Furbee R.B.","Toxicity and drug interactions associated with herbal products: Ephedra and St. John's Wort",2005,"Medical Clinics of North America",89,6,,1225,1257,,1,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-26844445307&partnerID=40&rel=R8.0.0","Division of Medical Toxicology, University of Virginia, Charlottesville, VA, United States; Department of Emergency Medicine, University of Virginia, Charlottesville, VA, United States; Department of Pediatrics, University of Virginia, Charlottesville, VA, United States; Blue Ridge Poison Center, University of Virginia, Charlottesville, VA, United States; Department of Internal Medicine, University of Washington, Seattle, WA, United States; Department of Emergency Medicine, Indiana University, School of Medicine, Indianapolis, IN, United States; Indiana Poison Center, Indianapolis, IN, United States; Clarian Health, Indianapolis, IN, United States; University of Virginia Health System, PO Box 800774, Charlottesville, VA 22908-0774, United States","Health care providers are being increasingly confronted with the use of herbal medications by their patients. It is imperative that patients be questioned regarding herbal preparation use and that health care providers become familiar with these agents. Research into the active components and mechanisms of action of various herbals is ongoing [350]. Long-range studies need to be performed to follow patients for efficacy or toxicity in chronic use [351,352]. Adverse reactions to herbal remedies should be reported to the FDA MedWatch at http://www.fda.gov/medwatch. As with any therapeutic agent, risk of use must always be weighed against potential benefits. © 2005 Elsevier Inc. All rights reserved.",,"4 aminobutyric acid receptor; alprazolam; amitriptyline; amsacrine; cyclosporin; digoxin; ephedrine derivative; etoposide; fexofenadine; herbaceous agent; hyperforin; hypericin; Hypericum perforatum extract; imatinib; indinavir; interleukin 6; methadone; midazolam; nevirapine; omeprazole; oral contraceptive agent; paroxetine; serotonin agonist; serotonin uptake inhibitor; simvastatin; theophylline; tricyclic antidepressant agent; unindexed drug; verapamil; warfarin; abdominal pain; abnormally high substrate concentration in blood; agitation; alcoholism; anorexia; antiinflammatory activity; antineoplastic activity; anxiety; arthralgia; asthma; atractylis gummifera; brain hemorrhage; brain vasculitis; breakthrough bleeding; bronchodilatation; callilepsis laureola; cancer; cardiomyopathy; cataract; cerebrovascular disease; Chelidonium; chill; Cimicifuga racemosa; clinical trial; comfrey; depression; diaphoresis; diarrhea; dizziness; drowsiness; drug activity; drug fatality; drug safety; dysosma pleianthum; dyspepsia; edema; enteritis; enuresis; Ephedra; Ephedra sinica; erythroderma; fatigue; flu like syndrome; gastritis; gastrointestinal disease; germander; hair loss; headache; heart infarction; heart muscle ischemia; heart palpitation; heat stroke; hedeoma pulegoides; human; Hypericum perforatum; hypertension; hypomania; hypotension; insomnia; irritability; ischialgia; larrea tridentata; lethargy; liver injury; mania; medicinal plant; mental disease; Mentha pulegium; meta analysis; microangiopathy; migraine; muscle weakness; mydriasis; narcolepsy; nausea; nephrolithiasis; neurosis; nonhuman; pain; parkinsonism; Piper methysticum; priority journal; pruritus; psychosis; rash; respiratory tract infection; retina injury; review; risk assessment; risk factor; scutellaria lateriflora; sedation; seizure; serotonin syndrome; sexual dysfunction; side effect; skin disease; stroke; syncope; systematic review; tachycardia; thirst; tobacco dependence; virus inhibition; vomiting; withdrawal syndrome; xerostomia; Ephedra; Herb-Drug Interactions; Humans; Hypericum; Phytotherapy",,"alprazolam, 28981-97-7; amitriptyline, 50-48-6, 549-18-8; amsacrine, 51264-14-3, 54301-15-4; cyclosporin, 79217-60-0; digoxin, 20830-75-5, 57285-89-9; etoposide, 33419-42-0; fexofenadine, 138452-21-8; hyperforin, 11079-53-1; hypericin, 548-04-9; imatinib, 152459-95-5, 220127-57-1; indinavir, 150378-17-9, 157810-81-6, 180683-37-8; methadone, 1095-90-5, 125-56-4, 23142-53-2, 297-88-1, 76-99-3; midazolam, 59467-70-8; nevirapine, 129618-40-2; omeprazole, 73590-58-6, 95510-70-6; paroxetine, 61869-08-7; simvastatin, 79902-63-9; theophylline, 58-55-9, 5967-84-0, 8055-07-0, 8061-56-1, 99007-19-9; verapamil, 152-11-4, 52-53-9; warfarin, 129-06-6, 2610-86-8, 3324-63-8, 5543-58-8, 81-81-2",,,"Eisenberg, D.M., Davis, R.B., Ettner, S.L., Trends in alternative medicine use in the United States, 1990-1997: Results of a follow-up national survey (1998) JAMA, 280, pp. 1569-1575; Hung, O.L., Shih, R.D., Chiang, W.K., Herbal preparation use among urban emergency department patients (1997) Acad Emerg Med, 4, pp. 209-213; Voelker, R., IOM points to need for more research, regulation in alternative medicine (2005) JAMA, 293, pp. 1178-1180; (2004) Acting FDA Commissioner Dr. Lester M. 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An important question for public safety (2002) Clin Pharmacol Ther, 71, pp. 411-413","Holstege, C.P.; University of Virginia Health System; PO Box 800774 Charlottesville, VA 22908-0774, United States; email: ch2xf@virginia.edu",,,,,,,,00257125,,MCNAA,10.1016/j.mcna.2005.08.002,"English","Medical Clinics of North America",Review,Scopus "Kirman C.R., Gargas M.L., Marsh G.M., Strother D.E., Klaunig J.E., Collins J.J., Deskin R.","Cancer dose-response assessment for acrylonitrile based upon rodent brain tumor incidence: Use of epidemiologic, mechanistic, and pharmacokinetic support for nonlinearity",2005,"Regulatory Toxicology and Pharmacology",43,1,,85,103,,1,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-24644449690&partnerID=40&rel=R8.0.0","Sapphire Group, Inc., Beachwood, OH, United States; Sapphire Group, Inc., Dayton, OH, United States; University of Pittsburgh, Pittsburgh, PA, United States; BP Chemical, Arlington, VA, United States; Indiana University, School of Medicine, Indianapolis, IN, United States; Dow Chemical Company, Midland, MI, United States; Cytec Industries, West Paterson, NJ, United States","A cancer dose-response assessment was conducted for acrylonitrile (AN) using updated information on mechanism of action, epidemiology, toxicity, and pharmacokinetics. Although more than 10 chronic bioassays indicate that AN produces multiple tumors in rats and mice, a number of large, well-conducted epidemiology studies provide no evidence of a causal association between AN exposure and cancer mortality of any type. The epidemiological data include early industry exposures that are far higher than occur today and that approach or exceed levels found to be tumorigenic in animals. Despite the absence of positive findings in the epidemiology data, a dose-response assessment was conducted for AN based on brain tumors in rats. Mechanistic studies implicate the involvement of oxidative stress in rat brain due to a metabolite (2-cyanoethylene oxide or CEO, cyanide), but do not conclusively rule out a potential role for the direct genotoxicity of CEO. A PBPK model was used to predict internal doses (peak CEO in brain) for 12 data sets, which were pooled together to provide a consistent characterization of the dose-response relationship for brain tumor incidence in the rat. The internal dose corresponding to a 5% increase in extra risk (ED05 = 0.017 mg/L brain) and its lower confidence limit (LED05 = 0.014 mg/L brain) was used as the point of departure. The weight-of-evidence supports the use of a nonlinear extrapolation for the cancer dose-response assessment. A quantitative comparison of the epidemiology exposure-response data (lung and brain cancer mortality) to the rat brain tumor data in terms of internal dose adds to the confidence in the nonlinear extrapolation. Uncertainty factors of 200 and 220 (for the oral and inhalation routes, respectively) were applied to the LED05 to account for interspecies variation, intraspecies variation, and the severity of the response measure. Accordingly, oral doses below 0.009 mg/kg-day and air concentrations below 0.1 mg/m3 are not expected to pose an appreciable risk to human populations exposed to AN. © 2004 Elsevier Inc. All rights reserved.","Acrylonitrile; Cancer dose-response assessment; Epidemiology; Mode of action; PBPK modeling; Species differences","acrylonitrile; cyanide; oxide; animal experiment; animal model; bioassay; brain cancer; brain tumor; carcinogenesis; comparative study; concentration (parameters); controlled study; disease severity; dose response; exposure; genotoxicity; human; incidence; lung cancer; medical assessment; metabolite; mortality; mouse; nonhuman; oxidative stress; priority journal; quantitative analysis; rat; review; risk assessment; rodent; toxicity; Acrylonitrile; Administration, Oral; Animals; Brain Neoplasms; Carcinogenicity Tests; Carcinogens; Dose-Response Relationship, Drug; Environmental Exposure; Humans; Incidence; Inhalation Exposure; Lung Neoplasms; Meta-Analysis; Mice; Models, Biological; Mutagenicity Tests; Nonlinear Dynamics; Rats; Animalia; Rodentia",,"acrylonitrile, 107-13-1; cyanide, 57-12-5; oxide, 16833-27-5; Acrylonitrile, 107-13-1; Carcinogens",,,"Abdel-Rahman, S.Z., Nouraldeen, A.M., Ahmed, A.E., Molecular interaction of [2,3-14C] acrylonitrile with DNA in gastric tissue of rat (1994) J. 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Report of the International Programme on Chemical Safety's collaborative study on in vitro assays; Zhang, H., Kamendulis, L.M., Klaunig, J.E., Mechanisms for the Induction of Oxidative Stress in Syrian Hamster Embryo Cells by Acrylonitrile (2002) Toxicol. Sci., 67, pp. 247-255; Zhang, H., Kamendulis, L.M., Jiang, J., Xu, Y., Klaunig, J.E., Acrylonitrile-induced morphological transformation in Syrian Hamster Embryo Cells (2000) Carcinogenesis, 21, pp. 727-733","Kirman, C.R.; Sapphire Group, Inc. Beachwood, OH, United States; email: crk@thesapphiregroup.com",,,,,,,,02732300,,RTOPD,10.1016/j.yrtph.2005.06.007,"English","Regulatory Toxicology and Pharmacology",Review,Scopus "Burris T.P., Krishnan V.","Estrogen: A mitochrondrial energizer that keeps on going",2005,"Molecular Pharmacology",68,4,,956,958,,4,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-25144509877&partnerID=40&rel=R8.0.0","Lilly Research Laboratories, Lilly Corporate Center, Indianapolis, IN, United States; Department of Pharmacology and Toxicology, Indiana University, School of Medicine, Indianapolis, IN, United States; Lilly Research Laboratories, Lilly Corporate Center, Indianapolis, IN 46285, United States","Estrogens demonstrate vasoprotective activity in many experimental models. These effects have been attributed to beneficial activity of these steroids on lipid metabolism as well as direct effects on the vasculature via modulation of nitric-oxide synthase and phosphatidylinositol-3 kinase/Akt signaling pathways. In this issue of Molecular Pharmacology, Stirone et al. (p. 959) present evidence suggesting that 17 β-estradiol may also exert vasoprotective effects in cerebral blood vessels via stimulation of mitochondrial energy production capacity and inhibition of reactive oxygen species production. These data indicate not only yet another potential mechanism underlying the vasoprotective effects of estrogens but also that the estrogen receptor may coordinate gene expression in both the nuclear and mitochondrial genomes. Copyright © 2005 The American Society for Pharmacology and Experimental Therapeutics.",,"conjugated estrogen; conjugated estrogen plus medroxyprogesterone acetate; estradiol; estrogen; estrogen receptor; gestagen; medroxyprogesterone acetate; mitochondrial protein; nitric oxide synthase; phosphatidylinositol 3 kinase; placebo; progesterone; protein kinase B; brain blood vessel; breast cancer; cerebrovascular disease; clinical trial; drug activity; drug mechanism; energy yield; estrogen activity; estrogen therapy; gene expression; gene expression regulation; genome; hormone substitution; human; lipid metabolism; mitochondrion; nonhuman; postmenopause; priority journal; protein expression; risk assessment; short survey; signal transduction; vascular disease; vascularization; Animals; Estradiol; Humans; Mitochondria; Reactive Oxygen Species",,"estradiol, 50-28-2; medroxyprogesterone acetate, 71-58-9; nitric oxide synthase, 125978-95-2; phosphatidylinositol 3 kinase, 115926-52-8; progesterone, 57-83-0; protein kinase B, 148640-14-6; Estradiol, 50-28-2; Reactive Oxygen Species",,,"An, J.P., Ribeiro, R.C.J., Webb, P., Gustafsson, J.A., Kushner, P.J., Baxter, J.D., Leitman, D.C., Estradiol repression of tumor necrosis factor-alpha transcription requires estrogen receptor activation function-2 and is enhanced by coactivators (1999) Proc Natl Acad Sci USA, 96, pp. 15161-15166; Anderson, G.L., Limacher, M., Assaf, A.R., Bassford, T., Beresford, S.A.A., Black, H., Bonds, D., Caan, B., Effects of conjugated, equine estrogen in postmenopausal women with hysterectomy - The women's health initiative randomized controlled trial (2004) J Am Med Assoc, 291, pp. 1701-1712; Arenas, I.A., Armstrong, S.J., Xu, Y., Davidge, S.T., Chronic tumor necrosis factor-alpha inhibition enhances NO modulation of vascular function in estrogen-deficient rats (2005) Hypertension, 46, pp. 76-81; Ballinger, S.W., Mitochondrial dysfunction in cardiovascular disease (2005) Free Radic Biol Med, 38, pp. 1278-1295; Ballinger, S.W., Patterson, C., Yan, C.N., Doan, R., Burow, D.L., Young, C.G., Yakes, F.M., Freeman, B.A., Hydrogen peroxide- and peroxynitrite-induced mitochondrial DNA damage and dysfunction in vascular endothelial and smooth muscle cells (2000) Circ Res, 86, pp. 960-966; 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Lesnefsky, E.J., Moghaddas, S., Tandler, B., Kerner, J., Hoppel, C.L., Mitochondrial dysfunction in cardiac disease: Ischemia-reperfusion, aging and heart failure (2001) J Mol Cell Cardiol, 33, pp. 1065-1089; Madamanchi, N.R., Hakim, Z.S., Runge, M.S., Oxidative stress in atherogenesis and arterial thrombosis: The disconnect between cellular studies and clinical outcomes (2005) Thromb Haemostasis, 3, pp. 254-267; Martin, M.B., Franke, T.F., Stoica, G.E., Chambon, P., Katzenellenbogen, B.S., Stoica, B.A., McLemore, M.S., Stoica, A., A role for Akt in mediating the estrogenic functions of epidermal growth factor and insulin-like growth factor I (2000) Endocrinology, 141, pp. 4503-4511; Miyagawa, K., Rosch, J., Stanczyk, F., Hermsmeyer, K., Medroxyprogesterone interferes with ovarian steroid protection against coronary vasospasm (1997) Nat Med, 3, pp. 324-327; Monje, P., Boland, R., Expression and cellular localization of naturally occurring beta estrogen receptors in uterine and mammary cell lines (2002) J Cell Biochem, 86, pp. 136-144; 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White, R.E., Estrogen and vascular function (2002) Vasc Pharmacol, 38, pp. 73-80; Yang, S.H., Liu, R., Perez, E.J., Wen, Y., Stevens, S.M., Valencia, T., Brun-Zinkernagel, A.M., Dykens, J., Mitochondrial localization of estrogen receptor beta (2004) Proc Natl Acad Sci USA, 101, pp. 4130-4135","Burris, T.P.; Lilly Research Laboratories; Lilly Corporate Center Indianapolis, IN 46285, United States; email: burris@lilly.com",,,,,,,,0026895X,,MOPMA,10.1124/mol.105.017335,"English","Molecular Pharmacology",Short Survey,Scopus "Stillwell W., Shaikh S.R., Zerouga M., Siddiqui R., Wassal S.R.","Docosahexaenoic acid affects cell signaling by altering lipid rafts",2005,"Reproduction Nutrition Development",45,5,,559,579,,24,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-27244437222&partnerID=40&rel=R8.0.0","Department of Biology, Indiana University, 723 West Michigan, Indianapolis, IN 46206, United States; Cellular Biochemistry Laboratory, Methodist Research Institute, Clarian Health Partners, 1801 N. Capitol Ave., Indianapolis, IN 46206, United States; Department of Physics, Indiana University, 402 North Balckford St., Indianapolis, IN 46202, United States","With 22 carbons and 6 double bonds docosahexaenoic acid (DHA) is the longest and most unsaturated fatty acid commonly found in membranes. It represents the extreme example of a class of important human health promoting agents known as omega-3 fatty acids. DHA is particularly abundant in retinal and brain tissue, often comprising about 50% of the membrane's total acyl chains. Inadequate amounts of DHA have been linked to a wide variety of abnormalities ranging from visual acuity and learning irregularities to depression and suicide. The molecular mode of action of DHA, while not yet understood, has been the focus of our research. Here we briefly summarize how DHA affects membrane physical properties with an emphasis on membrane signaling domains known as rafts. We report the uptake of DHA into brain phosphatidylethanolamines and the subsequent exclusion of cholesterol from the DHA-rich membranes. We also demonstrate that DHA-induced apoptosis in MDA-MB-231 breast cancer cells is associated with externalization of phosphatidylserine and membrane disruption (""blebbing""). We conclude with a proposal of how DHA incorporation into membranes may control cell biochemistry and physiology. © INRA, EDP Sciences, 2005.","Apoptosis; Docosahexaenoic acid; Lipid rafts; Membranes; Phospholipids","carbon; CD8 antigen; ceramide; cholesterol; docosahexaenoic acid; fish oil; long chain fatty acid; major histocompatibility antigen class 1; omega 3 fatty acid; phosphatidylcholine; phosphatidylethanolamine; phosphatidylserine; protein kinase C; rhodopsin; sphingomyelin; Thy 1 antigen; unsaturated fatty acid; antineoplastic activity; apoptosis; bilayer membrane; biochemistry; brain region; breast cancer; cell function; cell membrane fluidity; cell membrane permeability; chemical bond; depression; drug mechanism; drug structure; elasticity; human; learning disorder; lipid membrane; lipid raft; lipid storage; lipid transport; membrane damage; membrane structure; molecular dynamics; molecular interaction; nonhuman; physical parameters; retina; review; signal transduction; suicidal behavior; visual impairment; Animals; Apoptosis; Brain; Cell Membrane; Depressive Disorder, Major; Docosahexaenoic Acids; Humans; Membrane Lipids; Signal Transduction; Suicide",,"carbon, 7440-44-0; cholesterol, 57-88-5; docosahexaenoic acid, 25167-62-8, 32839-18-2; fish oil, 8016-13-5; phosphatidylcholine, 55128-59-1, 8002-43-5; phosphatidylethanolamine, 1405-71-6; protein kinase C, 141436-78-4; rhodopsin, 60383-01-9, 9009-81-8; sphingomyelin, 85187-10-6; Docosahexaenoic Acids, 25167-62-8; Membrane Lipids",,,"Stillwell, W., Wassall, S.R., Docosahexaenoic acid: Membrane properties of a unique fatty acid (2003) Chem. 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Acta, 1417, pp. 89-100","Stillwell, W.; Department of Biology; Indiana University; 723 West Michigan Indianapolis, IN 46202, United States; email: wstillwe@iupui.edu",,,,,,,,09265287,,RNDEE,10.1051/rnd:2005046,"English","Reproduction Nutrition Development",Review,Scopus "Yao Y., Kubota T., Takeuchi H., Sato K.","Prognostic significance of microvessel density determined by an anti-CD105/endoglin monoclonal antibody in astrocytic tumors: Comparison with an anti-CD31 monoclonal antibody",2005,"Neuropathology",25,3,,201,206,,10,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-27244431905&partnerID=40&rel=R8.0.0","Department of Neurosurgery, Faculty of Medical Sciences, University of Fukui, Fukui, Japan; Department of Microbiology and Immunology, Indiana University School of Medicine, Walther Oncology Center, 950 W. Walnut Street, Indianapolis, IN 46202, United States","There are conflicting reports as to whether the degree of angiogenesis as measured by microvessel density (MVD) has a prognostic value in astrocytic tumors. This may be due to the use of different antibodies against endothelial cells to highlight microvessels. It has been reported that unlike pan-endothelial antibodies, such as CD31, anti-CD105 antibodies preferentially react with endothelial cells in angiogenic tissues. To clarify the validity of anti-CD105 antibody in the evaluation of angiogenesis, we assessed MVD using an anti-CD105 monoclonal antibody (mAb) (CD105-MVD) and an anti-CD31 mAb (CD31-MVD) in a series of 50 astrocytic tumors, and correlated MVD with expression of the key angiogenic factor vascular endothelial growth factor (VEGF) and prognosis. The mean CD31-MVD and CD105-MVD was 36.7 and 24.8 for low-grade astrocytoma (LGA), 48.0 and 42.7 for anaplastic astrocytoma, 55.3 and 51.9 for glioblastoma multiforme (GBM), respectively. CD105-MVD was more closely correlated with VEGF expression than CD31-MVD. Patients with LGA and GBM showing higher CD105-MVD had a significantly shorter mean survival time (MST) than those with lower CD105-MVD tumors (P = 0.0381 and 0.0131, respectively). Whereas the MST of patients with higher CD31-MVD tumors seemed to be shorter than that of lower CD31-MVD patients within each tumor grade, the differences were not statistically significant. These findings suggest that anti-CD105 mAb may be a better marker than anti-CD31 mAb in evaluation of angiogenesis and prediction of prognosis in astrocytic tumors.","Angiogenesis; Anti-CD105 mAb; Glioma; Microvessel density; Prognosis","endoglin; monoclonal antibody; monoclonal antibody CD105; monoclonal antibody cd31; monoclonal antibody endoglin; unclassified drug; vasculotropin; CD31 antigen; cell surface receptor; diagnostic agent; ENG protein, human; leukocyte antigen; tumor marker; vascular cell adhesion molecule 1; vasculotropin A; adolescent; adult; aged; angiogenesis; article; astrocytoma; blood vessel diameter; cancer grading; clinical article; controlled study; female; glioblastoma; human; immunohistochemistry; male; microvasculature; priority journal; prognosis; protein expression; biosynthesis; brain tumor; comparative study; immunology; metabolism; middle aged; mortality; neovascularization (pathology); pathology; survival; survival rate; vascularization; Adolescent; Adult; Aged; Aged, 80 and over; Antibodies, Monoclonal; Antigens, CD; Antigens, CD31; Astrocytoma; Brain Neoplasms; Female; Humans; Immunohistochemistry; Male; Middle Aged; Neovascularization, Pathologic; Prognosis; Receptors, Cell Surface; Survival Analysis; Survival Rate; Tumor Markers, Biological; Vascular Cell Adhesion Molecule-1; Vascular Endothelial Growth Factor A",,"vasculotropin, 127464-60-2; vasculotropin A, 489395-96-2; Antibodies, Monoclonal; Antigens, CD; Antigens, CD31; ENG protein, human; Receptors, Cell Surface; Tumor Markers, Biological; Vascular Cell Adhesion Molecule-1; Vascular Endothelial Growth Factor A",,,"Folkman, J., Angiogenesis and tumor growth (1996) N Engl J Med, 334, p. 921; Fidler, I.J., Ellis, L.M., The implications of angiogenesis for the biology and therapy of cancer metastasis (1994) Cell, 79, pp. 185-188; Fox, S.B., Gatter, K.C., Harris, A., Tumor angiogenesis (1996) J Pathol, 179, pp. 232-237; Leon, S.P., Folkerth, R.D., Black, P.M., Microvessel density is a prognostic indicator for patients with astroglial brain tumors (1996) Cancer, 77, pp. 362-372; Abdulrauf, S.I., Edvardsen, K., Ho, K.L., Yang, X.Y., Rock, J.P., Rosenblum, M.L., Vascular endothelial growth factor expression and vascular density as prognostic marker of survival in patients with low-grade astrocytoma (1998) J Neurosurg, 88, pp. 513-520; Yao, Y., Kubota, T., Sato, K., Kitai, R., Takeuchi, H., Arishima, H., Prognostic value of vascular endothelial growth factor and its receptors flt-1 and flk-1 in astrocytic tumors (2001) Acta Neurochir, 143, pp. 159-166; Torp, S.H., Alsaker, M., Ki-67 immunoreactivity, basic fibroblastic growth factor (bFGF) expression, and microvessel density as supplementary prognostic tools in low-grade astrocytomas. An immunohistochemical study with special reference to the reliability of different Ki-67 antibodies (2002) Pathol Res Pract, 198, pp. 261-265; Kumar, P., Wang, J.M., Bernabeu, C., CD105 and angiogenesis (1996) J Pathol, 178, pp. 363-366; Vermeulen, P.B., Gasparini, G., Fox, P.B., Quantification of angiogenesis in solid human tumors: An international consensus on the methodology and criteria of evaluation (1996) Eur J Cancer, 32 A, pp. 2474-2484; Wang, J.M., Kumar, S., Pye, D., Haboubi, N., Al-Nakib, L., Breast carcinoma: Comparative study of tumor vasculature using two endothelial cell markers (1994) J Natl Cancer Inst, 86, pp. 386-388; Cheifetz, S., Bellon, T., Cales, C., Endoglin is a component of the transforming growth factor-beta receptor system in human endothelial cells (1992) J Biol Chem, 267, pp. 19027-19030; Li, C., Hampson, I.N., Hampson, L., Kumar, P., Bernabeu, C., Kumar, S., CD105 antagonizes the inhibitory signaling of transforming growth factor beta1 on human vascular endothelial cells (2000) FASEB J, 14, pp. 55-64; Li, D.Y., Sorensen, L.K., Brooke, B.S., Defective angiogenesis in mice lacking endoglin (1999) Science, 284, pp. 1534-1537; Wang, J.M., Kumar, S., Pye, D., Van Agthoven, A., Krupinski, J., Hunter, R.D., A monoclonal antibody detects heterogeneity in vascular endothelium of tumors and normal tissues (1993) Int J Cancer, 54, pp. 363-370; Seon, B.K., Matsuno, F., Haruta, Y., Kondo, M., Bareas, M., Long-lasting complete inhibition of human solid tumors in SCID mice by targeting endothelial cells of tumor vasculature with antihuman endoglin immunotoxin (1997) Clin Cancer Res, 3, pp. 1031-1044; Kumar, S., Ghellal, A., Li, C., Breast carcinoma: Vascular density determined using CD105 antibody correlates with tumor prognosis (1999) Cancer Res, 59, pp. 856-861; Tanaka, F., Otake, Y., Yanagihara, K., Evaluation of angiogenesis in non-small cell lung cancer: Comparison between anti-CD34 antibody and anti-CD105 antibody (2001) Clin Cancer Res, 7, pp. 3410-3415; Wikstrom, P., Lissbrant, I.F., Stattin, P., Egevad, L., Bergh, A., Endoglin (CD105) is expressed on immature blood vessels and is a marker for survival in prostate cancer (2002) Prostate, 51, pp. 268-275; Weidner, N., Carroll, P.R., Flax, J., Blumenfeld, W., Folkman, J., Tumor angiogenesis correlates with metastasis in invasive prostate carcinoma (1993) Am J Pathol, 143, pp. 401-409; Plate, K.H., Breier, G., Weich, H.A., Risau, W., Vascular endothelial growth factor is a potential tumor angiogenic factor in human gliomas in vivo (1992) Nature, 359, pp. 845-848; Folkerth, R.D., Descriptive analysis and quantification of angiogenesis in human brain tumors (2000) J Neurooncol, 50, pp. 165-172; Hasan, J., Byers, R., Jayson, G.C., Intra-tumoural microvessel density in human solid tumours (2002) Br J Cancer, 86, pp. 1566-1577; Staume, O., Akslen, L.A., Expression of vascular endothelial growth factor, its receptors (Flt-1, KDR) and TSP-1 related to microvessel density and patient outcome in vertical growth phase melanomas (2001) Am J Pathol, 159, pp. 223-235","Yao, Y.; Department of Microbiology and Immunology; Indiana University School of Medicine; Walther Oncology Center; 950 W. Walnut Street Indianapolis, IN 46202, United States; email: yonyao@iupui.edu",,,,,,,,09196544,,NOPAF,10.1111/j.1440-1789.2005.00632.x,"English","Neuropathology",Article,Scopus "Ahmed S.M., Cramer H., Ulbright T.M., Vance G.H., Hanna N.","Large cell carcinoma of the lung mimicking a germ cell tumor: The potential value of chromosome analysis",2005,"Lung Cancer",49,2,,271,274,,,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-22044441190&partnerID=40&rel=R8.0.0","Department of Internal Medicine, Indiana University, School of Medicine, Indianapolis, IN, United States; Department of Pathology and Laboratory Medicine, Indiana University, School of Medicine, Indianapolis, IN, United States; Department of Medical and Molecular Genetics, Indiana University, School of Medicine, Indianapolis, IN, United States; Division of Hematology/Oncology, Indiana University, School of Medicine, Indianapolis, IN, United States; RT 473, 535 Barnhill Drive, Indianapolis, IN 46202, United States",[No abstract available],"Chromosome 12; Fluorescent in situ hybridization; Germ cell cancers; HCG-beta; Isochromosomes; Large cell carcinomas; VIP chemotherapy combination","alpha fetoprotein; chorionic gonadotropin beta subunit; cisplatin; cytokeratin; etoposide; ifosfamide; thyroid transcription factor 1; adult; article; aspiration biopsy; blood chemistry; brain metastasis; cancer combination chemotherapy; cancer growth; case report; choriocarcinoma; chromosome 12p; chromosome analysis; computer assisted tomography; differential diagnosis; disease activity; echography; fluorescence in situ hybridization; germ cell tumor; gonadotropin blood level; gynecomastia; headache; histopathology; human; human tissue; isochromosome; large cell carcinoma; lifestyle; liver; lung carcinoma; lymphadenopathy; male; mediastinum; molecular probe; nuclear magnetic resonance imaging; priority journal; protein blood level; smoking; spleen; testis; tumor differentiation; visual impairment; Adult; Carcinoma, Large Cell; Choriocarcinoma; Chromosomes, Human; Humans; In Situ Hybridization, Fluorescence; Lung Neoplasms; Male; Mediastinal Neoplasms; Neoplasms, Germ Cell and Embryonal",,"cisplatin, 15663-27-1, 26035-31-4, 96081-74-2; etoposide, 33419-42-0; ifosfamide, 3778-73-2","vp 16",,"Downey, R.S., Sewell, C.W., Mansour, K.A., Large cell carcinoma of the lung: A highly aggressive tumor with dismal prognosis (1989) Ann Thorac Surg, 47, pp. 806-808; Group TIGCCC: Internation germ cell consensus classification: A prognostic factor-based staging system for metastatic germ cell cancers (1997) J Clin Oncol, 15, pp. 594-603; Bokemeyer, C., Nichols, C.R., Droz, J.-P., Schmoll, H.-J., Horwich, A., Gerl, A., Extragonadal germ cell tumors of the mediastinum and retroperitoneum: Results from an international analysis (2002) J Clin Oncol, 20, pp. 1864-1873; Zacahrias, J., Nicholson, A.G., Ladas, G.P., Goldstraw, P., Large cell neuroendocrine carcinoma and large cell carcinomas with neuroendocrine morphology of the lung: Prognosis after complete resection and systematic nodal dissection (2003) Ann Thorac Surg, 75, pp. 348-352; Kuhn, M., Weissbach, L., Localization, incidence, diagnosis and treatment of extratesticular germ cell tumors (1985) Urol Int, 40, pp. 166-172; Hotakainen, K., Ljungberg, B., Haglund, C., Nordling, S., Paju, A., Stenman, U.H., Expression of the free beta-subunit of human chorionic gonadotropin in renal cell carcinoma: Prognostic study on tissue and serum (2003) Int J Cancer, 104 (5), pp. 631-635; Louhimo, J., Carpelan-Holmstrom, M., Alfthan, H., Stenman, U.H., Jarvinen, H.J., Haglund, C., Serum HCG beta, CA 72-4 and CEA are independent prognostic factors in colorectal cancer (2002) Int J Cancer, 101 (6), pp. 545-548; Louhimo, J., Finne, P., Alfthan, H., Stenman, U.H., Haglund, C., Combination of HCG-beta, CA 19-9 and CEA with logistic regression improves accuracy in gastrointestinal malignancies (2002) Anticancer Res, 22 (3), pp. 1759-1764; Collins, R.J., Wong, L.C., Adenocarcinoma of the uterine cervix with beta-hCG production: A case report and review of the literature (1989) Gynecol Oncol, 33 (1), pp. 99-107; Rau, C.S., Lin, J.W., Liang, C.L., Lee, T.C., Chen, H.J., Lu, K., Production of human chorionic gonadotropin-beta subunit associated with an osteolytic meningioma. 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III. Cytogenetics and genes in testicular tumors (1996) J Urol, 155, pp. 1531-1556; Ullmann, R., Schwendel, A., Klemen, H., Wolf, G., Petersen, I., Popper, H.H., Unbalanced chromosomal aberrations in neuroendocrine lung tumors as detected by comparative genomic hybridization (1998) Hum Pathol, 29, pp. 1145-1149; Walch, A.K., Zitzelsberger, H.F., Aubele, M.M., Mattis, A.E., Bauchinger, M., Candidus, S., Typical and atypical carcinoid tumors of the lung are characterized by 11q deletions as detected by comparative genomic hybridization (1998) Am J Pathol, 153 (4), pp. 1089-1098; Li, J., Zhang, Z., Dai, Z., Plass, C., Morrison, C., Wang, Y., LOH of chromosome 12p correlates with Kras2 mutation in non-small cell lung cancer (2003) Oncogene, 22 (8), pp. 1243-1246; Hainsworth, J.D., Einhorn, L.H., Williams, S.D., Stewart, M., Greco, F.A., Advanced extragonadal germ-cell tumors. Successful treatment with combination chemotherapy (1982) Ann Intern Med, 97 (1), pp. 7-11; Bassetto, M.A., Pasini, F., Franceschi, T., Mustacchi, G., Cetto, G.L., Extragonadal germ cell tumor: A clinical study (1995) Anticancer Res, 15, pp. 2751-2754","Hanna, N.; RT 473; 535 Barnhill Drive Indianapolis, IN 46202, United States; email: nhanna@iupui.edu",,,,,,,,01695002,,LUCAE,10.1016/j.lungcan.2005.02.015,"English","Lung Cancer",Article,Scopus "Wagner J.D., Schauwecker D., Davidson D., Logan T., Coleman III J.J., Hutchins G., Love C., Wenck S., Daggy J.","Inefficacy of F-18 fluorodeoxy-D-glucose-positron emission tomography scans for initial evaluation in early-stage cutaneous melanoma",2005,"Cancer",104,3,,570,579,,27,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-22544441594&partnerID=40&rel=R8.0.0","Department of Surgery, Indiana University School of Medicine, Indiana University-Purdue University at Indianapolis, Indianapolis, IN, United States; Department of Radiology, Indiana University School of Medicine, Indiana University-Purdue University at Indianapolis, Indianapolis, IN, United States; Department of Pathology, Indiana University School of Medicine, Indiana University-Purdue University at Indianapolis, Indianapolis, IN, United States; Department of Medicine, Indiana University School of Medicine, Indiana University-Purdue University at Indianapolis, Indianapolis, IN, United States; Department of Biostatistics, Indiana University School of Medicine, Indiana University-Purdue University at Indianapolis, Indianapolis, IN, United States; Department of Surgery, Indiana University School of Medicine, Clearvista Parkway, Indianapolis, IN 46256, United States","BACKGROUND. The purpose of the current study was to determine the sensitivity and specificity of initial F-18 fluorodeoxy-D-glucose-positron emission tomography (FDG-PET) scanning for detection of occult lymph node and distant metastases in patients with early-stage cutaneous melanoma. METHODS. The authors conducted a prospective nonrandomized clinical trial. Inclusion criteria were patients with cutaneous melanoma tumors > 1.0 mm Breslow thickness, local disease recurrence, or solitary intransit metastases without regional lymph or distant metastases by standard clinical evaluation. All patients underwent whole-body FDG-PET scanning before surgical therapy. Abnormal PET findings were studied by targeted conventional imaging and/or biopsy. FDG-PET scans were interpreted in a blinded fashion. Regional lymph node basins were staged by sentinel lymph node biopsy (SLNB). PET scan findings in regional lymph nodes were compared with histology of SLNB specimens. Abnormal distant PET scan findings were studied with repeat conventional scan imaging at 3-6 months and were correlated with the first site(s) of clinical disease recurrence. Blinded PET scan findings were correlated with all information to determine sensitivity and specificity. RESULTS. There were 144 assessable patients with a mean tumor depth of 2.8 mm. The median follow-up for these patients was 41.4 months. Blinded interpretations of FDG-PET scan images showed that 31 patients (21%) had signs of metastatic disease, 13 patients had probable regional lymph node metastases, and 18 patients had 23 sites of possible distant metastases. SLNB and/or follow-up demonstrated regional lymph node metastases in 43 of 184 lymph node basins in 40 patients (27.8%). Compared with all clinical information, FDG-PET scan sensitivity for detection of regional lymph node metastases was 0.21 (95% confidence [CI], 0.10-0.36) and specificity was 0.97 (95% CI, 0.93-0.99). No distant sites were confirmed to be true positive by targeted conventional imaging/biopsy at the time of presentation. Thirty-four patients (23.6%) presented with 54 foci of metastatic disease at initial disease recurrence. FDG-PET scan sensitivity for prediction of the first site(s) of clinical disease recurrence was 0.11 (95% CI, 0.04-0.23). Excluding patients with brain metastases, FDG-PET scan sensitivity for detection of occult Stage IV disease in patients was 0.04 (95% CI, 0.001-0.20) and specificity was 0.86 (95% CI, 0.79-0.92). CONCLUSIONS. FDG-PET scanning did not impact the care of patients with early-stage melanoma already staged by standard techniques. Routine FDG-PET scanning was not recommended for the initial staging evaluation in this population. © 2005 American Cancer Society.","Fluorodeoxyglucose; Lymph nodes; Melanoma; Metastases; Positron emission tomography scan","fluorodeoxyglucose f 18; adult; aged; article; cancer recurrence; cancer staging; clinical trial; computer assisted emission tomography; controlled clinical trial; controlled study; correlation analysis; diagnostic accuracy; diagnostic value; female; histopathology; human; image analysis; lymph node biopsy; lymph node metastasis; lymphoscintigraphy; major clinical study; male; melanoma; metastasis; occult cancer; preoperative evaluation; priority journal; randomized controlled trial; sentinel lymph node; single blind procedure; skin cancer; thickness; tumor volume; validation process; Adult; Aged; Biopsy; Female; Fluorodeoxyglucose F18; Humans; Lymph Nodes; Lymphatic Metastasis; Male; Melanoma; Middle Aged; Neoplasm Staging; Prospective Studies; Radiopharmaceuticals; Sensitivity and Specificity; Skin Neoplasms; Tomography, Emission-Computed",,"fluorodeoxyglucose f 18, 63503-12-8; Fluorodeoxyglucose F18, 63503-12-8; Radiopharmaceuticals",,,"Balch, C.M., Buzaid, A.C., Atkins, M.B., A new American Joint Committee on Cancer staging system for cutaneous melanoma (2000) Cancer, 88, pp. 1484-1491; Gershenwald, J.E., Thompson, W., Mansfield, P.F., Multi-institutional melanoma lymphatic mapping experience: The prognostic value of sentinel lymph node status in 612 stage 1 or II melanoma patients (1999) J Clin Oncol, 17, pp. 976-983; Wagner, J.D., Ranieri, J., Evdokimow, D.Z., Patterns of initial recurrence and prognosis after sentinel node biopsy and selective lymphadenectomy for melanoma (2003) Plast Reconst Surg, 112, pp. 486-497; Gritters, L.S., Francis, I.R., Zasadny, K.R., Initial assessment of positron emission tomography using 2-fluorine-18-fluoro-2-deoxy-D-glucose in the imaging of malignant melanoma (1993) J Nucl Med, 34, pp. 1420-1427; Boni, R., Boni, P.J.A., Steinert, H., Staging of metastatic melanoma by whole body positron emission tomography using 2-fluorine-18-fluoro-2-deoxy-D-glucose (1995) Br J Dermatol, 132, pp. 556-562; Wagner, J.D., Schauwecker, D., Hutchins, G., Initial assessment of positron emission tomography for detection of subclinical regional lymphatic metastases in melanoma (1997) J Surg Oncol, 64, pp. 181-189; Steinert, H.C., Boni, R.A., Buck, A., Malignant melanoma: Staging with whole body positron emission tomography and 2-(F-18)-fluoro-2-deoxy-D-glucose (1995) Radiology, 195, pp. 705-709; Rinne, D., Baum, R.P., Hor, G., Primary staging and followup of high-risk melanoma patients with whole body 18 F-fluorodeoxyglucose positron emission tomography. Results of a prospective study of 100 patients (1998) Cancer, 82, pp. 1664-1671; Kirgan, D., Guenther, J., Bhattathiry, M., The importance of whole body PET scans on the management of metastatic malignant melanoma (1994) Proc Am Soc Clin Oncol, 13, p. 396; Blessing, C., Feine, U., Geiger, L., Positron emission tomography and ultrasonography: A comparative retrospective study assessing the diagnostic validity in lymph node metastases of malignant melanoma (1995) Arch Dermatol, 131, pp. 1394-1398; Damian, D.L., Fulham, M.J., Thompson, E., Positron emission tomography in the detection and management of metastatic melanoma (1996) Melanoma Res, 6, pp. 325-329; Macfarlane, D.J., Sondak, V., Johnson, T., Wahl, R., Prospective evaluation of 2-(18F)-2-deoxyglucose positron emission tomography in staging of regional lymph nodes in patients with cutaneous malignant melanoma (1998) J Clin Oncol, 16, pp. 1770-1776; Tyler, D.S., Onaitis, M., Kherani, A., Positron emission tomography scanning in malignant melanoma: Clinical utility in patients with stage III disease (2000) Cancer, 89, pp. 1019-1025; Mijnhout, S.G., Hoekstra, O.S., Van Tulter, M.W., Teule, G.J., Deville, W.L., Systematic review of the diagnostic accuracy of 18 f-fluorodeoxyglucose positron emission tomography in melanoma patients (2001) Cancer, 91, pp. 1530-1542; Wagner, J.D., Schauwecker, D.S., Davidson, D., Prospective study of fluorodeoxyglucose-positron emission tomography imaging of lymph node basins in melanoma patients undergoing sentinel node biopsy (1999) J Clin Oncol, 17, pp. 1508-1515; Balch, C.M., Buzaid, A.C., Soong, S.J., Final version of the American Joint Committee on Cancer staging system for cutaneous melanoma (2001) J Clin Oncol, 19, pp. 3635-3648; Acland, K.M., Healy, C., Calonje, E., Comparison of positron emission tomography scanning and sentinel node biopsy in the detection of micrometastases of primary cutaneous malignant melanoma (2001) J Clin Oncol, 19, pp. 2674-2678; Crippa, F., Leutner, M., Belli, F., Which kinds of lymph node metastases can fdg-pet detect? A clinical study in melanoma (2000) J Nucl Med, 41, pp. 1491-1494; Wagner, J.D., Schauwecker, D.S., Davidson, D., Wenck, S., Jung, S.H., Hutchins, G., FDG-PET sensitivity for melanoma lymph node metastases is dependent on tumor volume (2001) J Surg Oncol, 77, pp. 237-242; Wagner, J.D., Davidson, D., Coleman III, J.J., Lymph node tumor volumes in patients undergoing sentinel lymph node biopsy for cutaneous melanoma (1999) Ann Surg Oncol, 6, pp. 398-404","Wagner, J.D.; Department of Surgery; Indiana University School of Medicine; Clearvista Parkway Indianapolis, IN 46256, United States; email: jdwagner@insightbb.com",,,,,,,,0008543X,,CANCA,10.1002/cncr.21189,"English","Cancer",Article,Scopus "Van Meurs K.P., Wright L.L., Ehrenkranz R.A., Lemons J.A., Bethany Ball M., Kenneth Poole W., Perritt R., Higgins R.D., Oh W., Hudak M.L., Laptook A.R., Shankaran S., Finer N.N., Carlo W.A., Kennedy K.A., Fridriksson J.H., Steinhorn R.H., Sokol G.M., Ganesh Konduri G., Aschner J.L., Stoll B.J., D'Angio C.T., Stevenson D.K.","Inhaled nitric oxide for premature infants with severe respiratory failure",2005,"New England Journal of Medicine",353,1,,13,22,,51,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-21444459262&partnerID=40&rel=R8.0.0","Stanford University, School of Medicine, Palo Alto, CA, United States; National Institute of Child Health and Human Development (NICHD), Bethesda, MD, United States; Yale University, School of Medicine, New Haven, CT, United States; Indiana University, School of Medicine, Indianapolis, United States; Research Triangle Institute, Research Triangle Park, NC, United States; Women's and Infant's Hospital, Providence, RI, United States; University of Florida, Jacksonville, United States; Wayne State University, Detroit, United States; University of California at San Diego, San Diego, CA, United States; University of Alabama, Birmingham, AL, United States; University of Texas at Houston, Houston, TX, United States; College of Medicine, University of Cincinnati, Cincinnati, United States; Northwestern University, Chicago, United States; Medical College of Wisconsin, Milwaukee, WI, United States; Wake Forest University, School of Medicine, Winston-Salem, NC, United States; Emory University, School of Medicine, Atlanta, United States; University of Rochester, Rochester, NY, United States; Division of Neonatal and Developmental Medicine, Department of Pediatrics, Stanford University School of Medicine, 750 Welch Rd., Palo Alto, CA 94304, United States","Background: Inhaled nitric oxide is a controversial treatment for premature infants with severe respiratory failure. We conducted a multicenter, randomized, blinded, controlled trial to determine whether inhaled nitric oxide reduced the rate of death or bronchopulmonary dysplasia in such infants. Methods: We randomly assigned 420 neonates, born at less than 34 weeks of gestation, with a birth weight of 401 to 1500 g, and with respiratory failure more than four hours after treatment with surfactant to receive placebo (simulated flow) or inhaled nitric oxide (5 to 10 ppm). Infants with a response (an increase in the partial pressure of arterial oxygen of more than 10 mm Hg) were weaned according to protocol. Treatment with study gas was discontinued in infants who did not have a response. Results: The rate of death or bronchopulmonary dysplasia was 80 percent in the nitric oxide group, as compared with 82 percent in the placebo group (relative risk, 0.97; 95 percent confidence interval, 0.86 to 1.06; P=0.52), and the rate of bronchopulmonary dysplasia was 60 percent versus 68 percent (relative risk, 0.90; 95 percent confidence interval, 0.75 to 1.08; P=0.26). There were no significant differences in the rates of severe intracranial hemorrhage or periventricular leukomalacia. Post hoc analyses suggest that rates of death and bronchopulmonary dysplasia are reduced for infants with a birth weight greater than 1000 g, whereas infants weighing 1000 g or less who are treated with inhaled nitric oxide have higher mortality and increased rates of severe intracranial hemorrhage. Conclusions: The use of inhaled nitric oxide in critically ill premature infants weighing less than 1500 g does not decrease the rates of death or bronchopulmonary dysplasia. Further trials are required to determine whether inhaled nitric oxide benefits infants with a birth weight of 1000 g or more. Copyright © 2005 Massachusetts Medical Society.",,"nitric oxide; placebo; surfactant; oxygen; analytic method; arterial oxygen tension; article; birth weight; brain hemorrhage; child death; clinical trial; comparative study; confidence interval; controlled clinical trial; controlled study; critical illness; disease severity; drug response; encephalomalacia; flow; gas; gestational age; human; infant mortality; lung dysplasia; major clinical study; multicenter study; newborn; prematurity; priority journal; randomized controlled trial; respiratory failure; simulation; single blind procedure; statistical analysis; weaning; artificial ventilation; blood; female; inhalational drug administration; male; mortality; multimodality cancer therapy; neonatal respiratory distress syndrome; treatment outcome; very low birth weight; Administration, Inhalation; Bronchopulmonary Dysplasia; Cerebral Hemorrhage; Combined Modality Therapy; Female; Humans; Infant, Newborn; Infant, Premature; Infant, Premature, Diseases; Infant, Very Low Birth Weight; Leukomalacia, Periventricular; Male; Nitric Oxide; Oxygen; Respiration, Artificial; Respiratory Distress Syndrome, Newborn; Respiratory Insufficiency; Single-Blind Method; Treatment Outcome",,"nitric oxide, 10102-43-9; oxygen, 7782-44-7; Nitric Oxide, 10102-43-9; Oxygen, 7782-44-7",,,"Charafeddine, L., D'Angio, C.T., Phelps, D.L., Atypical chronic lung disease patterns in neonates (1999) Pediatrics, 103, pp. 759-765; Roze, J.-C., Storme, L., Echocardiographic investigation of inhaled nitric oxide in newborn babies with severe hypoxaemia (1994) Lancet, 344, pp. 303-305; Halliday, H., Hirschfeld, S., Riggs, T., Liebman, J., Fanaroff, A., Bormuth, C., Respiratory distress syndrome: Echocardiographic assessment of cardiovascular function and pulmonary vascular resistance (1977) Pediatrics, 60, pp. 444-449; Evans, N.J., Archer, L.N.J., Doppler assessment of pulmonary artery pressure and extrapulmonary shunting in the acute phase of hyaline membrane disease (1991) Arch Dis Child, 66, pp. 6-11; Skinner, J.R., Boys, R.J., Hunter, S., Hey, E.N., Pulmonary and systemic arterial pressure in hyaline membrane disease (1992) Arch Dis Child, 67, pp. 366-373; Walther, F.J., Benders, M.J., Leighton, J.O., Persistent pulmonary hypertension in premature neonates with severe respiratory distress syndrome (1992) Pediatrics, 90, pp. 899-904; Frostell, C., Fratacci, M.-D., Wain, J.C., Jones, R., Zapol, W.M., Inhaled nitric oxide: A selective pulmonary vasodilator reversing hypoxic pulmonary vasoconstriction (1991) Circulation, 83, pp. 2038-2047. , Erratum, Circulation 1991;84:2212; Rossaint, R., Falke, K.J., Lopez, F., Slama, K., Pison, U., Zalpol, W.M., Inhaled nitric oxide for the adult respiratory distress syndrome (1993) N Engl J Med, 328, pp. 399-405; Kinsella, J.P., Parker, T.A., Galan, H., Effects of inhaled nitric oxide on pulmonary edema and lung neutrophil accumulation in severe experimental hyaline membrane disease (1997) Pediatr Res, 41, pp. 457-463; Kinsella, J.P., Walsh, W.F., Bose, C.L., Inhaled nitric oxide in premature neonates with severe hypoxemic respiratory failure: A randomised controlled trial (1999) Lancet, 354, pp. 1061-1065; Early compared with delayed inhaled nitric oxide in moderately hypoxemic neonates with respiratory failure: A randomised controlled trial (1999) Lancet, 354, pp. 1066-1071. , Erratum, Lancet 1999;354:1826; Truffert, P., Llado-Paris, J., Mercier, J.-C., Dehan, M., Breart, G., Early inhaled nitric oxide in moderately hypoxemic preterm and term newborns with RDS: The RDS subgroup analysis of the Franco-Belgian iNO Randomized Trial (2003) Eur J Pediatr, 162, pp. 646-647; Subhedar, N.V., Ryan, S.W., Shaw, N.J., Open randomised controlled trial of inhaled nitric oxide and early dexamethasone in high risk premature infants (1997) Arch Dis Child Fetal Neonatal Ed, 77, pp. F185-F190; Barrington, K.J., Finer, N.N., Inhaled nitric oxide for respiratory failure in premature infants (2001) Cochrane Database Syst Rev, 4, pp. CD000509; Schreiber, M.D., Gin-Mestan, K., Marks, J.D., Huo, D., Lee, G., Srisuparp, P., Inhaled nitric oxide in premature infants with the respiratory distress syndrome (2003) N Engl J Med, 349, pp. 2099-2107; Jobe, A.H., Bancalari, E., Bronchopulmonary dysplasia (2001) Am J Respir Crit Care Med, 163, pp. 1723-1729; Schaffer, D.B., Palmer, E.A., Plotsky, D.F., Prognostic factors in the natural course of retinopathy of prematurity (1993) Ophthalmology, 100, pp. 230-237; Walsh, M.C., Yao, Q., Gettner, P., Impact of a physiologic definition on bronchopulmonary dysplasia rates (2004) Pediatrics, 114, pp. 1305-1311; Inhaled nitric oxide in full-term and nearly full-term infants with hypoxic respiratory failure (1997) N Engl J Med, 336, pp. 597-604.. , Erratum, N Engl J Med 1997;337:434; Konduri, G.G., Solimano, A., Sokol, G.M., A randomized trial of early versus standard inhaled nitric oxide therapy in term and near-term newborn infants with hypoxic respiratory failure (2004) Pediatrics, 113, pp. 559-564; Zou, G., A modified Poisson regression approach to prospective studies with binary data (2004) Am J Epidemiol, 159, pp. 702-706; O'Brien, P.C., Fleming, T.R., A multiple testing procedure for clinical trials (1979) Biometrics, 35, pp. 549-556; Furlong, B., Henderson, A.H., Lewis, M.J., Smith, J.A., Endothelium-derived relaxing factor inhibits in vitro platelet aggregation (1987) Br J Pharmacol, 90, pp. 687-692; Radomski, M.W., Palmer, R.M.J., Moncada, S., Endogenous nitric oxide inhibits human platelet adhesion to vascular endothelium (1987) Lancet, 2, pp. 1057-1058; Hogman, M., Frostell, C., Arnberg, H., Hedenstierna, G., Bleeding time prolongation and NO inhalation (1993) Lancet, 341, pp. 1664-1665; Cheung, P.-Y., Salas, E., Etches, P., Phillipos, E., Schultz, R., Radomski, M.W., Inhaled nitric oxide and inhibition of platelet aggregation in critically ill neonates (1998) Lancet, 351, pp. 1181-1182; George, T.N., Johnson, K.J., Bates, J.N., Segar, J.L., The effect of inhaled nitric oxide therapy on bleeding time and platelet aggregation in neonates (1998) J Pediatr, 132, pp. 731-734; Christou, H., Magnani, B., Morse, D., Inhaled nitric oxide does not affect adenosine 5'-diphosphate-dependent platelet activation in infants with persistent pulmonary hypertension of the newborn (1998) Pediatrics, 102, pp. 1390-1393; Van Meurs, K.P., Rhine, W.D., Asselin, J.M., Durand, D.J., Response of premature infants with severe respiratory failure to inhaled nitric oxide (1997) Pediatr Pulmonol, 24, pp. 319-323; Peliowski, A., Finer, N.N., Etches, P.C., Tierney, A.J., Ryan, C.A., Inhaled nitric oxide for premature infants after prolonged rupture of the membranes (1995) J Pediatr, 126, pp. 450-453; Mestan, K.K.L., Marks, J.D., Hecox, K., Neurodevelopmental outcomes of premature infants treated with inhaled nitric oxide (2005) N Engl J Med, 353, pp. 23-32; Use of inhaled nitric oxide (2000) Pediatrics, 106, pp. 344-345","Van Meurs, K.P.; Division of Neonatal and Developmental Medicine; Department of Pediatrics; Stanford University School of Medicine; 750 Welch Rd. Palo Alto, CA 94304, United States; email: vanmeurs@stanford.edu",,,,,,,,00284793,,NEJMA,10.1056/NEJMoa043927,"English","New England Journal of Medicine",Article,Scopus "Lo S.S., Chang E.L., Suh J.H.","Stereotactic radiosurgery with and without whole-brain radiotherapy for newly diagnosed brain metastases",2005,"Expert Review of Neurotherapeutics",5,4,,487,495,,7,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-22544471216&partnerID=40&rel=R8.0.0","Department of Radiation Oncology, Indiana Lions Gamma Knife Center, Indiana University Medical Center, 535 Barnhill Drive, Indianapolis, IN 46202, United States; Department of Radiation Oncology, University of Texas MD Anderson Cancer Center, 1515 Holcombe Blvd, Houston, TX 77030, United States; Brain Tumor Institute; Gamma Knife Center, Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, OH 44195, United States","Brain metastases develop in 20-40% of cancer patients and can cause significant morbidity. In selected patients with one to three lesions, stereotactic radiosurgery may be used to improve local control. However, it is unclear whether whole-brain radiotherapy is necessary for all patients who are candidates for stereotactic radiosurgery. While whole-brain radiotherapy may improve the locoregional control of brain metastases, it may cause long-term side effects and may not improve overall survival in some patients. Its benefits should be evaluated in the context of risks of neurocognitive deterioration, either from whole-brain radiotherapy or from uncontrolled brain metastases, and the possible need for salvage treatments with the omission of initial whole-brain radiotherapy. For certain radioresistant brain metastases, the benefit of whole-brain radiotherapy to patients who have stereotactic radiosurgery is uncertain. © 2005 Future Drugs Ltd.","Brain metastases; Radiosurgery; Whole-brain radiotherapy","gadolinium texaphyrin; brain edema; brain metastasis; cancer adjuvant therapy; cancer control; cancer radiotherapy; cancer recurrence; cancer survival; clinical trial; cognitive defect; gamma knife radiosurgery; histopathology; human; patient selection; radiation injury; radiation necrosis; radiosensitivity; review; risk assessment; seizure; stereotaxic surgery; treatment indication; Brain Neoplasms; Humans; Lung Neoplasms; Radiosurgery",,"gadolinium texaphyrin, 165254-24-0, 194083-75-5",,,"Cairncross, J.G., Kim, J.H., Posner, J.B., Radiation therapy for brain metastases (1980) Ann. Neurol., 7, pp. 529-541; Posner, J.B., Management of brain metastases (1992) Rev. 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Phys., 29, pp. 711-717; Mintz, A.H., Kestle, J., Rathbone, M.P., A randomized trial to assess the efficacy of surgery in addition to radiotherapy in patients with a single cerebral metastasis (1994) Cancer, 78 (7), pp. 1470-1476; Andrews, D.W., Scott, C.B., Sperduto, P.W., Whole brain radiation therapy with or without stereotactic radiosurgery boost for patients with one to three brain metastases: Phase III results of the RTOG 9508 randomised trial (2004) Lancet, 363 (9422), pp. 1665-1672; Larson, D.A., Flickinger, J.C., Loeffler, J.S., The radiobiology of radiosurgery (1993) Int. J. Radiat. Oncol. Biol. Phys., 25 (3), pp. 557-561; Auchter, R.M., Lamond, J.P., Alexander, E., A multi-institutional outcome and prognostic factor analysis of radiosurgery for resectable single brain metastasis (1996) Int. J. Radiat. Oncol. Biol. Phys., 35, pp. 27-35; Sanghavi, S.N., Miranpuri, S.S., Chappell, R., Radiosurgery for patients with brain metastases: A multi-institutional analysis, stratified by the RTOG recursive partitioning analysis method (2001) Int. J. Radiat. Oncol. Biol. Phys., 51, pp. 426-434; Kondziolka, D., Patel, A., Lunsford, L.D., Stereotactic radiosurgery plus whole brain radiotherapy versus radiotherapy alone for patients with multiple brain metastases (1999) Int. J. Radiat. Oncol. Biol. Phys., 45, pp. 427-434; Caspar, L., Scott, C., Rotman, M., Recursive partitioning analysis (RPA) of prognostic factors in three Radiation Therapy Oncology Group (RTOG) brain metastases trials (1997) Int. J. Radiat. Oncol. Biol. Phys., 37, pp. 745-751; Patchell, R.A., Tibbs, P.A., Regine, W.F., Postoperative radiotherapy in the treatment of single metastases to the brain: A randomized trial (1998) JAMA, 280 (17), pp. 1485-1489; Patchell, R.A., Regine, W.F., The rationale for adjuvant whole brain radiation therapy with radiosurgery in the treatment of single brain metastases (2003) Technol. Cancer Res. Treat., 2 (2), pp. 111-115; Regine, W.F., Huhn, J.L., Patchell, R.A., Risk of symptomatic brain tumor recurrence and neurologic deficit after radiosurgery alone in patients with newly diagnosed brain metastases: Results and implications (2002) Int. J. Radiat. Oncol. Biol. Phys., 52 (2), pp. 333-338; (2002) Int. J. Radiat. Oncol. Biol. Phys., 53 (1), p. 259. , Erratum; Sneed, P.K., Lamborn, K.R., Forstner, J.M., Radiosurgery for brain metastases: Is whole brain radiotherapy necessary? (1999) Int. J. Radiat. Oncol. Biol. Phys., 43 (3), pp. 549-558; Flickinger, J.C., Kondziolka, D., Lunsford, L.D., A multi-institutional experience with stereotactic radiosurgery for solitary brain metastasis (1994) Int. J. Radiat. Oncol. Biol. Phys., 28 (4), pp. 797-802; Aoyama, H., Shirato, H., Nakagawa, K., Interim report of the JROSG99-1 multi-institutional randomized trial, comparing radiosurgery alone vs. radiosurgery plus whole brain irradiation for 1-4 brain metastases (2004) J. Clin. Oncol., 22 (14 S), p. 1506. , ASCO Annual Meeting Proceedings (Post-Meeting Edition); Regine, W.F., Scott, C., Murray, K., Neurocognitive outcome in brain metastases patients treated with accelerated fractionation vs. accelerated hyperfractionated radiotherapy: An analysis from Radiation Therapy Oncology Group Study 91-104 (2001) Int. J. Radiat. Oncol. Biol. Phys., 51 (3), pp. 711-717; Taylor, B.V., Buckner, J.C., Cascino, T.L., Effects of radiation and chemotherapy on cognitive function in patients with high-grade glioma (1998) J. Clin. Oncol., 16 (6), pp. 2195-2201; Murray, K.J., Scott, C., Zachariah, B., Importance of the mini-mental status examination in the treatment of patients with brain metastases: A report from the Radiation Therapy Oncology Group protocol 91-04 (2000) Int. J. Radiat. Oncol. Biol. Phys., 48 (1), pp. 59-64; Chang, E.L., Wefel, J.S., Meyers, C.A., Prospective neurocognitive evaluation of patients with 1 to 3 newly diagnosed brain metastases treated with stereotactic radiosurgery alone (2004) Int. J. Radiat. Oncol. Biol. Phys., 60 (1), pp. S164-S165; Meyers, C.A., Smith, J.A., Bezjak, A., Neurocognitive function and progression in patients with brain metastases treated with whole-brain radiation and motexafin gadolinium: Results of a randomized Phase III trial (2004) J. Clin. Oncol., 22 (1), pp. 157-165; Pirzkall, A., Debus, J., Lohr, F., Radiosurgery alone or in combination with whole-brain radiotherapy for brain metastases (1998) J. Clin. Oncol., 16 (11), pp. 3563-3569; Sneed, P.K., Suh, J.H., Goetsch, S.J., A multi-institutional review of radiosurgery alone vs. radiosurgery with whole brain radiotherapy as the initial management of brain metastases (2002) Int. J. Radiat. Oncol. Biol. Phys., 53 (3), pp. 519-526; Byrne, T.N., Cascino, T.L., Posner, J.B., Brain metastasis from melanoma (1983) J. Neurooncol., 1 (4), pp. 313-317; Choi, K.N., Withers, H.R., Rotman, M., Intracranial metastases from melanoma. Clinical features and treatment by accelerated fractionation (1985) Cancer, 56 (1), pp. 1-9; Rate, W.R., Solin, L.J., Turrisi, A.T., Palliative radiotherapy for metastatic malignant melanoma: Brain metastases, bone metastases, and spinal cord compression (1988) Int. J. Radiat. Oncol. Biol. Phys., 15 (4), pp. 859-864; Stevens, G., Firth, I., Coates, A., Cerebral metastases from malignant melanoma (1992) Radiother. Oncol., 23 (3), pp. 185-191; Decker, D.A., Decker, V.L., Herskovic, A., Brain metastases in patients with renal cell carcinoma: Prognosis and treatment (1984) J. Clin. Oncol., 2 (3), pp. 169-173; Gay, P.C., Litchy, W.J., Cascino, T.L., Brain metastasis in hypernephroma (1987) J. Neurooncol., 5 (1), pp. 51-56; Maor, M.H., Frias, A.E., Oswald, M.J., Palliative radiotherapy for brain metastases in renal carcinoma (1988) Cancer, 62 (9), pp. 1912-1917; Wronski, M., Maor, M.H., Davis, B.J., External radiation of brain metastases from renal carcinoma: A retrospective study of 119 patients from the M. D. Anderson Cancer Center (1997) Int. J. Radiat. Oncol. Biol. 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(Wien), 140 (6), pp. 549-555; Brown, P.D., Brown, C.A., Pollock, B.E., Stereotactic radiosurgery for patients with radioresistant brain metastases (2002) Neurosurgery, 51 (3), pp. 656-667; Lavine, S.D., Petrovich, Z., Cohen-Gadol, A.A., Gamma knife radiosurgery for metastatic melanoma: An analysis of survival, outcome, and complications (1999) Neurosurgery, 44 (1), pp. 59-66; Mingione, V., Oliveira, M., Prasad, D., Gamma surgery for melanoma metastases in the brain (2002) J. Neurosurg., 96 (3), pp. 544-551; Mori, Y., Kondziolka, D., Flickinger, J.C., Stereotactic radiosurgery for cerebral metastatic melanoma: Factors affecting local disease control and survival (1998) Int. J. Radiat. Oncol. Biol. Phys., 42 (3), pp. 581-589; Seung, S.K., Sneed, P.K., McDermott, M.W., Gamma knife radiosurgery for malignant melanoma brain metastases (1998) Cancer J. Sci. Am., 4 (2), pp. 103-109; Grob, J.J., Regis, J., Laurans, R., Radiosurgery without whole brain radiotherapy in melanoma brain metastases (1998) Eur. J. Cancer, 34 (8), pp. 1187-1192. , Club de Cancerologie Cutanee; Gieger, M., Wu, J.K., Ling, M.N., Response of intracranial melanoma metastases to stereotactic radiosurgery (1997) Radiat. Oncol. Investig., 5 (2), pp. 72-80; Yu, C., Chen, J.C., Apuzzo, M.L., Metastatic melanoma to the brain: Prognostic factors after gamma knife radiosurgery (2002) Int. J. Radiat. Oncol. Biol. Phys., 52 (5), pp. 1277-1287; Selek, U., Chang, E.L., Hassenbusch III, S.J., Stereotactic radiosurgical treatment in 103 patients for 153 cerebral melanoma metastases (2004) Int. J. Radiat. Oncol. Biol. Phys., 59 (4), pp. 1097-1106; Chang, E.L., Selek, U., Hassenbusch, S.J., Outcome variation amoung ""radioresistant"" brain metastases treated with stereotactic radiosurgery (2005) Neurosurg., 56 (5), pp. 936-945; Mañon, R., Oneill, A., Mehta, M., Phase II trial of radiosurgery (RS) for 1 to 3 newly diagnosed brain metastases from renal cell, melanoma, and sarcoma: An Eastern Cooperative Oncology Group Study (E6397) (2004) J. Clin. Oncol., 22 (14 S), p. 1507. , ASCO Annual Meeting Proceedings (Post-Meeting Edition)","Lo, S.S.; Department of Radiation Oncology; Indiana Lions Gamma Knife Center; Indiana University Medical Center; 535 Barnhill Drive Indianapolis, IN 46202, United States; email: slo@iupui.edu",,,,,,,,14737175,,ERNXA,10.1586/14737175.5.4.487,"English","Expert Review of Neurotherapeutics",Review,Scopus "Batalis N.I., Galup L., Zaki S.R., Prahlow J.A.","West Nile virus encephalitis",2005,"American Journal of Forensic Medicine and Pathology",26,2,,192,196,,1,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-19544375063&partnerID=40&rel=R8.0.0","Medical University of South Carolina, Charleston, SC, United States; South Bend Medical Foundation, South Bend, IN, United States; Infectious Disease Pathology Activity, Centers for Disease Control and Prevention, Atlanta, GA, United States; Indiana University School of Medicine, South Bend Center for Medical Education, South Bend, IN, United States; Medical University of South Carolina, Children's Hospital, 165 Ashley Avenue, Charleston, SC 29407, United States","West Nile virus (WNV) is a mosquito-borne virus that has caused a large number of deaths in the United States since the first outbreak in New York City in 1998. The outbreak initially was limited to the northeast but has since spread across the entire continental United States. WNV causes a variety of clinical symptoms, but the most severe consequences result from central nervous system infection, resulting in meningitis, encephalitis, or meningoencephalitis. We present a case of a 62-year-old male with metastatic cancer, who died as a result of WNV encephalitis. This is followed by a discussion on the epidemiology of WNV and a detailed summary of the methods and resources available to make a diagnosis of WNV infection postmortem. The material presented in the discussion should provide the forensic pathologist with all the information necessary to make a diagnosis of WNV infection postmortem. If nothing else, the routine collection and storage of serum, cerebrospinal fluid, and tissue for every case can enable the forensic pathologist to make this diagnosis even in cases in which WNV is not suspected until after autopsy. Copyright © 2005 by Lippincott Williams & Wilkins.","Autopsy; Death; Encephalitis; Forensic pathology; West Nile virus","adult; article; autopsy; brain biopsy; case report; death; forensic pathology; geographic distribution; histopathology; human; male; terminal disease; tissue section; virus encephalitis; West Nile flavivirus; Brain; Carcinoma, Small Cell; Chills; Confusion; Fever; Forensic Pathology; Humans; Lung Neoplasms; Male; Middle Aged; Psychomotor Agitation; West Nile Fever",,,,,"Roehrig, J.T., Layton, M., Smith, P., The emergence of West Nile virus in North America: Ecology, epidemiology, and surveillance (2002) Curr Top Microbiol Immunol, 267, pp. 223-240; West Nile Virus, , http://www.cdc.gov/ncidod/dvbid/westnile/index.htm; Weiss, D., Carr, D., Kellachan, J., Clinical findings of West Nile virus infection in hospitalized patients, New York and New Jersey, 2000 (2001) Emerg Infect Dis, 7, pp. 654-658; Turell, M.J., Sardelis, M.R., O'Guinn, M.L., Potential vectors of West Nile virus in North America (2002) Curr Top Microbiol Immunol, 267, pp. 241-252; Campbell, G.L., Marfin, A.A., Lanciotti, R.S., West Nile virus (2002) Lancet Infect Dis, 2, pp. 519-529; Guidance for Industry: Revised Recommendations for the Assessment of Donor Suitability and Blood and Blood Product Safety in Cases of Known or Suspected West Nile Virus Infection, , http://www.fda.gov/cber/gdlns/wnvguid.htm; Iwamoto, M., Jernigan, J.B., Guasch, A., Transmission of West Nile virus from an organ donor to four transplant recipients (2003) N Engl J Med, 348, pp. 2196-2203; Peterson, L.R., Marfin, A.A., West Nile virus: A primer for the clinician (2002) Ann Intern Med, 137, pp. 173-179; Campbell, G.L., Grady, L.J., Huang, C., Laboratory testing for West Nile virus: Panel discussion (2001) Ann N Y Acad Sci, 951, pp. 179-194; Sampson, B.A., Ambrosi, C., Charlot, A., The pathology of human West Nile Virus infection (2000) Hum Pathol, 31, pp. 527-531; Shieh, W.J., Guarner, J., Layton, M., The role of pathology in an investigation of an outbreak of West Nile encephalitis in New York, 1999 (2000) Emerg Infect Dis, 6, pp. 370-372; Kelly, T.W., Prayson, R.A., Ruiz, A.I., The neuropathology of West Nile virus meningoencephalitis (2003) Am J Clin Pathol, 119, pp. 749-753; Batalis, N., Galup, L., Zaki, S.R., West Nile virus encephalitis (2003) American Society for Clinical Pathology Check Sample, FP03-6, pp. 75-91","Batalis, N.I.; Medical University of South Carolina; Children's Hospital; 165 Ashley Avenue Charleston, SC 29407, United States; email: batalini@musc.edu",,,,,,,,01957910,,AJFPD,10.1097/01.paf.0000163826.56278.da,"English","American Journal of Forensic Medicine and Pathology",Article,Scopus "Ganguli M., Dodge H.H., Shen C., Pandav R.S., DeKosky S.T.","Alzheimer disease and mortality: A 15-year epidemiological study",2005,"Archives of Neurology",62,5,,779,784,,13,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-18544384554&partnerID=40&rel=R8.0.0","Department of Epidemiology, University of Pittsburgh Graduate School of Public Health, Pittsburgh, PA, United States; Division of Geriatrics and Neuropsychiatry, Department of Psychiatry, University of Pittsburgh School of Medicine; Department of Neurology, Alzheimers Disease Research Center, University of Pittsburgh School of Medicine; Division of Biostatistics, Department of Medicine, Indiana University School of Medicine, Indianapolis, IN, United States; South-East Asia Regional Office, World Health Organization, New Delhi, India; Western Psychiatric Institute and Clinic, 3811 O'Hara St, Pittsburgh, PA 15213-2593, United States","Background: Alzheimer disease (AD) is considered a leading cause of death, but few studies have examined the contribution of AD to mortality based on follow-up of representative US cohorts. Objective: To examine mortality rates, duration of survival, causes of death, and the contribution of AD to the risk of mortality in an aging community-based cohort, controlling for other predictors. Design: Fifteen-year prospective epidemiological study. Mortality rates per 1000 person-years and the population-attributable risk of mortality were determined. Cox proportional hazards models were used to estimate relative risk of mortality due to AD, adjusting for relevant covariates. Death certificates were abstracted for listed causes of death. Setting: A largely blue-collar rural community in south-western Pennsylvania. Participants: A community-based cohort of 1670 adults 65 years and older at study enrollment. Main Outcome Measure: Mortality. Results: In the overall cohort, AD was a significant predictor of mortality, with a hazard ratio of 1.4 after adjusting for covariates. The population-attributable risk of mortality from AD was 4.9% based on the same model. Examining the sexes separately, AD increased mortality risk only among women. Death certificates of AD subjects were more likely to list dementia/AD, other brain disorders, pneumonia, and dehydration, and less likely to include cancer. Conclusions: Alzheimer disease was responsible for 4.9% of the deaths in this elderly cohort. Alzheimer disease increased the risk of mortality 40% in the cohort as a whole and separately in women but not in men. The mean (SD) duration of survival with AD was 5.9 (3.7) years, and longer with earlier age at onset.",,"aged; aging; Alzheimer disease; article; brain disease; cancer; cause of death; cohort analysis; controlled study; covariance; death certificate; dehydration; dementia; epidemiological data; female; follow up; human; major clinical study; male; mortality; onset age; pneumonia; priority journal; prospective study; survival time; United States; Age Factors; Age of Onset; Aged; Aged, 80 and over; Alzheimer Disease; Analysis of Variance; Cohort Studies; Female; Geriatric Assessment; Humans; Life Expectancy; Male; Retrospective Studies; Risk Factors; Survival Rate",,,,,"Katzman, R., Karasu, T.B., Differential diagnosis of dementia (1975) Neurological and Sensory Disorders of the Elderly, pp. 103-134. , Fields W, ed. 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Folstein, M.F., Folstein, S.E., McHugh, P.R., ""Mini-Mental State"": A practical method for grading the cognitive state of patients for the clinician (1975) J Psychiatr Res, 12, pp. 189-198; Ganguli, M., Gilby, J., Seaberg, E., Belle, S., Depressive symptoms and associated factors in a rural elderly population: The MoVIES project (1995) Am J Geriatr Psychiatry, 3, pp. 144-160; Fillenbaum, G.G., Screening the elderly: A brief instrumental activities of daily living measure (1985) J Am Geriatr Soc, 33, pp. 698-706; Mulsant, B.H., Ganguli, M., Seaberg, E.C., The relationship between self-rated health and depressive symptoms in an epidemiological sample of community-dwelling older adults (1997) J Am Geriatr Soc, 45, pp. 954-958; Morris, J.C., Heyman, A., Mohs, R.C., The Consortium to Establish a Registry for Alzheimer's Disease (CERAD), part I: Clinical and neuropsychological assessment of Alzheimer's disease (1989) Neurology, 39, pp. 1159-1165; (1987) Diagnostic and Statistical Manual of Mental Disorders, Revised Third Edition, , Washington, DC: American Psychiatric Association; McKhann, G., Drachman, D., Folstein, M., Katzman, R., Price, D., Stadlan, E.M., Clinical diagnosis of Alzheimer's disease: Report of the NINCDS-ADRDA work group under the auspices of Department of Health and Human Service Task Force on Alzheimer's disease (1984) Neurology, 34, pp. 939-944; Hughes, C.P., Berg, L., Danziger, W.L., Coben, L.A., Martin, R.L., A new clinical scale for the staging of dementia (1982) Br J Psychiatry, 140, pp. 566-572; Ganguli, M., Rodriguez, E., Reporting of dementia on death certificates: A community study (1999) J Am Geriatr Soc, 47, pp. 842-849; Wolfson, C., Wolfson, D.B., Asgharian, M., A re-evaluation of the duration of survival after the onset of dementia (2001) N Engl J Med, 344, pp. 1111-1116; Tschanz, J.T., Corcoran, C., Skoog, I., Dementia: The leading predictor of death in a defined elderly population: The Cache County Study (2004) Neurology, 62, pp. 1156-1162; Moritz, D.J., Fox, P.J., Luscombe, F.A., Kraemer, H.C., Neurological and psychiatric predictors of mortality in patients with Alzheimer disease in California (1997) Arch Neurol, 54, pp. 878-885; Stern, Y., Tang, M.X., Denaro, J., Mayeux, R., Increased risk of mortality in Alzheimer's disease patients with more advanced educational and occupational attainment (1995) Ann Neurol, 37, pp. 590-595; Gambassi, G., Francesco, L., Lapane, K., Sgadari, A., Mor, V., Bernabei, R., Predictors of mortality in patients with Alzheimer's disease living in nursing homes (1999) J Neurol Neurosurg Psychiatry, 67, pp. 59-65; Barclay, L.L., Zemcov, A., Blas, J.P., McDowell, F.H., Factors associated with duration of survival in Alzheimer's disease (1985) Biol Psychiatry, 20, pp. 86-93; Helmer, C., Joly, P., Letenneur, L., Commenges, D., Dartigues, J.F., Mortality with dementia: Results from a French prospective community-based cohort (2001) Am J Epidemiol, 154, pp. 642-648; Geerlings, M.I., Deeg, D.J., Penninx, B.W., Cognitive reserve and mortality in dementia: The role of cognition, functional ability and depression (1999) Psychol Med, 29, pp. 1219-1226; Baldereschi, M., DiCarlo, A., Maggi, S., Dementia is a major predictor of death among the Italian elderly (1999) Neurology, 52, pp. 709-713; Ostbye, T., Hill, G., Steenhuis, R., Mortality in elderly Canadians with and without dementia, a 5-year followup (1999) Neurology, 53, pp. 521-526; Evans, D.A., Smith, L.A., Scherr, P.A., Albert, M.S., Funkenstein, H.H., Hebert, L.E., Risk of death from Alzheimer's disease in a community population of older persons (1991) Am J Epidemiol, 134, pp. 403-412; Skoog, I., Hesse, C., Aevarsson, O., A population study of apoE genotype at the age of 85: Relation to dementia, cerebrovascular disease, and mortality (1998) J Neurol Neurosurg Psychiatry, 64, pp. 37-43; Aguero-Torres, H., Fratiglioni, L., Guo, Z., Viitanen, M., Winblad, B., Mortality from dementia in advanced age: A 5-year follow-up study of incident dementia cases (1999) J Clin Epidemiol, 52, pp. 737-743; Larson, E.B., Shadlen, M.F., Wang, L., Survival after initial diagnosis of Alzheimer disease (2004) Ann Intern Med, 140, pp. 501-509; Burns, A., Lewis, G., Jacoby, R., Levy, R., Factors affecting survival in Alzheimer's disease (1991) Psychol Med, 21, pp. 363-370; Ewbank, D.C., Deaths attributable to Alzheimer's disease in the United States (1999) Am J Public Health, 89, pp. 90-92; Anderson, R.N., Smith, B.L., Deaths: Leading causes for 2001 (2003) Natl Vital Stat Rep, 52, pp. 1-85; Lanska, D.J., Dementia mortality in the United States: Results of the 1986 National Mortality Followback Survey (1998) Neurology, 50, pp. 362-367; Olichney, J.M., Hofstetter, C.R., Galasko, D., Thai, L.J., Katzman, R., Death certificate reporting of dementia and mortality in an Alzheimer's Disease Research Center cohort (1995) J Am Geriatr Soc, 43, pp. 890-893; Kukull, W.A., Brenner, D.E., Speck, C.E., Causes of death associated with Alzheimer's disease: Variation by level of cognitive impairment before death (1994) J Am Geriatr Soc, 42, pp. 723-726; Molsa, P.K., Marttila, R.J., Rinne, U.K., Survival and cause of death in Alzheimer's disease and multi-infarct dementia (1986) Acta Neurol Scand, 74, pp. 103-107","Ganguli, M.; Western Psychiatric Institute and Clinic; 3811 O'Hara St Pittsburgh, PA 15213-2593, United States; email: gangulim@upmc.edu",,,,,,,,00039942,,ARNEA,10.1001/archneur.62.5.779,"English","Archives of Neurology",Article,Scopus "Teague S.D., Conces Jr. D.J.","Metastatic meningioma to the lungs",2005,"Journal of Thoracic Imaging",20,1,,58,60,,2,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-14644444461&partnerID=40&rel=R8.0.0","Department of Radiology, Indiana University, School of Medicine, Indianapolis, IN, United States; Department of Radiology, Indiana University, School of Medicine, 550 North University Blvd, Indianapolis, IN 46202, United States","Meningioma with extracranial metastases is a rare occurrence. However, the lungs are the most common site of extracranial metastases. We describe a case of a patient with recurrent intracranial meningioma and intrapulmonary metastases. Copyright © 2005 by Lippincott Williams & Wilkins.","Lung; Meningioma; Metastatic; Pulmonary","abdominal radiography; adult; article; aspiration biopsy; cancer recurrence; cancer surgery; case report; eosinophil; fluoroscopy; histopathology; human; male; meningioma; metastasis; nuclear magnetic resonance imaging; pelvis radiography; phlebography; pleura effusion; seizure; thorax radiography; Brain Neoplasms; Head and Neck Neoplasms; Humans; Lung; Lung Neoplasms; Magnetic Resonance Imaging; Male; Meningeal Neoplasms; Meningioma; Middle Aged; Neoplasm Recurrence, Local; Scalp; Seizures; Skin Neoplasms; Tomography, X-Ray Computed",,,,,"Adlakha, A., Rao, K., Adlakha, H., Meningioma metastatic to the lung (1999) Mayo Clin Proc, 74, pp. 1129-1133; Kaminski, J.M., Movsas, B., King, E., Metastatic meningioma to the lung with multiple pleural metastases (2001) Am J Clin Oncol, 24, pp. 579-582; Drummond, K.J., Bittar, R.G., Fearnside, M.R., Metastatic atypical meningioma: Case report and review of the literature (2000) J Clin Neurosci, 7, pp. 69-72; Figueroa, B.E., Quint, D.J., McKeever, P.E., Extracranial metastatic meningioma (1999) Br J Radiol, 72, pp. 513-516; Fukushima, T., Tsugu, H., Tomonaga, M., Papillary meningioma with pulmonary metastasis: Case report (1989) J Neurosurg, 70, pp. 478-482; Jestico, J.V., Lantos, P.L., Malignant meningioma with liver metastases and hypoglycemia: A case report (1976) Acta Neuropathol (Berl), 35, pp. 357-361; Kepes, J.J., Meningiomas: Biology, Pathology, and Differential Diagnosis (1982) Masson Monographs in Diagnostic Pathology, 4, pp. 190-200. , New York: Masson; Stoller, J.K., Kavuru, M., Mehta, A.C., Intracranial meningioma metastatic to the lung (1987) Cleve Clin J Med, 54, pp. 521-527; Lamszus, K., Meningioma pathology, genetics, and biology (2004) J Neuropathol Exp Neurol, 63, pp. 275-286; Ueyama, Y., Morita, K., Orchial, C., Xenotransplantation of a human meningioma and its lung metastasis in nude mice (1978) Br J Cancer, 37, pp. 644-647; Simpson, D., The recurrence of intracranial meningiomas after surgical treatment (1957) J Neurol Neurosurg Psychiatry, 20, pp. 22-39","Teague, S.D.; Department of Radiology; Indiana University; School of Medicine; 550 North University Blvd Indianapolis, IN 46202, United States; email: sdteague@iupui.edu",,,,,,,,08835993,,JTIME,10.1097/01.rti.0000139388.80395.6e,"English","Journal of Thoracic Imaging",Article,Scopus "Dropcho E.J.","Neurotoxicity of cancer chemotherapy",2004,"Seminars in Neurology",24,4,,419,426,,10,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-11344275310&partnerID=40&rel=R8.0.0","Department of Neurology, IN University School of Medicine, CL 291, 541 Clinical Drive, Indianapolis, IN 46202, United States; Department of Neurology, Indiana University Medical Center, Indianapolis Vet. Aff. Med. Center, Indianapolis, IN, United States","Neurological dysfunction is a common side effect of many chemotherapy drugs. For several agents neurotoxicity is common, severe, and can be dose-limiting. This is a review of the clinical features of chemotherapy-induced syndromes involving the central and peripheral nervous systems.","Chemotherapy adverse effects; Polyneuropathy","alpha interferon; antineoplastic agent; asparaginase; busulfan; carmustine; chlorambucil; chlormethine; cisplatin; clonazepam; corticosteroid; cytarabine; dexamethasone; diazepam; docetaxel; etoposide; fludarabine; fluorouracil; ifosfamide; interleukin 2; irinotecan; levamisole; methotrexate; methylene blue; paclitaxel; paroxetine; phenytoin; procarbazine; thiotepa; thymidine; unindexed drug; vincristine; acute lymphocytic leukemia; amnesia; anxiety; aseptic meningitis; auditory hallucination; behavior disorder; brain edema; brain hemorrhage; brain infarction; brain lymphoma; brain radiation; brain tumor; cerebellum disease; cerebral blindness; cerebral sinus thrombosis; cerebrovascular accident; clinical feature; colon carcinoma; computer assisted tomography; confusion; delirium; depression; drug fever; dysarthria; dysesthesia; extrapyramidal syndrome; gait disorder; glioma; headache; human; irritability; lethargy; leukemia; leukemic meningitis; leukoencephalopathy; lymphoma; microangiopathy; motor dysfunction; muscle rigidity; myoclonus; nausea; neck muscle; neurotoxicity; nuclear magnetic resonance imaging; peripheral neuropathy; personality disorder; pleocytosis; polyneuropathy; priority journal; quadriplegia; radiculopathy; review; risk factor; somnolence; spinal cord disease; tonic clonic seizure; tremor; visual hallucination; Cerebrovascular Disorders; Dose-Response Relationship, Drug; Drug Therapy; Humans; Neoplasms; Nervous System Diseases; Neurotoxicity Syndromes; Peripheral Nervous System Diseases",,"asparaginase, 9015-68-3; busulfan, 55-98-1; carmustine, 154-93-8; chlorambucil, 305-03-3; chlormethine, 51-75-2, 55-86-7, 82905-71-3; cisplatin, 15663-27-1, 26035-31-4, 96081-74-2; clonazepam, 1622-61-3; cytarabine, 147-94-4, 69-74-9; dexamethasone, 50-02-2; diazepam, 439-14-5; docetaxel, 114977-28-5; etoposide, 33419-42-0; fludarabine, 21679-14-1; fluorouracil, 51-21-8; ifosfamide, 3778-73-2; interleukin 2, 85898-30-2; irinotecan, 100286-90-6; levamisole, 14769-73-4, 16595-80-5; methotrexate, 15475-56-6, 59-05-2, 7413-34-5; methylene blue, 61-73-4; paclitaxel, 33069-62-4; paroxetine, 61869-08-7; phenytoin, 57-41-0, 630-93-3; procarbazine, 366-70-1, 671-16-9; thiotepa, 52-24-4; thymidine, 50-89-5; vincristine, 57-22-7","ara C; cpt 11; depocyt; taxol; taxotere; vp 16",,"Vassal, G., Deroussent, A., Hartmann, O., Dose-dependent neurotoxicity of high-dose busulfan in children: A clinical and pharmacological study (1990) Cancer Res, 50, pp. 6203-6207; Wyllie, A.R., Bayliff, C.D., Kovacs, M.J., Myodonus due to chlorambucil in two adults with lymphoma (1997) Ann Pharmacother, 31, pp. 171-174; Dropcho, E.J., Rosenfeld, S.S., Vitek, J., Guthrie, B.L., Morawetz, R.B., Phase II study of intracarotid or selective intracerebral infusion of cisplatin for treatment of recurrent anaplastic gliomas (1998) J Neurooncol, 36, pp. 191-198; 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Cheson, B.D., Vena, D.A., Foss, F.M., Sorensen, J.M., Neurotoxicity of purine analogs (1994) J Clin Oncol, 12, pp. 2216-2228; Cohen, R.B., Abdallah, J.M., Gray, J.R., Foss, F., Reversible neurologic toxicity in patients treated with standard-dose fludarabine phosphate for mycosis fungoides and chronic lymphocytic leukemia (1993) Ann Intern Med, 118, pp. 114-116; Feinberg, W.M., Swenson, M.R., Cerebrovascular complications of L-asparaginase therapy (1988) Neurology, 38, pp. 127-133; Mitchell, L.G., A prospective cohort study determining the prevalence of thrombotic events in children with acute lymphoblastic leukemia and a central venous line who are treated with L-asparaginase (2003) Cancer, 97, pp. 508-515; Icli, F., Karaoguz, H., Dincol, D., Severe vascular toxicity associated with cisplatin-based chemotherapy (1993) Cancer, 72, pp. 587-593; El Amrani, M., Henizlef, O., Debroucker, T., Brain infarction following 5-fluorouracil and cisplatin therapy (1998) Neurology, 51, pp. 899-901; Bernard, J.T., Ameriso, S., Kempf, R.A., Transient focal neurologic deficits complicating interleukin-2 therapy (1990) Neurology, 40, pp. 154-155; Walker, R.W., Allen, J.C., Rosen, G., Caparros, B., Transient cerebral dysfunction secondary to high-dose methotrexate (1986) J Clin Oncol, 4, pp. 1845-1850; Rubnitz, J.E., Relling, M.V., Harrison, P.L., Transient encephalopathy following high-dose methotrexate treatment in childhood acute lymphoblastic leukemia (1998) Leukemia, 12, pp. 1176-1181; Ay, H., Buonanno, F.S., Schaefer, P.W., Posterior leukoencephalopathy without severe hypertension: Utility of diffusion-weighted MRI (1998) Neurology, 51, pp. 1369-1376; Shin, R.K., Stern, J.W., Janss, A.J., Hunter, J.V., Liu, G.T., Reversible posterior leukoencephalopathy during the treatment of acute lymphoblastic leukemia (2001) Neurology, 56, pp. 388-391; Sanchez-Carpintero, R., Narbona, J., Lopez De Mesa, R., Arbizu, J., Sierrasesumaga, L., Transient posterior encephalopathy induced by chemotherapy in children (2001) Pediatr Neurol, 24, pp. 145-148; Henderson, R.D., Rajah, T., Nicol, A.J., Read, S.J., Posterior leukoencephalopathy following intrathecal chemotherapy with MRA-documented vasospasm (2003) Neurology, 60, pp. 326-328; Smith, G.A., Damon, L.E., Rugo, H.S., Ries, C.A., Linker, C.A., High-dose cytarabine dose modification reduces the incidence of neurotoxicity in patients with renal insufficiency (1997) J Clin Oncol, 15, pp. 833-839; Winkelman, M.D., Hines, J.D., Cerebellar degeneration caused by high-dose cytosine arabinoside: A clinicopathological study (1983) Ann Neurol, 14, pp. 520-S27; Brashear, A., Siemers, E., Focal dystonia after chemotherapy: A case series (1997) J Neurooncol, 34, pp. 163-167; Anderson, N.R., Tandon, D.S., Ifosfamide extrapyramidal neurotoxicity (1991) Cancer, 68, pp. 72-75; Resar, L.M., Phillips, P.C., Kastan, M.B., Acute neurotoxicity after intrathecal cytosine arabinoside in two adolescents with acute lymphoblastic leukemia of B-cell type (1993) Cancer, 71, pp. 117-123; Raney, B., Tefft, M., Heyn, R., Ascending myelitis after intensive chemotherapy and radiation therapy in children with cranial parameningeal sarcoma (1992) Cancer, 69, pp. 1498-1506; McLean, D.R., Clink, H.M., Ernst, P., Myelopathy after intrathecal chemotherapy (1994) Cancer, 73, pp. 3037-3040; Kleinschmidt-DeMasters, B.K., Yeh, M., ""Locked-in syndrome"" after intrathecal cytosine arabinoside therapy for malignant immunoblastic lymphoma (1992) Cancer, 70, pp. 2504-2507; Siegal, T., Haim, N., Cisplatin-induced peripheral neuropathy (1990) Cancer, 66, pp. 1117-1123; Cavaletti, G., Marzorati, L., Bogliun, G., Cisplatin-induced peripheral neurotoxicity is dependent on total-dose intensity and single-dose intensity (1992) Cancer, 69, pp. 203-207; Gill, J.S., Windebank, A.J., Cisplatin-induced apoptosis in rat dorsal root ganglion neurons is associated with attempted entry into the cell cycle (1998) J Clin Invest, 101, pp. 2842-2850; Krarup-Hansen, A., Rietz, B., Krarup, C., Histology and platinum content of sensory ganglia and sural nerves in patients treated with cisplatin and carboplatin: An autopsy study (1999) Neuropathol Appl Neurobiol, 25, pp. 29-40; Boogerd, W., Huinink, W.W., Dalesio, O., Hoppenbrouwers, W.J., Van Der Sande, J., Cisplatin induced neuropathy: Central, peripheral, and autonomic nerve involvement (1990) J Neurooncol, 9, pp. 255-263; Heinzlef, O., Lotz, J.P., Roullet, E., Severe neuropathy after high dose carboplatin in three patients receiving multidrug chemotherapy (1998) J Neurol Neurosurg Psychiatry, 64, pp. 667-669; Openshaw, H., Slatkin, N.E., Stein, A.S., Hinton, D.R., Forman, S.J., Acute polyneuropathy after high dose cytosine arabinoside in patients with leukemia (1996) Cancer, 78, pp. 1899-1905; Imrie, K.R., Couture, F., Turner, C.C., Sutcliffe, S.B., Keating, A., Peripheral neuropathy following high-dose etoposide and autologous bone marrow transplantation (1994) Bone Marrow Transplant, 13, pp. 77-79; Stein, M.E., Drumea, K., Yarnitsky, D., Benny, A., Tzuk-Shina, T., A rare event of 5-fluorouracil-associated peripheral neuropathy (1998) Am J Clin Oncol, 21, pp. 248-249; Patel, S.R., Forman, A.D., Benjamin, R.S., High-dose ifosfamide-induced exacerbation of peripheral neuropathy (1994) J Natl Cancer Inst, 86, pp. 305-306; Koh, S., Nelson, M.D., Kovanlikaya, A., Chen, L.S., Anterior lumbosacral radiculopathy after intrathecal methotrexate treatment (1999) Pediatr Neurol, 21, pp. 576-578; Gamelin, E., Gamelin, L., Bossi, L., Quasthoff, S., Clinical aspects and molecular basis of oxaliplatin neurotoxicity: Current management and development of preventive measures (2002) Semin Oncol, 29 (15 SUPPL.), pp. 21-33; Wilson, R.H., Lehky, T., Thomas, R.R., Acute oxaliplatin-induced peripheral nerve hyperexcitability (2002) J Clin Oncol, 20, pp. 1767-1774; Taieb, S., Trillet-Lenoir, V., Rambaud, L., Descos, L., Freyer, G., Lhermitte sign and urinary retention: Atypical presentation of oxaliplatin neurotoxicity in four patients (2002) Cancer, 94, pp. 2434-2440; Chaudhry, V., Eisenberger, M.A., Sinibaldi, V.J., A prospective study of suramin-induced peripheral neuropathy (1996) Brain, 119, pp. 2039-2052; Soliven, B., Dhand, U.K., Kobayashi, K., Evaluation of neuropathy in patients on suramin treatment (1997) Muscle Nerve, 20, pp. 83-91; Cavaletti, G., Bogliun, G., Marzorati, L., Peripheral neurotoxicity of taxol in patients previously treated with cisplatin (1995) Cancer, 75, pp. 1141-1150; Forsyth, P.S., Balmaceda, C., Peterson, K., Prospective study of paclitaxel-induced peripheral neuropathy with quantitative sensory testing (1997) J Neurooncol, 35, pp. 47-53; Hilkens, P.H., Verweij, J., Stoter, G., Peripheral neurotoxicity induced by docetaxel (1996) Neurology, 46, pp. 104-108; New, P.Z., Jackson, C.E., Rinaldi, D., Burris, H., Barohn, R.J., Peripheral neuropathy secondary to docetaxel (Taxotere) (1996) Neurology, 46, pp. 108-111; Van Den Bent, M.J., Hilkens, P.H., Sillevis Smitt, P.A., Lhermitte's sign following chemotherapy with docetaxel (1998) Neurology, 50, pp. 563-564; Chaudhry, V., Rowinsky, E.K., Sartorius, S.E., Donehower, R.C., Cornblath, D.R., Peripheral neuropathy from Taxol and cisplatin combination chemotherapy: Clinical and electrophysiological studies (1994) Ann Neurol, 35, pp. 304-311; Freilich, R.J., Balmaceda, C., Seidman, A.D., Rubin, M., DeAngelis, L.M., Motor neuropathy due to docetaxel and paclitaxel (1996) Neurology, 47, pp. 115-118; Chaudhry, V., Chaudhry, M., Crawford, T.O., Simmons-O'Brien, E., Griffin, J.W., Toxic neuropathy in patients with pre-existing neuropathy (2003) Neurology, 60, pp. 337-340; Berger, T., Malayeri, R., Doppelbauer, A., Neurological monitoring of neurotoxicity induced by paclitaxel/cisplatin chemotherapy (1997) Eur J Cancer, 33, pp. 1393-1399; Molloy, F.M., Floeter, M.K., Syed, N.A., Thalidomide neuropathy in patients treated for metastatic prostate cancer (2001) Muscle Nerve, 24, pp. 1050-1057; Chaudhry, V., Cornblath, D.R., Corse, A., Thalidomide-induced neuropathy (2002) Neurology, 59, pp. 1872-1875; Casey, E.B., Jellife, A.M., Le Quesne, P.M., Millett, Y.L., Vincristine neuropathy: Clinical and electrophysiological observations (1973) Brain, 96, pp. 69-86; Graf, W.D., Chance, P.F., Lensch, M.W., Severe vincristine neuropathy in Charcot-Marie-Tooth disease type 1A (1996) Cancer, 77, pp. 1356-1362; Weintraub, M., Adde, M.A., Venzon, D.J., Severe atypical neuropathy associated with administration of hematopoietic colony-stimulating factors and vincristine (1996) J Clin Oncol, 14, pp. 935-940; Pace, A., Bove, L., Nistico, C., Vinorelbine neurotoxicity: Clinical and neurophysiological findings in 23 patients (1996) J Neurol Neurosurg Psychiatry, 61, pp. 409-411; Apfel, S.C., Managing the neurotoxicity of paclitaxel and docetaxel with neurotrophic factors (2000) Cancer Invest, 18, pp. 564-573; Cavaletti, G., Zanna, C., Current status and future prospects for the treatment of chemotherapy-induced peripheral neurotoxicity (2002) Eur J Cancer, 38, pp. 1832-1837; Vahdat, L., Papadopoulos, K., Lange, D., Reduction of paclitaxel-induced peripheral neuropathy with glutamine (2001) Clin Cancer Res, 7, pp. 1192-1197; Cascinu, S., Catalano, V., Cordelia, L., Neuroprotective effect of reduced glutathione on oxaliplatin-based chemotherapy in advanced colorectal cancer (2002) J Clin Oncol, 20, pp. 3478-3483","Dropcho, E.J.; Department of Neurology; IN University School of Medicine; CL 291; 541 Clinical Drive Indianapolis, IN 46202, United States",,,,,,,,02718235,,SEMNE,10.1055/s-2004-861536,"English","Seminars in Neurology",Review,Scopus "Vilensky J.A., Sinish P.R.","Sir Felix Semon and semon's law",2004,"Clinical Anatomy",17,8,,605,606,,,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-7244224791&partnerID=40&rel=R8.0.0","Dept. of Anatomy and Cell Biology, Indiana University, School of Medicine, Fort Wayne, IN, United States; Indiana University, School of Medicine, 2101 Coliseum Blvd., E. Fort Wayne, IN 46805, United States",[No abstract available],,"brain cortex; clinical practice; experience; human; laryngeal nerve; laryngitis; larynx cancer; nerve paralysis; nonhuman; priority journal; short survey; thyroid surgery; tuberculosis; vocal cord paralysis; History, 20th Century; Humans; Laryngeal Diseases; Laryngeal Nerves; Neurology; Otolaryngology; Vocal Cord Paralysis",,,,,"Huizinga, E., Sir Felix Semon (1966) Arch Otolaryngol, 84, pp. 473-478; Negas, V., (1949) The Comparative Anatomy and Physiology of the Larynx, , London: William Heinemann Medical Books; Semon, F., Clinical remarks (1881) Arch Laryng, 2, pp. 197-222; Semon, F., On the probably cortical origin of some laryngeal paralyses (1899) Practitioner, 62, pp. 21-36; Semon, F., (1926) The Autobiography of Sir Felix Semon, , Semon H, McIntyre T, editors. London: Jarrold's Publishers; Semon, F., Horsley, V., An experimental investigation of the central motor innervation of the larynx (1890) Phil Trans Roy Soc Lond B, 181, pp. 187-211","Vilensky, J.A.; Indiana University; School of Medicine; 2101 Coliseum Blvd. E. Fort Wayne, IN 46805, United States; email: vilensk@ipfw.edu",,,,,,,,08973806,,CLANE,10.1002/ca.20045,"English","Clinical Anatomy",Short Survey,Scopus "Jakacki R.I., Feldman H., Jamison C., Boaz J.C., Luerssen T.G., Timmerman R.","A pilot study of preirradiation chemotherapy and 1800 cGy craniospinal irradiation in young children with medulloblastoma",2004,"International Journal of Radiation Oncology Biology Physics",60,2,,531,536,,10,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-4544365328&partnerID=40&rel=R8.0.0","Div. of Pediat. Hematology-Oncology, Children's Hospital of Pittsburgh, Pittsburgh, PA, United States; Child Development Unit, Children's Hospital of Pittsburgh, Pittsburgh, PA, United States; Div. of Pediat. Hematology/Oncology, St. Vincent Children's Hospital, Indianapolis, IN, United States; Department of Neurosurgery, Indiana University Medical Center, Indiana University, Indianapolis, IN, United States; Department of Radiation Therapy, Indiana University Medical Center, Indiana University, Indianapolis, IN, United States; Division of Hematology/Oncology, Children's Hospital of Pittsburgh, 3520 Fifth Ave., Suite 205, 15213, Pittsburgh, PA, United States","Purpose Craniospinal irradiation (CSI) is necessary in the treatment of medulloblastoma, although it results in significant long-term sequelae, particularly in young children. We prospectively evaluated the feasibility of giving preirradiation chemotherapy followed by 1800 cGy CSI to young children with localized medulloblastoma. Methods and materials Between January 1993 and July 1997, 7 consecutive patients (age, 20-64 months) with M0 medulloblastoma were enrolled. After surgical resection, patients received 4 months of multiagent chemotherapy followed by 1800 cGy CSI and 5400 cGy to the posterior fossa. Results Median follow-up is 8.9 years. No patient developed progressive disease during chemotherapy. One patient developed widespread metastatic recurrence 2 months after completing radiation therapy and died. Two additional patients developed isolated frontal horn relapses 32 and 36 months after initial diagnosis and received further irradiation and chemotherapy. Both of these patients remain alive 7.1 and 3.6 years from the time of recurrence. Four of the six survivors have endocrine deficits. All of the survivors require special assistance in school. Conclusions Craniospinal irradiation doses of 1800 cGy may not be adequate to prevent exoprimary recurrences. Despite the CSI dose reduction, neuroendocrine and neurocognitive sequelae are substantial. © 2004 Elsevier Inc.","Chemotherapy; Craniospinal; Medulloblastoma; Radiation therapy","Diagnosis; Diseases; Dosimetry; Drug dosage; Irradiation; Patient monitoring; Patient treatment; Surgery; Craniospinal irradiation (CSI); Medulloblastoma; Metastasis; Posterior fossa; Chemotherapy; antineoplastic agent; busulfan; carboplatin; cisplatin; cyclophosphamide; etoposide; granulocyte colony stimulating factor; thiotepa; vincristine; article; bacteremia; brain tumor; cancer combination chemotherapy; cancer growth; cancer radiotherapy; cancer recurrence; cancer surgery; cancer survival; child; clinical article; clinical trial; controlled clinical trial; controlled study; drug dose reduction; drug megadose; electrolyte disturbance; endocrine disease; fever; follow up; hearing loss; human; medulloblastoma; metastasis; neuropsychological test; neutropenia; ototoxicity; peripheral neuropathy; priority journal; prospective study; skull irradiation; thrombocytopenia; Antineoplastic Combined Chemotherapy Protocols; Cerebellar Neoplasms; Child, Preschool; Cognition Disorders; Combined Modality Therapy; Cranial Irradiation; Feasibility Studies; Growth Hormone; Humans; Infant; Medulloblastoma; Pilot Projects; Prospective Studies; Radiotherapy Dosage; Recurrence",,"busulfan, 55-98-1; carboplatin, 41575-94-4; cisplatin, 15663-27-1, 26035-31-4, 96081-74-2; cyclophosphamide, 50-18-0; etoposide, 33419-42-0; thiotepa, 52-24-4; vincristine, 57-22-7; Growth Hormone, 9002-72-6","vp 16",,"Duffner, P.K., Cohen, M.E., Thomas, P.R., The long-term effects of cranial irradiation on the central nervous system (1985) Cancer, 56, pp. 1841-1847; Silber, J.H., Radcliffe, J., Peckham, V., Whole-brain irradiation and decline in intelligence: The influence of dose and age on IQ score (1992) J Clin Oncol, 10, pp. 1390-1396; Geyer, R., Jennings, M., Boyett, J., Chemotherapy in infants with malignant brain tumors (1998) Proc ASCO, 17, p. 526; Duffner, P.K., Horowitz, M.E., Krischer, J.P., The treatment of malignant brain tumors in infants and very young children: An update of the Pediatric Oncology Group experience (1999) Neuro-Oncology, 1, pp. 152-161; Packer, R.J., Goldwein, J.W., Nicholson, H.S., Treatment of children with medulloblastomas with reduced-dose craniospinal radiation therapy and adjuvant chemotherapy: A Children's Cancer Group Study (1999) J Clin Oncol, 17, pp. 2127-2136; Ris, M.D., Packer, R.J., Goldwein, J., Intellectual outcome after reduced-dose radiation therapy plus adjuvant chemotherapy for medulloblastoma: A Children's Cancer Group Study (2001) J Clin Oncol, 19, pp. 3470-3476; Goldwein, J., Radcliffe, J., Packer, R.N., Results of a pilot study of low-dose craniospinal radiation therapy plus chemotherapy for children younger than 5 years with primitive neuroectodermal tumors (1993) Cancer, 71, pp. 2647-2652; Sparrow, S., Balla, D., Cicchetti, D., (1984) Vineland Adaptive Behavior Scales: Interview Edition Survey Form Manual, , Circle Pines, NM: American Guidance Service, Inc; Bouffet, E., Bernard, J.L., Frappaz, D., M4 protocol for cerebellar medulloblastoma: Supratentorial radiotherapy may not be avoided (1992) Int J Radiat Oncol Biol Phys, 24, pp. 79-85; Pomeroy, S.L., Tamayo, P., Gaasenbeek, M., Prediction of central nervous system embryonal tumor outcome based on gene expression (2002) Nature, 415, pp. 436-442; Goldwein, J.W., Radcliffe, J., Johnson, J., Updated results of a pilot study of low dose craniospinal irradiation plus chemotherapy for children under five with cerebellar primitive neuroectodermal tumors (medulloblastoma) (1996) Int J Radiat Oncol Biol Phys, 14, pp. 899-904; Daum, I., Ackerman, H., Cerebellar contributions to cognition (1994) Behav Brain Res, 67, pp. 201-210; Marien, P., Engelborghs, S., De Deyn, P.P., Cerebellar neurocognition: A new avenue (2001) Acta Neurologica Belgica, 101, pp. 96-109; Paradiso, S., Andreasen, N.C., O'Leary, D.S., Cerebellar size and cognition: Correlation with IQ, verbal memory and motor dexterity (1997) Neuropsychiatry Neuropsychol Behav Neurol, 10, pp. 1-8; Grill, J., Kieffer-Renaux, V., Bulteau, C., Long-term intellectual outcome in children with posterior fossa tumors according to radiation doses and volumes (1999) Int J Radiat Oncol Biol Phys, 45, pp. 137-145; Giaccone, G., Dalesio, O., McVie, G.J., Maintenance chemotherapy in small-cell lung cancer: Long term results of a randomized trial (1993) J Clin Oncol, 11, pp. 1230-1240; Einhorn, L.H., Williams, S.D., Troner, M., The role of maintenance therapy in disseminated testicular cancer (1981) N Engl J Med, 305, pp. 727-731; Hortabagyi, G.N., Treatment of breast cancer (1998) New Engl J Med, 339, pp. 974-984; Gentet, J.C., Bouffet, E., Doz, F., Preirradiation chemotherapy including ""eight drugs in 1 day"" regimen and high dose methotrexate in childhood medulloblastoma: Results of the M7 French Cooperative Study (1995) J Neurosurg, 82, pp. 608-614; Heideman, R.L., Kovnar, E.H., Kellie, S.J., Preirradiation chemotherapy with carboplatin and etoposide in newly diagnosed embryonal pediatric CNS tumors (1995) J Clin Oncol, 13, pp. 2247-2254; Packer, R.J., Sutton, L.N., Elterman, R., Outcome for children with medulloblastoma treated with radiation and cisplatin, CCNU and vincristine chemotherapy (1994) J Neurosurg, 81, pp. 690-698; Yock, T.I., Friedman, H., Kun, L., Barnes, P., Tarbell, N.J., Response to pre-radiation chemotherapy is predictive of improved survival in high-risk medulloblastoma: Results from Pediatric Oncology Group (POG 9031) (2001) Int J Radiat Oncol Biol Phys, 51, p. 120; Schell, M.J., McHaney, V.A., Green, A.A., Hearing loss in children and young adults receiving cisplatin with or without prior cranial irradiation (1989) J Clin Oncol, 7, pp. 754-760; Bergman, I., Jakacki, R., Heller, G., Finlay, J., Treatment of standard risk medulloblastoma with craniospinal irradiation, carboplatin and vincristine (1997) Med Ped Oncol, 29, pp. 563-567","Jakacki, R.I.; Div. of Pediat. Hematology-Oncology; Children's Hospital of Pittsburgh Pittsburgh, PA, United States; email: regina.jakacki@chp.edu",,,,,,,,03603016,,IOBPD,10.1016/j.ijrobp.2004.03.027,"English","International Journal of Radiation Oncology Biology Physics",Article,Scopus "Neville K., Blaney S., Bernstein M., Thompson P., Adams D., Aleksic A., Berg S.","Pharmacokinetics of O6-benzylguanine in pediatric patients with central nervous system tumors: A Pediatric Oncology Group study",2004,"Clinical Cancer Research",10,15,,5072,5075,,4,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-4143146385&partnerID=40&rel=R8.0.0","Department of Pediatrics, Baylor College of Medicine, Houston, TX, United States; Sainte-Justine Hospital, University of Montreal, Montreal, Que., Canada; Univ. of Vermont College of Medicine, Burlington, VT, United States; Riley Children's Hospital, Indiana University, Indianapolis, IN 46202, United States; Children's Oncology Group, P.O. Box 60012, Arcadia, CA, United States","Purpose: To report the results of the first pharmacokinetic study in pediatric patients of O6-benzylguanine (O6BG), which irreversibly inactivates the DNA repair protein alkylguanine-alkyltransferase, thus enhancing the cytotoxicity of nitrosoureas. Experimental Design: As part of a Pediatric Oncology Group Phase I study, 120 mg/m2 of O 6BG was administered i.v. over 1 h, before 1,3-bis(2-chloroethyl)-1- nitrosourea administration in children with recurrent or refractory brain tumors. Serial blood samples for plasma pharmacokinetic studies were obtained. Concentrations of O6BG and its active metabolite O 6-benzyl-8-oxoguanine (8-oxo-O6BG) were measured by high-performance liquid chromatography. A pharmacokinetic model and additional first-order elimination rate constants for each compound were developed. Results: O6BG concentration versus time data were evaluated for 25 patients. The peak concentration of O6BG (mean ± SD) was 11 ± 4 μM, and the peak concentration of its active metabolite, 8-oxo-O6BG, was 35 ± 10 μM. O6BG was rapidly eliminated with a half-life of 85 ± 140 min, area under the curve of 795 ± 320 μM · min and clearance of 760 ± 400 ml/min/m 2. The area under the curve of 8-oxo-O6BG when extrapolated to infinity was 22,700 ± 11,800 μM · min. The clearance and terminal half-life of 8-oxo-O6BG were 30 ± 15 ml/min/m2 and 360 ± 220 min, respectively. Conclusions: There is rapid elimination of O6BG after i.v. administration over 1 h. In contrast, the terminal half-life for the active metabolite, 8-oxo-O 6BG, is 4-fold longer. The pharmacokinetic parameters for O 6BG and 8-oxo-O6BG are similar to those reported previously in adults.",,"6 o alkylguanine DNA alkyltransferase; 6 o benzylguanine; carmustine; drug metabolite; guanine derivative; nitrosourea derivative; o6 benzyl 8 oxoguanine; unclassified drug; area under the curve; article; cancer chemotherapy; cancer recurrence; central nervous system tumor; child; childhood cancer; clinical article; clinical trial; drug blood level; drug clearance; drug cytotoxicity; drug effect; drug elimination; drug half life; enzyme inactivation; high performance liquid chromatography; human; oncology; phase 1 clinical trial; priority journal; Adolescent; Adult; Antineoplastic Agents; Area Under Curve; Brain Neoplasms; Central Nervous System Neoplasms; Chromatography, High Pressure Liquid; DNA Repair; Dose-Response Relationship, Drug; Enzyme Inhibitors; Guanine; Humans; Neoplasms; O(6)-Methylguanine-DNA Methyltransferase; Time Factors; Treatment Outcome",,"6 o benzylguanine, 19916-73-5; carmustine, 154-93-8; Antineoplastic Agents; Enzyme Inhibitors; Guanine, 73-40-5; O(6)-benzylguanine, 19916-73-5; O(6)-Methylguanine-DNA Methyltransferase, EC 2.1.1.63","nsc 637037, National Cancer Institute","National Cancer Institute","Srivenugopal, K., Formation and disappearance of DNA interstrand crosslinks in human colon cancer cell lines with different levels of resistance to chlorozotocin (1992) Biochem Pharmacol, 433, pp. 1159-1163; Trey, J., Gerson, S., The role of O6-alkylguanine DNA alkyltransferase in limiting nitrosurea-induced sister chromatid exchanges in proliferating human lymphocytes (1989) Cancer Res, 49, pp. 1889-1902; Wiencke, J., Bodell, W., N-Methyl-N-nitrosurea potentiation of cytogenetic damage induced by 1,3-bis(2-chloroethyl)-1-nitrosurea in normal human lymphocytes (1985) Cancer Res, 45, pp. 4798-4803; Day, R.I., Ziolowski, C., Scudiero, D., Moyer, S., Mattern, M., Human tumor cell strains defective in the repair of alkylation damage (1980) Carcinogenesis (Lond), 1, pp. 21-32; Pegg, A., Dolan, M., Moschel, R., Structure, function and inhibition of O6-alkylguanine DNA alkyltransferase (1995) Prog Nucleic Acid Res Mol Biol, 51, pp. 167-223; Pegg, A., Mammalian O6-alkylguanine DNA alkyltransferase: Regulation and importance in response to alkylation carcinogenic and therapeutic agents (1990) Cancer Res, 50, pp. 6119-6129; Pegg, A., Beyers, T., Repair of DNA containing O6-alkylguanine (1992) FASEB J, 6, pp. 2302-2310; Yarosh, D., Rice, M., Day, R., Foote, R., Mitra, S., O6-methylguanine-DNA methyltransferase in human cells (1984) Mutat Res, 131, pp. 27-36; Roy, S., Korzekwa, K., Gonzalez, F., Moschel, R., Dolan, M., Role of human liver microsomal and human cDNA-expressed cytochrome P450 in oxidative metabolism of O6-benzylguanine (1995) Proc Am Assoc Cancer Res, 36, pp. A846; Dolan, M., Chae, M.-Y., Pegg, A., Mullen, J., Friedman, H., Moschel, R., Metabolism of O6-benzylguanine, an inactivator of O 6-alkylguanine-DNA alkyltransferase (1994) Cancer Res, 54, pp. 5123-5130; Knott, G., MLAB - A mathematical modeling tool (1979) Comput Programs Biomed, 10, pp. 271-280; Belanich, M., Pastor, M., Randall, T., Retrospective study of the correlation between the DNA repair protein alkyltransferase and survival of brain tumor patients treated with carmustine (1996) Cancer Res, 56, pp. 783-788; Hongeng, S., Brent, T., Sanford, R., Li, H., Kun, L., Heideman, R., O6-methylguanine-DNA methyltransferase protein levels in pediatric brain tumors (1997) Clin Cancer Res, 3, pp. 2459-2463; Wiestler, O., Kleihues, P., Pegg, A., O6-alkylguanine-DNA alkyltransferase activity in human brain and brain tumors (1984) Carcinogenesis (Lond), 5, pp. 121-124; Schold Jr., S.C., Brent, T.P., Von Hofe, E., O6-alklylguanine-DNA alkyltransferase and sensitivity to procarbazine in human brain tumor xenografts (1989) J Neurosurg, 70, pp. 573-577; Jaeckle, K., Eyre, H., Townsend, J., Correlation of tumor O6 methylguanine-DNA methyltransferase levels with survival of malignant astrocytoma patients treated with bis-chloroethylnitrosurea: A Southwest Oncology Group study (1998) J Clin Oncol, 16, pp. 3310-3315; Lefkowitz, I., Evans, A., Sposto, C., Hammond, D., Adjuvant chemotherapy of childhood posterior fossa (PF) ependymoma; craniospinal irradiation with and without CCNU, vincristine (VCR), and prednisone (P) (1989) Am Soc Clin Oncol, 8, p. 87; Ward, H., CCNU in treatment of recurrent medulloblastoma (1974) Br Med J, 1, p. 642; Spiro, T., Gerson, S., Liu, L., O6-benzylguanine: A clinical trial establishing the biochemical modulatory dose in tumor tissue for alkyltransferase-directed DNA repair (1999) Cancer Res, 59, pp. 2402-2410; Friedman, H., Kokkinakis, D., Pluda, J., Phase I trial of O6-benzylguanine for patients undergoing surgery for malignant glioma (1998) J Clin Oncol, 16, pp. 3570-3575; Tserng, K.-Y., Ingalls, S., Boczko, E., Pharmacokinetics of O6-benzylguanine (NSC637037) and its metabolite, 8-oxo-O6-benzylguanine (2003) J Clin Pharmacol, 43, pp. 881-893; Dolan, M., Roy, S., Fasanmade, A., Paras, P., Schilsky, R., Ratain, M., O6-benzylguanine in humans: Metabolic, pharmacokinetic, and pharmacodynamic findings (1998) J Clin Oncol, 16, pp. 1803-1810; Quinn, J.A., Pluda, J., Dolan, M.E., Phase II trial of carmustine plus O(6)-benzylguanine for patients with nitrosourea-resistant recurrent or progressive malignant glioma (2002) J Clin Oncol, 20, pp. 2277-2283","Blaney, S.; Children's Oncology Group; P.O. Box 60012 Arcadia, CA, United States; email: sblaney@bcm.txccc.org",,,,,,,,10780432,,CCREF,10.1158/1078-0432.CCR-03-0123,"English","Clinical Cancer Research",Article,Scopus "Dropcho E.J.","Low-grade gliomas in adults",2004,"Current Treatment Options in Neurology",6,4,,265,271,,,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-3142706536&partnerID=40&rel=R8.0.0","Department of Neurology, Indiana University Medical Center, Indianapolis Veterans Affairs Med., Indianapolis, IN 46202, United States","Adult patients with a magnetic resonance scan suggestive of a supratentorial low-grade glioma should generally undergo at least a stereotactic biopsy to confirm the diagnosis and rule out an anaplastic glioma or a non-neoplastic lesion. Early tumor treatment should be given to patients with newly diagnosed low-grade gliomas who are over age 50 years, those who have headaches or neurologic deficits other than seizures, or those whose neuroimaging studies show tumor growth or mass effect. For younger patients presenting with seizures and no other neurologic symptoms, it is reasonable to defer therapy until there is clinical or radiographic tumor progression. When it is judged that intervention is necessary, patients should undergo to maximal surgical tumor resection, which preserves or improves neurologic function. For younger (<50 years) astrocytoma patients with a good tumor resection, radiation may be deferred until tumor progression. Early radiation should be given to astrocytoma patients who are older than 50 years of age at diagnosis (regardless of the type of surgery) or to younger patients who are judged to require early intervention but who are not candidates for aggressive surgical resection. The radiation dose for low-grade glioma should be 4500 to 5000 cGy, preferably with three-dimensional conformal ports. The same guidelines for management apply to patients with low-grade oligodendroglioma or oligoastrocytoma, except that chemotherapy is a reasonable alternative to radiation when it is judged that treatment other than surgical resection is required. Copyright © 2004 by Current Science Inc.",,"anticonvulsive agent; antineoplastic agent; carmustine; lomustine; procarbazine; temozolomide; vincristine; adult; astrocytoma; brain biopsy; cancer grading; cancer growth; headache; human; neuroimaging; neurologic disease; nuclear magnetic resonance imaging; oligodendroglioma; practice guideline; radiation dose; review; seizure; symptomatology",,"carmustine, 154-93-8; lomustine, 13010-47-4; procarbazine, 366-70-1, 671-16-9; temozolomide, 85622-93-1; vincristine, 57-22-7",,,"Leighton, C., Fisher, B., Bauman, G., Supratentorial low-grade glioma in adults: An analysis of prognostic factors and timing of radiation (1997) J. Clin. Oncol., 15, pp. 1294-1301; Lote, K., Egeland, T., Hager, B., Survival, prognostic factors, and therapeutic efficacy in low-grade glioma: A retrospestive study in 379 patients (1997) J. Clin. Oncol., 15, pp. 3129-3140; van Veelen, M.L., Avezaat, C.J., Kros, J.M., Supratentorial low grade astrocytoma: Prognostic factors, dedifferentiation, and the issue of early versus late surgery (1998) J. Neurol. Neorosurg. Psychiatr., 64, pp. 581-587; Olson, J.D., Riedel, E., DeAngelis, L.M., Long-term outcome of low-grade oligodendroglioma and mixed glioma (2000) Neurology, 54, pp. 1442-1448; Perry, A., Pathology of low grade gliomas: An update of emerging concepts (2003) Neuro-oncol., 5, pp. 168-178; Azzarelli, B., Miravalle, L., Vidal, R., Immunolocalization of the oligodendrocyte transcription factor 1 (Olig1) in brain tumors (2004) J. Neuropathol. Exp. Neurol., 63, pp. 170-179; Fisher, B.J., Naumova, E., Leighton, C.C., ki-67: A prognostic factor for low-grade glioma? (2002) Int. J. Rad. Oncol. Biol. Phys., 52, pp. 966-1001; Hirose, Y., Aldape, K.D., Chang, S., Grade II astrocytomas are subgrouped by chromosome aberrations (2003) Cancer Gener. Cytogenet., 142, pp. 1-7; Wessels, P.H., Hopman, A.H., Kubat, B., Proliferation and aneusomy predict survival of young patients with astrocytoma grade 2 (2003) Brit. J. Cancer, 89, pp. 128-134; Sasaki, H., Zlatescu, M.C., Betensky, R.A., Histopathological-molecular genetic correlations on referral pathologist-diagnosed low-grade ""oligodendroglioma"" (2002) J. Neuropathol. Exp. Neurol., 61, pp. 58-63; Reifenberger, G., Louis, D.N., Oligodendroglioma: Toward molecular definitions in diagnostic neuro-oncology (2003) J. Neuropathol. Exp. Neurol., 62, pp. 111-126; van den Bent, M.J., Looijenga, L.H., Langenberg, K., Chromosomal anomalies in oligodendroglial tumors are correlated with clinical features (2003) Cancer, 97, pp. 1276-1284; Mueller, W., Hartmann, C., Hoffmann, A., Genetic signature of oligoastrocytomas correlates with tumor location and denotes distinct molecular subsets (2002) Am. J. Pathol., 161, pp. 313-319; Pignatti, E., van den Bent, M., Curran, D., Prognostic factors for survival in adult patients with cerebral low-grade glioma (2003) J. Clin. Oncol., 20, pp. 2076-2084; Shaw, E., Arusell, R., Scheithauer, B., Prospective randomized trial of low-dose versus high-dose radiation therapy in adults with supratentorial low-grade glioma (2002) J. Clin. Oncol., 20, pp. 2267-2276; Bauman, G., Lote, K., Larson, D., Pretreatment factors predict overall survival for patients with low-grade glioma: A recursive partitioning analysis (1999) Int. J. Rad. Oncol. Biol. Phys., 45, pp. 923-929; Berger, M.S., Rostomily, R.C., Low grade gliomas: Functional mapping resection strategies, extent of resection, and outcome (1997) J. Neurooncol., 34, pp. 85-101; Keles, G.E., Lamborn, K.R., Berger, M.S., Low-grade hemispheric gliomas in adults: A critical review of extent of resection as a factor influencing outcome (2001) J. Neurosurg., 95, pp. 735-745; Lo, S.S., Cho, K.H., Hall, W.A., Does the extent of surgery have an impact on the survival of patients who receive postoperative radiation therapy for supratentorial low-grade gliomas? (2001) Int. J. Cancer, 96 (SUPPL.), pp. 71-78; Karim, A.B., Maat, B., Hatlevoll, R., A randomized trial on does-response in radiation therapy of low-grade cerebral glioma: European Organization for Research and Treatment of Cancer study 22844 (1996) Int. J. Rad. Oncol. Biol. Phys., 36, pp. 549-556; Karim, A.B., Afra, D., Cornu, P., Randomized trial on the efficacy of radiotherapy for cerebral low-grade glioma in the adult (2002) Int. J. Rad. Oncol. Biol. Phys., 52, pp. 316-324; Armstrong, C.L., Hunter, J.V., Ledakis, G.E., Late cognitive and radiographic changes related to radiotherapy: Initial prospective findings (2002) Neurology, 59, pp. 40-48; Postma, T.J., Klein, M., Verstappen, C.C., Radiotherapy-induced cerebral abnormalities in patients with low-grade glioma (2002) Neurology, 59, pp. 121-123; Surma-aho, O., Niemela, M., Vilkki, J., Adverse long-term effects of brain radiotherapy in adult low-grade glioma patients (2001) Neurology, 56, pp. 1285-1290; Klein, M., Heimans, J.J., Aaronson, N.K., Effect of radiotherapy and other treatment-related factors on mid-term to long-term cognitive sequelae in low-grade gliomas: A comparative study (2002) Lancet, 360, pp. 1361-1368; Torres, I.J., Mundt, A.J., Sweeney, P.J., A longitudinal neuropsychological study of partial brain radiation in adults with brain tumors (2003) Neurology, 60, pp. 1113-1118; Buckner, J.C., Gesme, D., O'Fallon, J.R., Phase II trial of procarbazine, lomustine, and vincristine as initial therapy for patients with low-grade oligodendroglioma or oligoastrocytoma: Efficacy and associations with chromosomal abnormalities (2003) J. Clin. Oncol., 21, pp. 251-255; Quinn, J.A., Reardon, D.A., Friedman, A.H., Phase II trial of temozolomide in patients with progressive low-grade glioma (2003) J. Clin. Oncol., 21, pp. 646-651; van den Bent, M.J., Taphoorn, M.J., Brandes, A.A., Phase II study of first-line chemotherapy with temozolomide in recurrent oligodendroglial tumors: The EORTC brain tumor group study 26971 (2003) J. Clin. Oncol., 21, pp. 2525-2528; Klein, M., Engelberts, N.H., van der Ploeg, H.M., Epilepsy in low-grade gliomas: The impact on cognitive function and quality of life (2003) Ann. Neurol., 54, pp. 514-520","Dropcho, E.J.; Department of Neurology; Indiana University Medical Center; Indianapolis Veterans Affairs Med. Indianapolis, IN 46202, United States; email: edropcho@iupui.edu",,,,,,,,10928480,,CTONB,,"English","Current Treatment Options in Neurology",Review,Scopus "Manon R., Hui S., Chinnaiyan P., Suh J., Chang E., Timmerman R., Phan S., Das R., Mehta M.","The impact of mid-treatment MRI on defining boost volumes in the radiation treatment of glioblastoma multiforme",2004,"Technology in Cancer Research and Treatment",3,3,,303,307,,5,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-2942666236&partnerID=40&rel=R8.0.0","University of Wisconsin, Department of Radiation Oncology, 600 Highland Ave, Madison, WI 53792, United States; Cleveland Clinic Foundation, Dept. Radiation Oncology, 9500 Euclid Ave, Cleveland, OH 44195, United States; MD Arderson Cancer Center, Box 97, 1515 Holcombe Blvd., Houston, TX 77030, United States; Indiana University Medical Center, 535 Barnhill Dr. RT 041, Indianapolis, IN 46202, United States; Pharmacyclics Inc., 995 East Arques Ave, Sunnyvale, CA 94085-4521, United States","Radiation therapy is a central modality in the treatment of glioblastoma multiforme (GBM). Integral to adequate radiation therapy delivery is the appropriate determination of tumor volume and extent at the time treatment is being delivered. As a matter of routine practice, radiation therapy treatment fields are designed based on tumor volumes evident on pre-operative or immediate post-operative MRIs; another MRI is generally not obtained for planning boost fields. In some instances the time interval from surgery to radiotherapy initiation is up to 5 weeks and the boost or ""cone-down phase"" commences 4-5 weeks later. The contrast enhanced T1 MRI may not be a totally reliable indicator of active tumor, especially in regions where such blood-brain barrier breakdown has not occurred. Moreover, these volumes may change during the course of treatment. This may lead to a geographic miss when mid-treatment boost volumes are designed based on a pre-radiotherapy MRI. The goal of this study is to examine how a mid-treatment MRI impacts the delineation and definition of the boost volume in GBM patients in comparison to the pre-treatment MRI scan, particularly when the tumor-specific agent Motexafin-Gadolinium is used.","Glioblastoma treatment planning; Motexafin gadolinium; Target volumes","gadolinium texaphyrin; article; blood brain barrier; cancer radiotherapy; cancer surgery; clinical article; contrast enhancement; disease activity; drug specificity; glioblastoma; human; nuclear magnetic resonance imaging; postoperative period; preoperative evaluation; treatment planning; tumor volume; Brain Neoplasms; Clinical Trials; Combined Modality Therapy; Contrast Media; Glioblastoma; Humans; Magnetic Resonance Imaging; Metalloporphyrins; Postoperative Period; Radiotherapy; Radiotherapy Planning, Computer-Assisted; Tumor Burden",,"gadolinium texaphyrin, 165254-24-0, 194083-75-5; Contrast Media; Metalloporphyrins; motexafin gadolinium",,,"Leibel, S.A., Scott, C.B., Loeffler, J.S., Contemporary approaches to the treatment of malignant gliomas with radiation therapy (1994) Seminars in Oncology, 21, pp. 198-219; Kelly, P.J., Daumas-Duport, C., Scheithauer, B.W., Stereotactic histologic correlations of computed tomography and magnetic resonance imaging-defined abnormalities in patients with glial neoplasms (1987) Mayo Clinic Proceedings, 62, pp. 450-459; Masukado, Y.M.C., Kernohan, J.W., The growth of glioblastoma multiforme (astrocytoma grades 3 and 4) in neurosurgical practice (1961) J. Neurosurg., 18, pp. 636-644; Burger, P.C., Heinz, E.R., Shibata, T., Topographic anatomy and CT correlations in the untreated glioblastoma multiforme (1988) Journal of Neurosurgery, 68, pp. 698-704; Hochberg, F.H., Pruitt, A., Assumptions in the radiotherapy of glioblastoma Neurology; Oppitz, U., Maessen, D., Zunterer, H., 3D-recurrence-patterns of glioblastomas after CT-planned postoperative irradiation (1999) Radiotherapy & Oncology, 53, pp. 53-57; Wallner, K.E., Galicich, J.H., Krol, G., Patterns of failure following treatment for glioblastoma multiforme and anaplastic astrocytoma (1989) International Journal of Radiation Oncology, Biology, Physics, 16, pp. 1405-1409; Holodny, A.I., Nusbaum, A.O., Festa, S., Correlation between the degree of contrast enhancement and the volume of peritumoral edema in meningiomas and malignant gliomas (1999) Neuroradiology, 41, pp. 820-825; Jacobs, A.H., Winkler, A., Dittmar, C., Molecular and functional imaging technology for the development of efficient treatment strategies for gliomas (2002) Technology in Cancer Research & Treatment, 1, pp. 187-204; Pirzkall, A., McKnight, T.R., Graves, E.E., MR-spectroscopy guided target delineation for high-grade gliomas (2001) International Journal of Radiation Oncology, Biology, Physics, 50, pp. 915-928; Miller, R.A., Woodburn, K., Fan, Q., In vivo animal studies with gadolinium (III) texaphyrin as a radiation enhancer (1999) International Journal of Radiation Oncology, Biology, Physics, 45, pp. 981-989; Young, S.W., Qing, F., Harriman, A., Gadolinium(III) texaphyrin: A tumor selective radiation sensitizer that is detectable by MRI (1996) Proceedings of the National Academy of Sciences of the United States of America, 93, pp. 6610-6615; (1999) Proc. Natl. Acad. Sci. USA, 96, p. 2569. , Erratum appears; De Stasio, G., Casalbore, P., Pallini, R., Gadolinium in human glioblastoma cells for gadolinium neutron capture therapy (2001) Cancer Research, 61, pp. 4272-4277; Carde, P., Timmerman, R., Mehta, M.P., Multicenter phase Ib/II trial of the radiation enhancer motexafin gadolinium in patients with brain metastases (2001) Journal of Clinical Oncology, 19, pp. 2074-2083; Ford, J.M.E.J., Alger, J.R., Earle, J., Miles, D., Phan, S., A phase I dose escalation trial of motexafin gadolinium (Gadolinium Texaphyrin, XcytrinR) as a radiation sensitizer in patients with newly diagnosed glioblastoma multiforme (2001) Int. J. Radiat. Oncol. Biol. Phys., 51, p. 205; Rosenthal, D.I., Nurenberg, P., Becerra, C.R., A phase I single-dose trial of gadolinium texaphyrin (Gd-Tex), a tumor selective radiation sensitizer detectable by magnetic resonance imaging (1999) Clinical Cancer Research, 5, pp. 739-745; Albert, F.K., Forsting, M., Sartor, K., Early postoperative magnetic resonance imaging after resection of malignant glioma: Objective evaluation of residual tumor and its influence on regrowth and prognosis (1994) Neurosurgery, 34, pp. 45-60. , [See Comment]; discussion 60-41; Rabin, B.M., Meyer, J.R., Berlin, J.W., Radiation-induced changes in the central nervous system and head and neck (1996) Radiographics, 16, pp. 1055-1072; Rowley, H.A.D.W., Iatrogenic white matter diseases (1993) Neuroimaging Clinics of North America, 3, pp. 379-404","Manon, R.; University of Wisconsin; Department of Radiation Oncology; 600 Highland Ave Madison, WI 53792, United States; email: manon@humonc.wisc.edu",,,,,,,,15330346,,TCRTB,,"English","Technology in Cancer Research and Treatment",Article,Scopus "Salvan C.V., Ulmer J.L., DeYoe E.A., Wascher T., Mathews V.P., Lewis J.W., Prost R.W.","Visual Object Agnosia and Pure Word Alexia: Correlation of Functional Magnetic Resonance Imaging and Lesion Localization",2004,"Journal of Computer Assisted Tomography",28,1,,63,67,,3,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-0347355232&partnerID=40&rel=R8.0.0","Department of Radiology, Division of Neuroradiology, Medical College of Wisconsin, Milwaukee, WI, United States; Neurospine Center of Wisconsin, Green Bay, WI, United States; Department of Radiology, Indiana University Medical Center, Indianapolis, IN, United States; Department of Radiology, Medical College of Wisconsin, 9200 W. Wisconsin Ave., Milwaukee, WI 53226, United States","We present a case of a 64-year-old, right-handed female with a metastatic breast cancer lesion involving the left posterior inferior temporal lobe causing complete loss of the ability to recognize visually common objects and words. After her symptoms resolved on corticosteroid therapy, functional magnetic resonance imaging (fMRI) mapping demonstrated strong left-hemispheric dominance for word recognition and right-hemispheric dominance for object recognition. The case illustrates the relationships among ventral occipito-temporal cortical activation, lesion localization, and lesion-induced deficits of higher visual function. The relationship between hemispheric dominance determined by fMRI and risk of postoperative deficit depends on the specific visual function of interest.","Bold oxygen level dependent (BOLD); Functional magnetic resonance imaging (fMRI); Object recognition; Ventral occipito-temporal cortex (VOTC); Word recognition","adult; agnosia; alexia; article; brain mapping; brain metastasis; breast cancer; case report; diagnostic imaging; female; hemispheric dominance; human; neuroradiology; nuclear magnetic resonance imaging; occipital cortex; preoperative evaluation; priority journal; task performance; temporal lobe; treatment planning; vision; word recognition; Agnosia; Brain Mapping; Brain Neoplasms; Breast Neoplasms; Cerebral Cortex; Dominance, Cerebral; Dyslexia, Acquired; Female; Humans; Magnetic Resonance Imaging; Middle Aged; Temporal Lobe; Visual Perception",,,,,"Laurito, J.T., Bryan, R.N., Mathews, U.P., (2000) Functional Brain Mapping. Categorial Course in Diagnostic Radiology: Neuroradiology, pp. 79-104. , Oak Brook, IL: RSNA; Holodny, A.I., Schulder, M., Liu, W.C., The effect of brain tumors on BOLD functional MR imaging activation in the adjacent motor cortex: Implications for image-guided neurosurgery (2000) AJNR Am J Neuroradiol, 21, pp. 1415-1422; DeYoe, E.A., Occipital lobe (2002) Encyclopedia of the Human Brain, pp. 677-715. , Ramachandran VS ed Elsevier Science; Trobe, J.D., (2001) The Neurology of Vision, 36-39, pp. 346-366. , New York: Oxford University Press; Purves, D., Augustine, G.J., Fitzpatrick, D., (2001) Neuroscience. 2nd Ed., pp. 117-140. , Sunderland, MA: Sinauer Associates; Humphreys, G.W., Forde, E.M.E., Hierarchies, similarity, and interactivity in object recognition: ""category-specific"" neuropsychological deficits (2001) Behav Brain Sci, 24, pp. 453-509; Gerlach, C., Law, I., Gade, A., Perceptual differentiation and category effects in normal object recognition (1999) Brain, 122, pp. 2159-2170; Moore, C., Price, C.J., A functional neuroimaging study of the variables that generate category-specific object processing differences (1999) Brain, 122, pp. 943-962; Kanwisher, N., McDermott, J., Chun, M.M., The fusiform face area: A module in human extrastriate cortex specialized for face perception (1997) J Neurosci, 17, pp. 4302-4311; Gauthier, I., Skudlarski, P., Gore, J.C., Expertise for cars and birds recruits brain areas involved in face recognition (2000) Nat Neurosci, 3, pp. 191-197; Grill-Spector, K., Kourtzi, Z., Kanwisher, N., The lateral occipital complex and its role in object recognition (2001) Vision Res, 41, pp. 1409-1422; Brazis, P.W., Masdeu, J.C., Biller, J., (2001) Localization in Clinical Neurology. 4th Ed., pp. 453-521. , Lippincott Williams & Wilkins: Philadelphia, PA; Jankowiak, J., Albert, M.L., (1994) Localization and Neuroimaging in Neuropsychology, pp. 429-467. , Kertesz A, ed. San Diego, CA: Academic Press; Cohen, L., Lehericy, S., Chochon, F., Language-specific tuning of visual cortex? Functional properties of the visual word form area (2002) Brain, 125, pp. 1054-1069; Cox, R.W., Hyde, J.S., Software tools for analysis and visualization of fMRI data (1997) NMR Biomed, 10, pp. 171-178; Laurito, J.T., Kareken, D.A., Lowe, M.J., Comparison of rhyming and word generation with fMRI (2000) Hum Brain Mapp, 10, pp. 99-106; Mima, T., Oluwatimilehin, T., Hiraoka, T., Transient interhemispheric neuronal synchrony correlates with object recognition (2001) J Neurosci, 21, pp. 3942-3948; Black, S.E., Behrmann, M., (1994) Localization and Neuroimaging in Neuropsychology, pp. 331-359. , Kertesz A, ed. San Diego, CA: Academic Press; Koutstaal, W., Wagner, A.D., Rotte, M., Perceptual specificity in visual object priming: Functional magnetic resonance imaging evidence for a laterality difference in fusiform cortex (2001) Neuropsychologia, 39, pp. 184-199; Fiebach, C.J., Friederici, A.D., Mueller, K., Functional MRI evidence for dual routes to the mental lexicon in visual word recognition (2002) J Cogn Neurosci, 14, pp. 11-23; Kuschinsky, W., (1999) Functional MRI, pp. 15-23. , Moonen CTW, Bandettini PA, eds. Berlin: Springer; Ulmer, J.L., Krouwer, H.G., Mueller, W.M., Pseudo-reorganization of language cortical function in fMRI: A consequence of tumor-induced neurovascular uncoupling (2003) AJNR Am J Neuroradiol, 24, pp. 213-217","Ulmer, J.L.; Department of Radiology; Medical College of Wisconsin; 9200 W. Wisconsin Ave. Milwaukee, WI 53226, United States; email: julmer@mcw.edu",,,,,,,,03638715,,JCATD,10.1097/00004728-200401000-00010,"English","Journal of Computer Assisted Tomography",Article,Scopus "DesRosiers C., Mendonca M.S., Tyree C., Moskvin V., Bank M., Massaro L., Bigsby R.M., Caperell-Grant A., Valluri S., Dynlacht J.R., Timmerman R.","Use of the Leksell Gamma Knife for Localized Small Field Lens Irradiation in Rodents",2003,"Technology in Cancer Research and Treatment",2,5,,449,454,,4,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-10744223297&partnerID=40&rel=R8.0.0","Department of Radiation Oncology, Indiana Univ. Schools of Med./Dent., Indianapolis, IN 46202, United States; Dept. Maxillo-Facial Prosthetics, Indiana Univ. Schools of Med./Dent., Indianapolis, IN 46202, United States; Department Obstetrics, Indiana Univ. Schools of Med./Dent., Indianapolis, IN 46202, United States; Department of Ophthalmology, Indiana Univ. Schools of Med./Dent., Indianapolis, IN 46202, United States; Department of Radiation Oncology, Indiana University, 535 Barnhill Drive, Indianapolis, IN 46202, United States","For most basic radiobiological research applications involving irradiation of small animals, it is difficult to achieve the same high precision dose distribution realized with human radiotherapy. The precision for irradiations performed with standard radiotherapy equipment is ±2 mm in each dimension, and is adequate for most human treatment applications. For small animals such as rodents, whose organs and tissue structures may be an order of magnitude smaller than those of humans, the corresponding precision required is closer to ±0.2 mm, if comparisons or extrapolations are to be made to human data. The Leksell Gamma Knife is a high precision radiosurgery irradiator, with precision in each dimension not exceeding 0.5 mm, and overall precision of 0.7 mm. It has recently been utilized to treat ocular melanoma and induce targeted lesions in the brains of small animals. This paper describes the dosimetry and a technique for performing irradiation of a single rat eye and lens with the Gamma Knife while allowing the contralateral eye and lens of the same rat to serve as the ""control"". The dosimetry was performed with a phantom in vitro utilizing a pinpoint ion chamber and thermoluminescent dosimeters, and verified by Monte Carlo simulations. We found that the contralateral eye received less than 5% of the administered dose for a 15 Gy exposure to the targeted eye. In addition, after 15 Gy irradiation 15 out of 16 animals developed cataracts in the irradiated target eyes, while 0 out of 16 contralateral eyes developed cataracts over a 6-month period of observation. Experiments at 5 and 10 Gy also confirmed the lack of cataractogenesis in the contralateral eye. Our results validate the use of the Gamma Knife for cataract studies in rodents, and confirmed the precision and utility of the instrument as a small animal irradiator for translational radiobiology experiments.","Cataractogenesis; Cataracts; Radiation","animal experiment; animal model; article; cancer radiotherapy; cataract; cataractogenesis; controlled study; dosimetry; gamma knife; gamma knife radiosurgery; irradiation; linear accelerator; Monte Carlo method; nonhuman; rat; thermoluminescence; tumor localization; Animals; Cataract Extraction; Image Processing, Computer-Assisted; Lens, Crystalline; Radiation Dosage; Radiosurgery; Rats; Rats, Sprague-Dawley",,,,,"Emami, B., Lyman, J., Brown, A., Coia, L., Tolerance of Normal Tissue to Therapeutic Irradiation (1991) Int. J. Radiat. Oncol. Biol. Phys., 21, pp. 109-122; Raabe, A., Beck-Bornholdt, H.P., Krull, A., Zieron, J.O., Impact of Pulmonary Metastases of the R1H-tumour on Radiation Tolerance of Rat Lung (2001) Int. J. Radiat. 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Phys., 21, pp. 581-618; Maitz, A.H., Wu, A., Lunsford, L.D., Flickinger, J.C., Quality Assurance for Gamma Knife Stereotactic Radiosurgery (1995) Int. J. Radiat. Oncol. Biol. Phys., 32, pp. 1465-1471; Mehta, M.P., The Physical, Biologic, and Clinical Basis of Radiosurgery (1995) Curr. Probl. Cancer, 19, pp. 265-329; Kamiryo, T., Lopes, M.B., Berr, S.S., Lee, K.S., Occlusion of the Anterior Cerebral Artery after Gamma Knife Irradiation in a Rat (1996) Acta Neurochir. (Wien), 138, pp. 983-990. , discussion 990-981; Rey, M., Valliccioni, P.A., Vial, M., Porcheron, D., Experimental Radiosurgery in Rats using Gamma a ""Gamma Knife"". Description of a Stereotactic Device for Small Laboratory Animals (1996) Neurochirurgie, 42, pp. 289-293; Regis, J., Kerkerian-Legoff, L., Rey, M., Vial, M., First Biochemical Evidence of Differential Functional Effects Following Gamma Knife Surgery (1996) Stereotact. Funct. Neurosurg., 66 (SUPPL. 1), pp. 29-38; Kamiryo, T., Berr, S.S., Lee, K.S., Kassell, N.F., Steiner, L., Enhanced Magnetic Resonance Imaging of the Rat Brain using a Stereotactic Device with a Small Head Coil: Technical Note (1995) Acta. Neurochir. (Wien), 133, pp. 87-92; Kondziolka, D., Lacomis, D., Niranjan, A., Mori, Y., Histological Effects of Trigeminal Nerve Radiosurgery in a Primate Model: Implications for Trigeminal Neuralgia Radiosurgery (2000) Neurosurgery, 46, pp. 971-976. , discussion 976-977; Kamiryo, T., Han, K., Golfinos, J., Nelson, P.K., A Stereotactic Device for Experimental Rat and Mouse Irradiation using Gamma Knife Model B: Technical Note (2001) Acta. Neurochir. (Wien), 143, pp. 83-87. , discussion 87-88; Rand, R.W., Khonsary, A., Brown, W.J., Winter, J., Leksell Stereotactic Radiosurgery in the Treatment of Eye Melanoma (1987) Neurol. Res., 9, pp. 142-146; Salvat, F., Fernandez-Varea, J.M., Sempau, J., Mazurier, J., Practical Aspects of Monte Carlo Simulation of Charged Particle Transport: Mixed Algorithms and Variance Reduction Techniques (1999) Radiat. Environ. Biophys., 38, pp. 15-22; Sempau, J., Sanchez-Reyes, A., Salvat, F., Ben Tahar, H.O., Monte Carlo Simulation of Electron Beams from an Accelerator Head using PENELOPE (2001) Phys. Med. Biol., 46, pp. 1163-1186; Moskvin, V., DesRosiers, C., Papiez, L., Timmerman, Monte Carlo Simulation of the Leksell Gamma Knife: I. Source Modelling and Calculations in Homogeneous Media (2002) Phys. Med. Biol., 47, pp. 1995-2011; Livesey, J.C., Wiens, L.W., Von Seggern, D.J., Inhibition of Radiation Cataractogenesis by WR-77913 (1995) Radiat. Res., 141, pp. 99-104; Stone, H.B., McBride, W.H., Coleman, C.N., Modifying Normal Tissue Damage Postirradiation (2002) Radiat. Res., 157, pp. 204-223. , Report of a Workshop Sponsored by the Radiation Research Program, National Cancer Institute, Bethesda, Maryland, September 6-8, 2000; Dublineau, I., Morel, E., Griffiths, N.M., Characterization of Altered Absorptive and Secretory Functions in the Rat Colon After Abdominal Irradiation: Comparison with the Effects of Total-body Irradiation (2002) Radiat. Res., 157, pp. 52-61","Dynlacht, J.R.; Department of Radiation Oncology; Indiana University; 535 Barnhill Drive Indianapolis, IN 46202, United States; email: jdynlach@iupui.edu",,,,,,,,15330346,,TCRTB,,"English","Technology in Cancer Research and Treatment",Article,Scopus "Witzmann F., Grant R.A.","Pharmacoproteomics in drug development",2003,"Pharmacogenomics Journal",3,2,,69,76,,11,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-0038312125&partnerID=40&rel=R8.0.0","Dept. Cellular/Integrative Physiol., Indiana University Sch. of Medicine, 1345 W. 16th St., Indianapolis, IN 46202, United States; Corporate Res.-Biotechnology Div., The Procter/Gamble Company, Cincinnati, OH, United States","The field of proteomics is taking on increased significance as the relevance of investigating and understanding protein expression in disease and drug development is appreciated. Recent advances in proteomics have been driven by the availability of numerous annotated whole-genome sequences and a broad range of technological and bioinformatic developments that underscore the complexity of the proteome. This review briefly addresses some of the various technologies that comprise Expression Proteomics and Functional Proteomics, citing examples where these emerging approaches have been applied to pharmacology, toxicology, and the development of drugs.","Drug development; Mass spectrometry; Protein array; Protein interactions; Proteomics; Toxicology; Two-dimensional electrophoresis","biological marker; cyclosporin A; daunorubicin; DNA; fluindostatin; gentamicin; heat shock protein 70; hydroxymethylglutaryl coenzyme A reductase; hydroxymethylglutaryl coenzyme A reductase inhibitor; isotope; manumycin; mevinolin; monoclonal antibody; protein farnesyltransferase inhibitor; proteome; pyrimidine derivative; Ras protein; binding affinity; bioinformatics; brain disease; breast cancer; cancer cell culture; cell organelle; diagnostic value; DNA microarray; drug efficacy; drug resistance; drug safety; gene mutation; gene sequence; histopathology; human; kidney disease; liquid chromatography; mass spectrometry; matrix assisted laser desorption ionization time of flight mass spectrometry; nonhuman; ovary cancer; pancreas cancer; pharmacogenetics; polyacrylamide gel electrophoresis; priority journal; protein analysis; protein expression; protein function; protein interaction; protein isolation; protein purification; proteomics; review; technology; two dimensional gel electrophoresis; two hybrid system; Animals; Drug Design; Humans; Organelles; Pharmacogenetics; Pharmacology, Clinical; Protein Biosynthesis; Proteins",,"cyclosporin A, 59865-13-3, 63798-73-2; daunorubicin, 12707-28-7, 20830-81-3, 23541-50-6; DNA, 9007-49-2; fluindostatin, 93957-54-1; gentamicin, 1392-48-9, 1403-66-3, 1405-41-0; hydroxymethylglutaryl coenzyme A reductase, 37250-24-1; manumycin, 52665-74-4; mevinolin, 75330-75-5; Proteins","lescol; mevacorProteinChip, Ciphergen, United States","Ciphergen, United States","Tew, K.D., Glutathione-associated enzymes in the human cell lines of the national cancer institute drug screening program (1996) Mol. 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Cell Biol., 19, pp. 1720-1730; Ideker, T., Thorsson, V., Ranish, J.A., Christmas, R., Buhler, J., Eng, J.K., Integrated genomic and proteomic analyses of a systematically perturbed metabolic network (2001) Science, 292, pp. 929-934; Moller, A., Soldan, M., Volker, U., Maser, E., Two-dimensional gel electrophoresis: A powerful method to elucidate cellular responses to toxic compounds (2001) Toxicology, 160, pp. 129-138; Steiner, S., Witzmann, F.A., Proteomics: Applications and opportunities in preclinical drug development (2000) Electrophoresis, 21, pp. 2099-2104; Liebler, D.C., Introduction to Proteomics: Tools for the New Biology (2002), Humana Press: Totowa, NJWasinger, V.C., Corthals, G.L., Proteomic tools for biomedicine (2002) J. Chromatogr. B. Analyt. Technol. Biomed. Life Sci., 771, pp. 33-48; Kennedy, S., The role of proteomics in toxicology: Identification of biomarkers of toxicity by protein expression analysis (2002) Biomarkers, 7, pp. 269-290; Witzmann, F.A., Li, J., Proteomics: Core technologies and applications in physiology (2002) Am. J. Physiol. GI Liver Physiol., 282, pp. G735-G741; Molloy, M.P., Herbert, B.R., Walsh, B.J., Tyler, M.I., Traini, M., Sanchez, J.C., Extraction of membrane proteins by differential solubilization for separation using two-dimensional gel electrophoresis (1998) Electrophoresis, 19, pp. 837-844; Herbert, B., Righetti, P.G., A turning point in proteome analysis: Sample prefractionation via multicompartment electrolyzers with isoelectric membranes (2000) Electrophoresis, 21, pp. 3639-3648; Cordwell, S.J., Nouwens, A.S., Verrills, N.M., Basseal, D.J., Walsh, B.J., Subproteomics based upon protein cellular location and relative solubilities in conjunction with composite two-dimensional electrophoresis gels (2000) Electrophoresis, 21, pp. 1094-1103; Scheler, C., Lamer, S., Pan, Z., Li, X.P., Salnikow, J., Jungblut, P., Peptide mass fingerprint sequence coverage from differently stained proteins on two-dimensional electrophoresis patterns by matrix assisted laser desorption/ionization-mass spectrometry (MALDI-MS) (1998) Electrophoresis, 19, pp. 918-927; Perkins, D.N., Pappin, D.J., Creasy, D.M., Cottrell, J.S., Probability-based protein identification by searching sequence databases using mass spectrometry data (1999) Electrophoresis, 20, pp. 3551-3567; Eng, J.K., McCormack, A.L., Yates J.R. III, An approach to correlate tandem mass spectral data of peptides with amino acid sequences in a protein database (1994) J. Am. Soc. Mass Spectrom., 5, pp. 976-989; Shevchenko, A., Jensen, O.N., Podtelejnikov, A.V., Sagliocco, F., Wilm, M., Vorm, O., Linking genome and proteome by mass spectrometry: Large-scale identification of yeast proteins from two dimensional gels (1996) Proc. Natl. Acad. Sci. USA, 93, pp. 14440-14445; Keough, T., Lacey, M.P., Fieno, A.M., Grant, R.A., Sun, Y., Bauer, M.D., Tandem mass spectrometry methods for definitive protein identification in proteomics research (2000) Electrophoresis, 21, pp. 2252-2265; Medzihradszky, K.F., Campbell, J.M., Baldwin, M.A., Falick, A.M., Juhasz, P., Vestal, M.L., The characteristics of peptide collision-induced dissociation using a high-performance MALDI-TOF/TOF tandem mass spectrometer (2000) Anal. Chem., 72, pp. 552-558; Anderson, N.L., Copple, D.C., Bendele, R.A., Probst, G.S., Richardson, F.C., Covalent protein modifications and gene expression changes in rodent liver following administration of methapyrilene: A study using two-dimensional electrophoresis (1992) Fundam. Appl. Toxicol., 18, pp. 570-580; Steiner, S., Aicher, L., Raymackers, J., Meheus, L., Esquer-Blasco, R., Anderson, N.L., Cyclosporine A decreases the protein level of the calcium-binding protein calbindin-D 28 kDa in rat kidney (1996) Biochem. Pharmacol., 51, pp. 253-258; Varela, M.C., Arce, A., Greiner, B., Schwald, M., Aicher, L., Wahl, D., Cyclosporine A-induced decrease in calbindin-D 28 kDa in rat kidney but not in cerebral cortex and cerebellum (1998) Biochem. 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Cellular/Integrative Physiol.; Indiana University Sch. of Medicine; 1345 W. 16th St. Indianapolis, IN 46202, United States; email: fwitzman@iupui.edu",,,,,,,,1470269X,,PJHOA,10.1038/sj.tpj.6500164,"English","Pharmacogenomics Journal",Review,Scopus "Holmes A.M., Deb P.","The effect of chronic illness on the psychological health of family members",2003,"Journal of Mental Health Policy and Economics",6,1,,13,22,,9,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-0043032659&partnerID=40&rel=R8.0.0","School of Public/Environ. Affairs, Indiana University, Purdue University Indianapolis, 801 W. Michigan Street, Indianapolis, IN 46202, United States; Department of Economics, Hunter College, City University of New York, Flushing, NY, United States; Department of Economics, Indiana University, Purdue University Indianapolis, 801 W. Michigan Street, Indianapolis, IN 46202, United States","Background: Chronic illness in a family member can cause emotional distress throughout the family, and may impair the family's ability to support the patient. Objectives: We compare the familial impact of mental illness to other common chronic conditions. We examine the impact of a person's chronic illness on the psychological health of all persons in his or her family and identify both individual and family-level risk factors associated with psychological spillovers. Methods: Our analysis is based on data from the 1996 Medical Expenditure Panel Survey (MEPS) that, because of its sample design, can be used to model both individual and family health status. Psychological distress is measured using responses to the general mental health question for each family member. The chronic conditions considered include cancer, diabetes, stroke-related disorders, arthritis, asthma, and mental illness (including dementia). We estimate the relationships of interest using a semi-parametric method, the discrete random effects probit model. Results: Brain-related conditions, including mental illness, impose the most significant risk to the psychological well-being of family members. The effects of the other chronic conditions studied, while not as significant, are notable in that their negative impacts on the psychological health of family members are sometimes larger than their direct psychological impacts on the patient. Economic distress not only directly increases the chance that an individual will experience emotional distress, but it appears it also reduces the family's ability as a whole to cope psychologically with chronic illness. Discussion: Our analysis suffers from problems common to all cross-sectional designs, although the impact of selection bias appeared to be small in sensitivity analysis. While health conditions were based on unverified self-reports, condition categories were broadly defined to reduce the required precision of such reports.",,"accuracy; adult; arthritis; article; asthma; brain disease; cancer; child; chronic disease; controlled study; coping behavior; data analysis; dementia; diabetes mellitus; distress syndrome; emotional stress; family health; health care cost; health economics; health status; health survey; human; major clinical study; medical parameters; mental disease; mental health; nonbiological model; psychological aspect; questionnaire; randomization; risk assessment; risk factor; self report; sensitivity analysis; stroke; wellbeing; Chronic Disease; Cost of Illness; Cross-Sectional Studies; Family; Family Health; Family Relations; Female; Health Status; Humans; Male; Mental Health; Risk Factors; Stress, Psychological; United States",,,,,"Lowery, K., Mynt, P., Aisbett, J., Dixon, T., O'Brien, J., Ballard, C., Depression in the carers of dementia sufferers: A comparison of the carers of patients suffering from dementia with Lewy bodies and the carers of patients with Alzheimer's disease (2000) J. 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Meas., 13, pp. 61-375; Carlson, B.L., Cohen, S.B., Johnson, A.E., Family unit constructs, dynamics, and analysis in the household component of the NMES (1994) J. Econ. Soc. Meas., 20 (3), pp. 215-235; Altman, B.M., Cooper, P.F., Cunningham, P.J., The case of disability in the family: Impact on health care utilization and expenditures for nondisabled members (1999) Milbank Q., 77 (1), pp. 39-75; Cuellar, N., Butts, J.B., Caregiver distress: What nurses in rural settings can do to help (1999) Nurs. Forum, 34 (3), pp. 24-30","Holmes, A.M.; School of Public/Environ. Affairs; Indiana University; Purdue University Indianapolis; 801 W. Michigan Street Indianapolis, IN 46202, United States; email: aholmes@iupui.edu",,,,,,,,10914358,,JMHPA,,"English","Journal of Mental Health Policy and Economics",Article,Scopus "van der Wal E.P.J., Azzarelli B., Edwards-Brown M.","Malignant transformation of a chiasmatic pilocytic astrocytoma in a patient with diencephalic syndrome",2003,"Pediatric Radiology",33,3,,207,210,,12,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-0038182113&partnerID=40&rel=R8.0.0","Department of Radiology, Indiana University, James Whitcomb Riley Child. Hospital, 702 Barnhill Drive, Indianapolis, IN 46202-5200, United States; Department of Pathology, Division of Neuropathology, Indiana University, 635 Barbhill Drive, Indianapolis, IN 46202-5120, United States","Chiasmatic gliomas with metastatic spread are rare in children and are usually associated with diencephalic syndrome. They are mostly pilocytic astrocytomas and their transformation to high-grade astrocytomas has never previously been reported in the pediatric population. We report leptomeningeal spread of a chiasmatic pilocytic astrocytoma in a child presenting with diencephalic syndrome. He was treated with chemotherapy and radiation. The tumor recurred with transformation into a high-grade astrocytoma. Radiation therapy may have played a role in transformation of the tumor, but more research is needed to further clarify the biological behavior of this tumor.","Chiasmatic pilocytic astrocytoma; Diencephalic syndrome; Malignant transformation; Metastatic spread","carboplatin; etoposide; glial fibrillary acidic protein; ifosfamide; vincristine; article; astrocytoma; brain biopsy; brain tumor; brain ventricle peritoneum shunt; cancer chemotherapy; cancer grading; cancer research; case report; cell nucleus; diencephalon; facial nerve paralysis; histopathology; human; human cell; human tissue; immunohistochemistry; male; malignant transformation; meningeal metastasis; mental health; nerve paralysis; nuclear magnetic resonance imaging; priority journal; school child; tumor cell; tumor growth; tumor recurrence; Antineoplastic Combined Chemotherapy Protocols; Astrocytoma; Biopsy, Needle; Cell Transformation, Neoplastic; Child, Preschool; Combined Modality Therapy; Cranial Irradiation; Diencephalon; Follow-Up Studies; Humans; Immunohistochemistry; Magnetic Resonance Imaging; Male; Meningeal Neoplasms; Neoplasm Invasiveness; Optic Chiasm; Optic Nerve Neoplasms; Risk Assessment; Syndrome",,"carboplatin, 41575-94-4; etoposide, 33419-42-0; ifosfamide, 3778-73-2; vincristine, 57-22-7","vp 16",,"Poussaint, T.Y., Barnes, P.D., Nichols, K., Diencephalic syndrome: Clinical features and imaging findings (1997) AJNR, 18, pp. 1499-1505; Namba, S., Nishimoto, A., Yagyu, Y., Diencephalic syndrome of emaciation (Russell's syndrome) (1985) Surg. Neurol., 23, pp. 581-588; Perilongo, G., Carollo, C., Salviati, L., Diencephalic syndrome and disseminated juvenile pilocytic astrocytomas of the hypothalamic-optic chiasm region (1997) Cancer, 80, pp. 142-146; Waga, S., Shimizu, T., Sakakura, M., Diencephalic syndrome of emaciation (Russell's syndrome) (1982) Surg. Neurol., 17, pp. 141-146; Tihan, T., Fisher, P., Kepner, J.L., Pediatric astrocytomas with monomorphous pilomyxoid features and a less favorable outcome (1999) J. Neuropathol. Exp. Neurol., 58, pp. 1061-1068; Mclendon, R., Enterline, D., Tien, R., Tumors of the central neuroepithelial origin (1998) Russell and Rubinstein's Pathology of Tumors of the Central Nervous System, pp. 308-528. , 6th edn; Savoiardo, M., Harwood-Nash, D., Tadmor, R., Gliomas of the intracranial optic pathways in children (1981) Radiology, 138, pp. 601-610; Harrison, M.J., Wolfe, D.E., Lau, T.S., Radiation induced meningiomas: Experience at Mount Sinai Hospital and review of the literature (1991) J. Neurosurg., 75, pp. 564-574; Kumar, P.P., Good, R.R., Skultety, F.M., Radiation induced neoplasms of the brain (1987) Cancer, 59, pp. 1174-1282; Wilson, W.B., Feinsod, M., Hoyt, W.F., Malignant evolution of childhood chiasmal pilocytic astrocytoma (1976) Neurology, 26, pp. 322-325","Edwards-Brown, M.; Department of Radiology; Indiana University; James Whitcomb Riley Child. Hospital; 702 Barnhill Drive Indianapolis, IN 46202-5200, United States; email: medward@IUPUI.edu",,,,,,,,03010449,,PDRYA,,"English","Pediatric Radiology",Article,Scopus "Kavanagh B.D., Timmerman R.D., Benedict S.H., Wu Q., Schefter T.E., Stuhr K., McCourt S., Newman F., Cardinale R.M., Gaspar L.E.","How should we describe the radiobiologic effect of extracranial stereotactic radiosurgery: Equivalent uniform dose or tumor control probability?",2003,"Medical Physics",30,3,,321,324,,19,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-0141611848&partnerID=40&rel=R8.0.0","Department of Radiation Oncology, Univ. of Colorado Hlth. Sci. Center, Aurora, CO 80010-0510, United States; Department of Radiation Oncology, Indiana University, Bloomington, IN, United States; Department of Radiation Oncology, Virginia Commonwealth University, Richmond, VA, United States; Department of Radiation Oncology, Anschutz Cancer Center, Univ. of Colorado Hlth. Sci. Center, 1665 N. Ursula St., Aurora, CO 80010-0510, United States","Extracranial stereotactic radiosurgery (ESR) is now undergoing clinical investigation at numerous institutions as a treatment for solitary malignant lesions. Because there is no standard ESR technique, the same minimum dose might be applied through widely variable target dose-volume histograms. For multicenter trials of ESR or interinstitutional comparisons, a reliable index of radiobiological dose equivalency might facilitate the evaluation of dose-response relationships. Equivalent uniform dose (EUD) and tumor control probability (TCP) were considered for this application. While EUD appears more robust for the prospective description of ESR, TCP is expected to remain more valuable for a post hoc estimation of radiosensitivity parameters. © 2003 American Association of Physicists in Medicine.","EUD; Extracranial; Radiosurgery; Stereotactic; TCP","article; cancer control; dose response; malignant neoplastic disease; priority journal; probability; radiation dose; radiobiology; radiosensitivity; radiosurgery; stereotaxic surgery; brain; brain tumor; cell survival; comparative study; computer assisted radiotherapy; evaluation; human; methodology; radiation exposure; radiometry; sensitivity and specificity; standard; treatment outcome; Brain; Brain Neoplasms; Cell Survival; Humans; Radiation Tolerance; Radiometry; Radiosurgery; Radiotherapy Dosage; Radiotherapy Planning, Computer-Assisted; Sensitivity and Specificity; Treatment Outcome",,,,,"Blomgren, H., Lax, I., Naslund, I., Svanstrom, R., Stereotactic high dose fraction radiation therapy of extracranial tumors using an accelerator: Clinical experience of the first thirty-one patients (1995) Acta Oncol., 34, pp. 861-870; Niemierko, A., Reporting and analyzing dose distributions: A concept of an equivalent uniform dose (1997) Med. Phys., 24, pp. 103-110; Sanchez-Nieto, B., Nahum, A.E., The delta-TCP concept: A clinically useful measure of tumor control probability (1999) Int. J. Radiat. Oncol., Biol., Phys., 44, pp. 369-380; Webb, S., Nahum, A.E., A model for calculating tumour control probability in radiotherapy including the effects of inhomogeneous distributions of dose and clonogenic cell density (1993) Phys. Med. Biol., 38, pp. 653-666; Elkind, M.M., Swain, R.W., Alescio, T., Sutton, H., Moses, W.B., Oxygen, nitrogen, recovery, and radiation therapy (1965) Cellular Radiation Biology, pp. 442-461. , Williams & Wilkins, Baltimore; Khandelwal, S.R., Kavanagh, B.D., Lin, P., Truong, Q.T., Lu, J., Abraham, D.J., Schmidt-Ullrich, R.K., RSR13, an allosteric effector of hemoglobin, and carbogen radiosensitize FSAII and SCCVII tumors in C3H mice (1999) Br. J. Cancer, 79, pp. 814-820; Kavanagh, B.D., Secomb, T.W., Hsu, R., Lin, P., Venitz, J., Dewhirst, M.W., A theoretical model for the effects of reduced hemoglobin-oxygen affinity on tumor oxygenation (2002) Int. J. Radiat. Oncol., Biol., Phys., 53, pp. 172-179; Ljungkvist, A.S., Bussink, J., Rijken, P.F., Kaanders, J.H., Van der Kogel, A.J., Denekamp, J., Vascular architecture, hypoxia, and proliferation in first-generation xenografts of human head-and-neck squamous cell carcinomas (2002) Int. J. Radiat. Oncol., Biol., Phys., 54, pp. 215-228; Tome, W.A., Fowler, J.F., On cold spots in tumor subvolumes (2002) Med. Phys., 29, pp. 1590-1598","Kavanagh, B.D.; Department of Radiation Oncology; Anschutz Cancer Center; Univ. of Colorado Hlth. Sci. Center; 1665 N. Ursula St. Aurora, CO 80010-0510, United States; email: Brian.Kavanagh@uchsc.edu",,,,,,,,00942405,,MPHYA,10.1118/1.1543571,"English","Medical Physics",Article,Scopus "Villain M.A., Pageaux G.P., Veyrac M., Arnaud B., Harris A., Greenfield D.S.","Effect of acetazolamide on ocular hemodynamics in pseudotumor cerebri associated with inflammatory bowel disease",2002,"American Journal of Ophthalmology",134,5,,778,780,,5,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-0036844822&partnerID=40&rel=R8.0.0","Service d'Ophtalmologie, Hôpital Gui De Chauliac, Universitaire De Montpellier, Montpellier, France; Bascom Palmer Eye Institute, University of Miami, School of Medicine, Miami, FL, United States; Service Des Maladies De l'Appareil Digestif, Hôpital St Eloi, Centre Hospitalo-Universitaire De Montpellier, Montpellier, France; Department of Ophthalmology, Indiana University, School of Medicine, Indianapolis, IN, United States; Service d'Ophtalmologie, Hôpital Gui De Chauliac, 80, avenue Augustin Fliche, 34 295 Montpellier Cedex 5, France","PURPOSE: To describe the hemodynamic effect of oral acetazolamide administration on ocular perfusion in a patient with pseudotumor cerebri associated with Crohn disease. DESIGN: Interventional case report. METHODS: A 20-year-old woman with a 5-year history of Crohn disease presented with a 2-week history of headache and blurred vision in both eyes. Ophthalmologic examination was normal. Fluorescein angiography showed a profound delay in retinal and choroidal perfusion. Lumbar puncture showed an opening pressure of 320 mm water. Therapy was initiated with oral acetazolamide 750 mg per day. RESULTS: A subjective improvement of symptoms was noted over 4 days. Repeat fluorescein angiography showed resolution of the ocular perfusion deficit. No recurrent symptoms were noted 19 months after cessation of therapy. CONCLUSIONS: Crohn disease may present with pseudotumor cerebri and severe ocular perfusion deficits that are reversible with oral acetazolamide therapy. © 2002 by Elsevier Science Inc. All rights reserved.",,"acetazolamide; prednisone; water; adult; arterial pressure; article; body weight; brain pseudotumor; cancer chemotherapy; case report; cerebrospinal fluid analysis; choroid plexus; clinical feature; Crohn disease; disease course; drug effect; drug withdrawal; female; fluorescence angiography; follow up; headache; hemodynamic monitoring; hemodynamics; human; intraocular pressure; laboratory test; lumbar puncture; nuclear magnetic resonance imaging; ophthalmology; priority journal; recurrent disease; retina; steroid therapy; treatment outcome; visual acuity; visual impairment; Acetazolamide; Administration, Oral; Adult; Carbonic Anhydrase Inhibitors; Choroid; Crohn Disease; Female; Fluorescein Angiography; Headache; Hemodynamic Processes; Humans; Intracranial Pressure; Papilledema; Pseudotumor Cerebri; Retinal Vessels; Visual Acuity; Visual Fields",,"Acetazolamide, 59-66-5; Carbonic Anhydrase Inhibitors",,,"Rubin, R.C., Henderson, E.S., Ommaya, A.K., Walker, M.D., Rall, D.P., The production of cerebrospinal fluid in man and its modification by acetazolamide (1966) J Neurosurg, 25, pp. 430-436; Rassam, S.M.B., Patel, V., Kohner, E.M., The effect of acetazolamide on the retinal circulation (1993) Eye, 7, pp. 697-702; Miller, N.R., Papilledema (1998) Walsh & Hoyt's clinical neuro-ophthalmology, 1, pp. 487-548. , N.R. Miller, & N.J. Newman. Baltimore, MD: Williams and Wilkins; Harris, A., Tippke, S., Sievers, C., Picht, G.D., Lieb, W., Martin, B., Acetazolamide and CO2: Acute effects on cerebral and retrobulbar hemodynamics (1996) J Glaucoma, 5, pp. 39-45; Greenfield, D.S., Wanichwecharungruang, B., Liebman, J.M., Ritch, R., Pseudotumor cerebri appearing with unilateral papilledema after trabeculectomy (1997) Arch Ophthalmol, 115, pp. 423-426","Villain, M.A.; Service d'Ophtalmologie; Hôpital Gui de Chauliac; 80, avenue Augustin Fliche 34 295 Montpellier Cedex 5, France; email: villainmax@aol.com",,,,,,,,00029394,,AJOPA,10.1016/S0002-9394(02)01650-1,"English","American Journal of Ophthalmology",Article,Scopus "Coldiron Jr. A.D., Sanders R.A., Watkins III J.B.","Effects of combined Quercetin and coenzyme Q10 treatment on oxidative stress in normal and diabetic rats",2002,"Journal of Biochemical and Molecular Toxicology",16,4,,197,202,,8,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-0036396164&partnerID=40&rel=R8.0.0","Medical Sciences Program, Indiana University, School of Medicine, Bloomington, IN 47405-7005, United States","Reactive oxygen species may be actively involved in the genesis of various pathological states such as ischemia-reperfusion injury, cancer, and diabetes. Our objective was to determine if subacute treatment with combined antioxidants quercetin and coenzyme Q10 (10 mg/kg/day ip for 14 days) affects the activities of antioxidant enzymes in normal and 30-day streptozotocin-induced diabetic Sprague-Dawley rats. Quercetin treatment raised blood glucose concentrations in normal and diabetic rats, whereas treatment with coenzyme Q10 did not. Liver, kidney, heart, and brain tissues were excised and the activities of catalase, glutathione reductase, glutathione peroxidase, superoxide dismutase, and concentrations of oxidized and reduced glutathione were determined. In the liver of diabetic rats, superoxide dismutase, glutathione peroxidase, and levels of both oxidized and reduced glutathione were significantly decreased from the non-diabetic control, and these effects were not reversed when antioxidants were administered. In kidney, glutathione peroxidase activity was significantly elevated in the diabetic rats as compared to nondiabetic rats, and antioxidant treatment did not return the enzyme activity to nondiabetic levels. In heart, catalase activity was increased in diabetic animals and restored to normal levels after combined treatment with quercetin and coenzyme Q10. Cardiac superoxide dismutase was lower than normal in quercetin- and quercetin + coenzyme Q10-treated diabetic rats. There were no adverse effects on oxidative stress markers after treatment with quercetin or coenzyme Q10 singly or in combination. In spite of the elevation of glucose, quercetin may be effective in reversing some effects of diabetes, but the combination of quercetin + coenzyme Q10 did not increase effectiveness in reversing effects of diabetes. © 2002 Wiley Periodicals, Inc. J Biochem Mol Toxicol.","Catalase; Coenzyme Q10; Diabetes; Glutathione peroxidase; Glutathione reductase; Heart; Kidney; Liver; Oxidative stress; Quercetin; Streptozotocin; Superoxide dismutase","antioxidant; catalase; glucose; glutathione; glutathione disulfide; glutathione peroxidase; glutathione reductase; quercetin; reactive oxygen metabolite; superoxide dismutase; ubidecarenone; animal experiment; animal model; animal tissue; article; brain tissue; cancer; controlled study; drug efficacy; enzyme activity; excision; female; glucose blood level; heart; ischemia; kidney parenchyma; liver; nonhuman; oxidative stress; rat; rat strain; reperfusion injury; streptozocin diabetes; Animals; Body Weight; Brain; Diabetes Mellitus, Experimental; Female; Kidney; Liver; Myocardium; Organ Size; Oxidative Stress; Quercetin; Rats; Rats, Sprague-Dawley; Ubiquinone; Animalia",,"coenzyme Q10, 303-98-0; Quercetin, 117-39-5; Ubiquinone, 1339-63-5",,,"Kehrer, J.P., Free radicals as mediators of tissue injury and disease (1993) Crit. Rev. Toxicol, 23, pp. 21-48; Baynes, J.W., Thorpe, S.R., Role of oxidative stress in diabetic complications: A new perspective on an old paradigm (1999) Diabetes, 48, pp. 1-9; Ernster, L., Forsmark-Andree, P., Ubiquinol: An endogenous antioxidant in aerobic organisms (1993) Clin. Investig, 71, pp. S60-S65; Ernster, L., Dallner, G., Biochemical, physiological and medical aspects of ubiquinone function (1995) Biochim. Biophys. Acta, pp. 195-204. , 1271; Greenberg, S., Frishman, W.H., Co-enzyme Q10: A new drug for cardiovascular disease (1990) J. Clin. Pharmacol, 30, pp. 596-608; Kamei, M., Fujita, T., Kanbe, T., Sasaki, K., Oshiba, K., Otani, S., Matsui-Yuasa, I., Morisawa, S., The distribution and content of ubiquinone in foods (1986) Int. J. Vitam. Nutr. Res, 56, pp. 57-63; Lenaz, G., Bovina, C., Formiggini, G., Castelli, G.P., Mitochondria, oxidative stress, and antioxidant defences (1999) Acta Biochim. Pol, 46, pp. 1-21; Lass, A., Sohal, R.S., Electron transport-linked ubiquinone-dependent recycling of alpha-tocopherol inhibits autooxidation of mitochondrial membranes (1998) Arch. Biochem. Biophys, 352, pp. 229-236; Henriksen, J.E., Andersen, C.B., Hother-Nielsen, O., Vaag, A., Mortensen, S.A., Beck-Nielsen, H., Impact of ubiquinone (coenzyme Q10) treatment on glycaemic control, insulin requirement and well-being in patients with Type 1 diabetes mellitus (1999) Diabet. Med, 16, pp. 312-318; Rauscher, F.R., Sanders, R.A., Watkins, J.B., Effects of coenzyme Q10 treatment on antioxidant pathways in normal and streptozotocin-induced diabetic rats (2001) J. Biochem. Mol. Toxicol, 15, pp. 41-46; Niki, E., Saito, T., Kawakami, A., Kamiya, Y., Inhibition of oxidation of methyl linoleate in solution by vitamin E and vitamin C (1984) J. Biol. Chem, 259, pp. 4177-4182; Niki, E., Antioxidants in relation to lipid peroxidation (1987) Chem. Phys. Lipids, 44, pp. 227-253; Afanas'ev, I.B., Dorozhko, A.I., Brodskii, A.V., Kostyuk, V.A., Potapovitch, A.I., Chelating and free radical scavenging mechanisms of inhibitory action of rutin and quercetin in lipid peroxidation (1989) Biochem. Pharmacol, 38, pp. 1763-1769; Candlish, J.K., Das, N.P., Antioxidants in food and chronic degenerative diseases (1996) Biomed. Environ. Sci, 9, pp. 117-123; Morand, C., Crespy, V., Manach, C., Besson, C., Demigne, C., Remesy, C., Plasma metabolites of quercetin and their antioxidant properties (1998) Am. J. Physiol, 275, pp. R212-R219; Plumb, G.W., Price, K.R., Williamson, G., Antioxidant properties of flavonol glycosides from green beans (1999) Redox Rep, 4, pp. 123-127; Rankin, S.M., de Whalley, C.V., Hoult, J.R., Jessup, W., Wilkins, G.M., Collard, J., Leake, D.S., The modification of low density lipoprotein by the flavonoids myricetin and gossypetin (1993) Biochem. Pharmacol, 45, pp. 67-75; Negre-Salvayre, A., Salvayre, R., Quercetin prevents the cytotoxicity of oxidized LDL on lymphoid cell lines (1992) Free Radical Biol. Med, 12, pp. 101-106; Josephy, P.D., (1997) Molecular Toxicology, , New York: Oxford University Press; Saxena, A.K., Srivastava, P., Kale, R.K., Baquer, N.Z., Impaired antioxidant status in diabetic rat liver: Effect of vanadate (1993) Biochem. Pharmacol, 45, pp. 539-542; Mukherjee, B., Mukherjee, J.R., Chatterjee, M., Lipid peroxidation, glutathione levels and changes in glutathione-related enzyme activities in streptozotocin-induced diabetic rats (1994) Immunol. Cell. Biol, 72, pp. 109-114; Kakkar, R., Kalra, J., Mantha, S.V., Prasad, K., Lipid peroxidation and activity of antioxidant enzymes in diabetic rats (1995) Mol. Cell. Biochem, 151, pp. 113-119; Godin, D.V., Wohaieb, S.A., Garnett, M.E., Goumeniouk, A.D., Antioxidant enzyme alterations in experimental and clinical diabetes (1988) Mol. Cell. Biochem, 84, pp. 223-231; Rauscher, F.M., Sanders, R.A., Watkins, J.B., Effects of new antioxidant compounds PNU-104067F and PNU-74389G on antioxidant defense in normal and diabetic rats (2000) J. Biochem. Mol. Toxicol, 14, pp. 189-194; Rauscher, F.M., Sanders, R.A., Watkins, J.B., Effects of piperine on antioxidant pathways in tissues from normal and streptozotocin-induced diabetic rats (2000) J. Biochem. Mol. Toxicol, 14, pp. 329-334; Guide for the Care and Use of Laboratory Animals (1996), National Research Council. Washington DC: National Academy PressLuck, H., Catalase (1963) Methods of Enzymatic Analysis, pp. 885-888. , Bergmeyer H-U, editor. New York: Academic Press; Tappel, A.L., Glutathione peroxidase and hydroperoxides (1978) Meth. Enzymol, 52, pp. 506-513; Carlberg, I., Mannervik, B., Purification and characterization of the flavoenzyme glutathione reductase from rat liver (1975) J. Biol. Chem, 250, pp. 5475-5480; Crapo, J.D., McCord, J.M., Fridovich, I., Preparation and assay of superoxide dismutases (1978) Meth. Enzymol, 53, pp. 382-393; Hissin, P.J., Hilf, R., A fluorometric method for determination of oxidized and reduced glutathione in tissues (1976) Anal. Biochem, 74, pp. 214-226; Lowry, O., Rosebrough, N.J., Farr, A.L., Randall, R.J., Protein measurements with Folin phenol reagent (1951) J. Biol. Chem, 193, pp. 265-275; Baynes, J.W., Role of oxidative stress in development of complications in diabetes (1991) Diabetes, 40, pp. 405-412; Wohaieb, S.A., Godin, D.V., Alterations in free radical tissue-defense mechanisms in streptozocin-induced diabetes in rat. Effects of insulin treatment (1987) Diabetes, 36, pp. 1014-1018; Mak, D.H., Ip, S.P., Li, P.C., Poon, M.K., Ko, K.M., Alterations in tissue glutathione antioxidant system in streptozotocin-induced diabetic rats (1996) Mol. Cell. Biochem, 162, pp. 153-158; Kakkar, R., Mantha, S.V., Radhi, J., Prasad, K., Kalra, J., Antioxidant defense system in diabetic kidney: A time course study (1997) Life Sci, 60, pp. 667-679; Mukai, K., Tsuzuki, N., Ishizu, K., Ouchi, S., Fukuzawa, K., Electron spin resonance and electron nuclear double resonance studies of cation radicals derived from tocopherol model compounds (1984) Chem. Phys. Lipids, 35, pp. 199-208; Nohl, H., Gille, L., Kozlov, A.V., Critical aspects of the antioxidant function of coenzyme Q in biomembranes (1999) Biofactors, 9, pp. 155-161; Mellors, A., Tappel, A.L., The inhibition of mitochondrial peroxidation by ubiquinone and ubiquinol (1966) J. Biol. Chem, 241, pp. 4353-4356; Rauchova, H., Drahota, Z., Lenaz, G., Function of coenzyme Q in the cell: Some biochemical and physiological properties (1995) Physiol. Res, 44, pp. 209-216; Yamamoto, Y., Yamashita, S., Plasma ratio of ubiquinol and ubiquinone as a marker of oxidative stress (1997) Mol. Aspects. Med, 18 (SUPPL.), pp. S79-S84; Kontush, A., Schippling, S., Spranger, T., Beisiegel, U., Plasma ubiquinol-10 as a marker for disease: Is the assay worthwhile? (1999) Biofactors, 9, pp. 225-229; Laughton, M.J., Evans, P.J., Moroney, M.A., Hoult, J.R., Halliwell, B., Inhibition of mammalian 5-lipoxygenase and cyclo-oxygenase by flavonoids and phenolic dietary additives. Relationship to antioxidant activity and to iron ion-reducing ability (1991) Biochem. Pharmacol, 42, pp. 1673-1681; Rauscher, F.M., Sanders, R.A., Watkins J.B. III, Effects of isoeugenol on oxidative stress pathways in normal and streptozotocin-induced diabetic rats (2001) J. Biochem. Mol. Toxicol, 15, pp. 159-164; Sanders, R.A., Rauscher, F.M., Watkins J.B. III, Effects of quercetin on antioxidant defense in streptozotocin-induced diabetic rats (2001) J. Biochem. Mol. Toxicol, 15, pp. 143-149; Kato, R., Yamazoe, Y., Sex-specific cytochrome P450 as a cause of sex- and species-related differences in drug toxicity (1992) Toxicol. Lett, 64-65, pp. 661-667. , (Spec No); Packer, L., Rimbach, G., Virgili, F., Antioxidant activity and biologic properties of a procyanidin-rich extract from pine (Pinus maritima) bark, pycnogenol (1999) Free Radical Biol. Med, 27, pp. 704-724; Rice-Evans, C.A., Miller, N.J., Antioxidant activities of flavonoids as bioactive components of food (1996) Biochem. Soc. Trans, 24, pp. 790-795","Watkins III, J.B.; Medical Sciences Program; Indiana Univ. School of Medicine Bloomington, IN 47405-7005, United States; email: watkins@indiana.edu",,,,,,,,10956670,,JBMTF,10.1002/jbt.10035,"English","Journal of Biochemical and Molecular Toxicology",Article,Scopus "Pritz M.B.","Ruptured true posterior communicating artery aneurysm and cystic craniopharyngioma",2002,"Acta Neurochirurgica",144,9,,937,939,,1,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-0036379170&partnerID=40&rel=R8.0.0","Section of Neurological Surgery, Indiana University, School of Medicine, Indianapolis, United States",[No abstract available],,"adult; aneurysm rupture; article; brain angiography; brain artery aneurysm; brain ventricle peritoneum shunt; cancer radiotherapy; case report; controlled study; craniopharyngioma; craniotomy; disease course; female; human; hydrocephalus; priority journal; subarachnoid hemorrhage; surgical technique; treatment outcome; Aneurysm, Ruptured; Brachytherapy; Cerebral Angiography; Combined Modality Therapy; Craniopharyngioma; Female; Follow-Up Studies; Humans; Intracranial Aneurysm; Middle Aged; Neoplasm Recurrence, Local; Pituitary Neoplasms; Postoperative Complications; Radiotherapy, Adjuvant; Subarachnoid Hemorrhage; Tomography, X-Ray Computed; Vasospasm, Intracranial",,,,,"Azzarelli, B., Moore, J., Gilmor, R., Muller, J., Edwards, M., Mealey, J., Multiple fusiform intracranial aneurysms following curative radiation therapy for surpasellar germinoma. Case report (1984) J Neurosurg, 61, pp. 1141-1145; Liu, S.S., Zabramski, J.M., Spetzler, R.F., Fusiform aneurysm after surgery for craniopharyngioma (1991) J Neurosurg, 75, pp. 670-671; Muneda, K., Yoshizu, H., Terada, H., True posterior communicating artery aneurysm (2001) No Shinkei Geka, 29, pp. 163-168; Pia, H.W., Obrador, S., Martin, J.G., Association of brain tumours and arterial intracranial aneurysms (1972) Acta Neurochir (Wien), 27, pp. 189-204; Sutton, L.N., Gusnard, D., Bruce, D.A., Fried, A., Packer, R.J., Zimmerman, R.A., Fusiform dilatations of the carotid artery following radical surgery of childhood craniopharyngiomas (1991) J Neurosurg, 74, pp. 695-700","Pritz, M.B.; Section of Neurological Surgery; Indiana University Sch. of Medicine; 545 Barnhill Drive Indianapolis, IN 46202-5124, United States",,,,,,,,00016268,,ACNUA,10.1007/s00701-002-0943-4,"English","Acta Neurochirurgica",Article,Scopus "Hanna N.H., Einhorn L.H.","Small-cell lung cancer: State of the art",2002,"Clinical Lung Cancer",4,2,,87,94,,6,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-0036749809&partnerID=40&rel=R8.0.0","Department of Medicine, Division of Oncology, Indiana University, 535 Barnhill Drive, Indianapolis, IN 46202, United States","Thirty years ago, there was a pervasive atmosphere of pessimism concerning the management of small-cell lung cancer (SCLC). Surgery or radiation therapy alone resulted in few cures since these techniques utilize a local therapy for a disseminated disease. Chemotherapy remains the backbone of treatment for all patients with SCLC, regardless of stage. For patients with limited-stage disease (LD), the addition of thoracic radiation to chemotherapy is standard. The optimal timing, dose, and schedule of radiation remains undefined. The majority of studies demonstrate equivalent or superior survival for early radiation when compared to delayed radiation. Approximately 50% of patients with LD will achieve a complete remission with chemoradiation and will be candidates for prophylactic cranial irradiation (PCI). While phase III trials have failed to demonstrate a statistically significant survival for PCI, brain relapse is clearly reduced, and a metaanalysis reports a small long-term survival advantage favoring patients receiving PCI. Unfortunately, unlike LD SCLC, advances in extensive-stage disease have been elusive, despite the testing of numerous strategies. Four courses of cisplatin (or carboplatin) plus etoposide remain standard first-line therapy. Promising results have been seen with irinotecan/cisplatin, but confirmatory trials are still needed. A plateau has been reached with chemotherapy regimens, and novel strategies are greatly needed to improve survival for patients with SCLC.","Carboplatin; Chemoradiation; Cisplatin; Etoposide; Irinotecan; Prophylactic cranial irradiation; Topotecan","carboplatin; carmustine; cisplatin; cyclophosphamide; DNA topoisomerase inhibitor; doxorubicin; epirubicin; etoposide; gastrin releasing peptide; gemcitabine; granulocyte macrophage colony stimulating factor; herbimycin A; ifosfamide; imatinib; irinotecan; lomustine; marimastat; matrix metalloproteinase inhibitor; methotrexate; monoclonal antibody; navelbine; paclitaxel; platelet derived growth factor; platinum; protein tyrosine kinase inhibitor; somatomedin; stem cell factor receptor; taxane derivative; topotecan; unindexed drug; vincristine; advanced cancer; brain metastasis; brain radiation; cancer combination chemotherapy; cancer radiotherapy; cancer recurrence; cancer regression; cancer staging; cancer survival; clinical trial; continuous infusion; controlled clinical trial; controlled study; diarrhea; disseminated cancer; dose response; drug effect; drug efficacy; drug megadose; drug response; drug tolerability; hematologic disease; human; long term care; lung small cell cancer; lung surgery; maintenance therapy; meta analysis; neutropenia; radiation dose; review; standard; statistical analysis",,,"gleevec",,"Greenlee, R.T., Hill-Harmon, M., Murray, T., Cancer Statistics 2001 (2001) CA Cancer J. 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This suggests a functional screen for transforming genes is required to identify genetic mutations that are missed by cytogenetic analyses. We utilized a retrovirus-based cDNA expression system to identify transforming genes expressed in cytogenetically normal AML patients. We identified a new member of the Ras guanyl nucleotide-releasing protein (RasGRP) family of Ras guanine nucleotide exchange factors, designating it RasGRP4. Subsequently, cDNA sequences encoding rodent and human RasGRP4 proteins were deposited in GenBank™. RasGRP4 contains the same protein domain structure as other members of the RasGRP family, including a Ras exchange motif, a CDC25 homology domain, a C1/diacyglycerol-binding domain, and putative calcium-binding EF hands. We show that expression of RasGRP4 induces anchorage-independent growth of Rat1 fibroblasts. RasGRP4 is a Ras-specific activator and, interestingly, is highly expressed in peripheral blood leukocytes and myeloid cell lines. Unlike other RasGRP proteins, RasGRP4 is not expressed in the brain or in lymphoid cells. We demonstrated that 32D myeloid cells expressing RasGRP4 have elevated levels of activated Ras compared with control cells, and phorbol 12-myristate 13-acetate (PMA) treatment greatly enhanced Ras activation. PMA induced membrane localization of RasGRP4 and 32D cells expressing RasGRP4 were capable of cytokine-independent proliferation in the presence of PMA. We conclude that RasGRP4 is a member of the RasGRP family of Ras guanine nucleotide exchange factors that may play a role in myeloid cell signaling growth regulation pathways that are responsive to diacylglycerol levels.",,"Brain; DNA sequences; Genes; Mutations; Biochemistry; diacylglycerol; gene product; phorbol 13 acetate 12 myristate; Ras guanyl nucleotide releasing protein 4; Ras protein; unclassified drug; acute granulocytic leukemia; article; brain cell; cancer cell culture; carboxy terminal sequence; cell growth; cell proliferation; cellular distribution; controlled study; cytogenetics; gene activation; gene expression; gene mutation; gene sequence; gene structure; genetic code; growth regulation; human; human cell; nucleotide sequence; oncogene ras; priority journal; protein domain; protein motif; sequence analysis; sequence homology; signal transduction; Amino Acid Sequence; Animals; Base Sequence; Cytokines; Genes, ras; Guanine Nucleotide Exchange Factors; Humans; Leukemia, Myelocytic, Acute; Molecular Sequence Data; ras Guanine Nucleotide Exchange Factors; Rats; Tetradecanoylphorbol Acetate; Rodentia; unidentified retrovirus","GENBANK: AF448437","Cytokines; Guanine Nucleotide Exchange Factors; ras Guanine Nucleotide Exchange Factors; RASGRP4 protein, human; Tetradecanoylphorbol Acetate, 16561-29-8",,,"Miller, K.B., (1995) Hematology: Basic Principles and Practice, pp. 993-1014. , (Hoffman, R., Benz, E. 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Biol., 7, pp. 794-797; Der, C.J., Weissman, B., MacDonald, M.J., (1988) Oncogene, 3, pp. 105-112; Mitelman, F., Johansson, B., Mertens, F., (2002) Mitelman Database of Chromosome Aberrations in Cancer, , cgap.nci.nih.gov/Chromosomes/Mitelman; Bos, J.L., Verlaan-de Vries, V.M., Van der Eb, A.J., Janssen, J.W., Delwel, R., Lowenberg, B., Colly, L.P., (1987) Blood, 69, pp. 1237-1241; Needleman, S.W., Kraus, M.H., Srivastava, S.K., Levine, P.H., Aaronson, S.A., (1986) Blood, 67, pp. 753-757; Gilliland, D.G., (2001) Curr. Opin. Hematol., 8, pp. 189-191; Towatari, M., Iida, H., Tanimoto, M., Iwata, H., Hamaguchi, M., Saito, H., (1997) Leukemia, 11, pp. 479-484","Reuther, G.W.; University of North Carolina; Lineberger Compreh. Cancer Center Chapel Hill, NC 27599-7295, United States; email: greuther@med.unc.edu",,,,,,,,00219258,,JBCHA,10.1074/jbc.M111330200,"English","Journal of Biological Chemistry",Article,Scopus "Hanna N.H., Sandler A.B., Loehrer Sr. P.J., Ansari R., Jung S.H., Lane K., Einhorn L.H.","Maintenance daily oral etoposide versus no further therapy following induction chemotherapy with etoposide plus ifosfamide plus cisplatin in extensive small-cell lung cancer: A Hoosier Oncology Group randomized study",2002,"Annals of Oncology",13,1,,95,102,,19,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-0036230962&partnerID=40&rel=R8.0.0","Department of Medicine, Indiana University Medical Center, Indianapolis, IN, United States; Hoosier Oncology Group, Indianapolis, IN, United States; Walther Cancer Institute, Indianapolis, IN, United States; Michiana Oncology Associates, South Bend, IN, United States; Division of Biostatistics, Indiana University, Indianapolis, IN, United States; 535 Barnhill Drive, Indianapolis, IN 46202, United States","Background: We performed this phase III study to determine whether the addition of 3 months of oral etoposide in non-progressing patients with extensive small-cell lung cancer (SCLC) treated with four cycles of etoposide plus ifosfamide plus cisplatin (VIP) improves progression-free survival (PFS) or overall survival. Patients and methods: Patients with extensive SCLC with a Karnofsky performance score (KPS) ≥50, adequate renal function and bone marrow reserve were eligible. Patients with CNS metastasis were eligible and received concurrent whole-brain radiotherapy. All patients received etoposide 75 mg/m2, ifosfamide 1.2 g/m2 and cisplatin 20 mg/m2 intravenously on days 1-4 every 3 weeks for four cycles. Non-progressing patients were randomized to oral etoposide 50 mg/m2 for 21 consecutive days every 4 weeks for three courses versus no further therapy until progression. Results: From September 1993 to June 1998, 233 patients were entered and treated with VIP with 144 non-progressing patients subsequently randomized to oral etoposide (n = 72) or observation (n = 72). Minimum follow up for all patients is 2 years. Toxicity with oral etoposide was mild. There was an improvement in median PFS favoring the maintenance arm of 8.23 versus 6.5 months (P = 0.0018). There was a trend towards an improvement in median (12.2 versus 11.2 months), 1-year (51.4% versus 40.3%), 2-year (16.7% versus 6.9%) and 3-year (9.1% versus 1.9%) survival (P = 0.0704) favoring the maintenance arm. Conclusions: Three months of oral etoposide in non-progressing patients with extensive SCLC was associated with a significant improvement in PFS and a trend towards improved overall survival.","Lung cancer; Maintenance; Small cell; VIP","cisplatin; etoposide; ifosfamide; mesna; adult; aged; alopecia; article; blood toxicity; bone marrow; cancer growth; cancer survival; cardiotoxicity; clinical trial; controlled clinical trial; controlled study; female; human; kidney function; liver toxicity; lung small cell cancer; lung toxicity; maintenance therapy; major clinical study; male; metastasis; nausea; neurotoxicity; phase 3 clinical trial; priority journal; prognosis; randomized controlled trial; statistical analysis; stomatitis; Administration, Oral; Adult; Aged; Antineoplastic Combined Chemotherapy Protocols; Carcinoma, Small Cell; Cisplatin; Disease Progression; Etoposide; Female; Humans; Ifosfamide; Lung Neoplasms; Male; Middle Aged; Survival Rate; Time Factors",,"Cisplatin, 15663-27-1; Etoposide, 33419-42-0; Ifosfamide, 3778-73-2",,,"Greenlee, R.T., Murray, T., Buldea, S., Cancer Statistics, 2000 (2000) CA Cancer J. 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Oncol, 5, pp. 921-928; Broder, L., Sridhar, K., Selawry, O., A randomized clinical trial in bronchogenic small-cell carcinoma evaluating alternating maintenance therapy of vincristine, adriamycin, procarbazine, and etoposide (VAPE) with cyclophosphamide, CCNU, and CCM maintenance alone in complete responders following VAPE induction and late intensification (1994) Am. J. Clin. Oncol, 17, pp. 527-537; Sculier, J.P., Berghman, T., Castaigne, C., Maintenance chemotherapy for small cell lung cancer: A critical review of the literature (1998) Lung Cancer, 19, pp. 141-151","Hanna, N.H.; Department of Medicine; Indiana University Medical Center; The Hoosier Oncology Group; 535 Barnhill Drive Indianapolis, IN 46202, United States; email: nhanna@iupui.edu",,,,,,,,09237534,,ANONE,10.1093/annonc/mdf014,"English","Annals of Oncology",Article,Scopus "Dropcho E.J.","Remote neurologic manifestations of cancer",2002,"Neurologic Clinics",20,1,,85,122,,22,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-0036157185&partnerID=40&rel=R8.0.0","Department of Neurology, Indiana University Medical Center, Richard Roudebush Veterans Affairs Medical Center, Indianapolis, IN, United States; Department of Neurology, CL 365, Indiana University Medical Center, Indianapolis, IN 46202, United States","In patients with or without a known cancer diagnosis, a number of clinical neurologic syndromes should raise suspicion for a paraneoplastic disorder. For some of these disorders, the presence of specific autoantibodies is a useful diagnostic marker. The actual immunopathogenetic mechanisms for most paraneoplastic syndromes are still unclear. Although many patients affected by paraneoplastic disorders suffer severe and permanent neurologic deficits, a significant number of patients benefits from prompt diagnosis and aggressive treatment.",,"3,4 diaminopyridine; alpha interferon; aminoglycoside antibiotic agent; autoantibody; azathioprine; baclofen; beta adrenergic receptor blocking agent; carbamazepine; chlorambucil; clonazepam; corticosteroid; corticotropin; cryoglobulin; cyclophosphamide; diazepam; fludarabine; immunoglobulin; immunosuppressive agent; melphalan; myelin associated glycoprotein antibody; ofloxacin; phenytoin; prednisone; procainamide; quinidine; quinoline derived antiinfective agent; retinoic acid; tamoxifen; tumor antigen; unclassified drug; unindexed drug; autoimmunity; cancer; carcinoma; cerebellum degeneration; clinical feature; clinical trial; cryoglobulinemia; demyelinating neuropathy; diagnostic procedure; disease association; Eaton Lambert syndrome; encephalomyelitis; human; immunoadsorption; immunosuppressive treatment; immunotherapy; limbic system; lymphoma; motor neuron disease; myeloma; myoclonus; myokymia; myopathy; opsoclonus; paraneoplastic neuropathy; pathogenesis; plasmapheresis; practice guideline; priority journal; retina degeneration; review; sensory neuropathy; side effect; spinal cord disease; stiff man syndrome; Autoantibodies; Brain; Cerebellum; Demyelinating Diseases; Encephalomyelitis; Glycoproteins; Humans; Lambert-Eaton Myasthenic Syndrome; Limbic System; Motor Neuron Disease; Neoplasms; Nerve Degeneration",,"Autoantibodies; Glycoproteins",,,"Ahern, G.L., O'Connor, M., Dalmau, J., Paraneoplastic temporal lobe epilepsy with testicular neoplasm and atypical amnesia (1994) Neurology, 44, pp. 1270-1274; Alamowitch, S., Graus, F., Uchuya, M., Limbic encephalitis and small cell lung cancer: Clinical and immunological features (1997) Brain, 120, pp. 923-928; Albert, M.L., Austin, L.M., Darnell, R.B., Detection and treatment of activated T cells in the cerebrospinal fluid of patients with paraneoplastic cerebellar degeneration (2000) Ann Neurol, 47, pp. 9-17; 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Methods: A total of 1207 patients with advanced non-small-cell lung cancer were randomly assigned to a reference regimen of cisplatin and paclitaxel or to one of three experimental regimens: cisplatin and gemcitabine, cisplatin and docetaxel, or carboplatin and paclitaxel. Results: The response rate for all 1155 eligible patients was 19 percent, with a median survival of 7.9 months (95 percent confidence interval, 7.3 to 8.5), a 1-year survival rate of 33 percent (95 percent confidence interval, 30 to 36 percent), and a 2-year survival rate of 11 percent (95 percent confidence interval, 8 to 12 percent). The response rate and survival did not differ significantly between patients assigned to receive cisplatin and paclitaxel and those assigned to receive any of the three experimental regimens. Treatment with cisplatin and gemcitabine was associated with a significantly longer time to the progression of disease than was treatment with cisplatin and paclitaxel but was more likely to cause grade 3, 4, or 5 renal toxicity (in 9 percent of patients, vs. 3 percent of those treated with cisplatin plus paclitaxel). Patients with a performance status of 2 had a significantly lower rate of survival than did those with a performance status of 0 or 1. Conclusions: None of four chemotherapy regimens offered a significant advantage over the others in the treatment of advanced non-small-cell lung cancer. Copyright © 2002 Massachusetts Medical Society.",,"carboplatin; cisplatin; docetaxel; gemcitabine; paclitaxel; adult; advanced cancer; aged; article; brain metastasis; cancer chemotherapy; cancer staging; cancer survival; clinical trial; confidence interval; controlled clinical trial; controlled study; dose response; drug efficacy; drug safety; female; human; lung small cell cancer; major clinical study; male; nephrotoxicity; priority journal; randomized controlled trial; treatment outcome; Adult; Aged; Aged, 80 and over; Antineoplastic Combined Chemotherapy Protocols; Carcinoma, Non-Small-Cell Lung; Cisplatin; Deoxycytidine; Disease-Free Survival; Female; Humans; Lung Neoplasms; Male; Middle Aged; Paclitaxel; Survival Analysis; Taxoids",,"Cisplatin, 15663-27-1; Deoxycytidine, 951-77-9; docetaxel, 114977-28-5; gemcitabine, 103882-84-4; Paclitaxel, 33069-62-4; Taxoids",,,"Rapp, E., Pater, J.L., Willan, A., Chemotherapy can prolong survival in patients with advanced non-small-cell lung cancer - Report of a Canadian multicenter randomized trial (1988) J Clin Oncol, 6, pp. 633-641; Marino, P., Pampallona, S., Preatoni, A., Cantoni, A., Invernizzi, F., Chemotherapy vs. supportive care in advanced non-small-cell lung cancer: Results of a meta-analysis of the literature (1994) Chest, 106, pp. 861-865; Chemotherapy in non-small cell lung cancer: A meta-analysis using updated data on individual patients from 52 randomised clinical trials (1995) BMJ, 311, pp. 899-909; Grilli, R., Oxman, A.D., Julian, J.A., Chemotherapy for advanced non-small-cell lung cancer: How much benefit is enough? 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Review of biological basis, technique and preliminary clinical experience",2002,"Oncologia",25,4,,19,25+i,,5,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-0036054273&partnerID=40&rel=R8.0.0","Indiana University Sch. of Medicine, Radiation Oncology Department, 525 Barnhill Dr, Indianapolis, IN 46202, United States","Extracranial stereotactic radioablation (ESR) is a new and exiting treatment modality of delivering high dose, hypofractionated irradiation, to extracranial tumors. In the present article we will briefly review the rationale, biological implications of ""extreme"" hypofractionation, treatment technique and published data. In addition data from an ongoing Phase I clinical trial in patients with clinical stage I, medically inoperable, non-small cell lung cancer, conducted at Indiana University will be presented.","Biological basis; Clinical experience; Extracranial; Stereotactic radioablation","brain metastasis; cancer grading; cancer staging; experience; gamma knife radiosurgery; human; lung non small cell cancer; radiation dose fractionation; review; stereotaxis; technique; treatment planning",,,,,"Lax, I., Blomgren, H., Naslund, I., Svanstrom, R., Stereotactic radiotherapy of extracranial targets (1994) Z. Med. Phys., 4, pp. 112-113; Lax, I., Blomgren, H., Naslund, I., Svanstrom, R., Stereotactic radiotherapy of malignancies in the abdomen. Methodological aspects (1994) Acta Oncol., 33, pp. 677-683; Fowler, J., Brief summary of radiobiological principles in fractionated radiotherapy (1992) Sem. Rad. Oncol., 2, p. 1621; Hall, E., Repair of radiation damage and the dose-rate effect Radiobiology for the Radiologist. 4th Edition, pp. 107-131. , J. B. Lippincott Co; Lax, I., Blomgren, H., Larson, D., Naslund, I., Extracranial stereotactic radiosurgery of localized targets (1998) J. Neurosurg., 1, pp. 135-148; Blomgren, H., Lax, I., Naslund, I., Svanstrom, R., Stereotactic high dose fraction radiation therapy of extracranial tomors using a linear accelerator (1995) Acta Oncol., 34, pp. 861-870; Blomgren, H., Lax, I., Goranson, H., Kraepelien, T., Nilsson, B., Naslund, I., Svastrom, R., Tilikidis, A., Radiosurgery of tumors in the body: Clinical experience using a new method (1998) J. Radiosurg., 1, pp. 63-74; Papiez, L., Timmerman, R., DesRosiers, C., Randall, M., Extracranial stereotactic radioablation: Physical principles Int. J. Rad. Oncol. Biol. Phys., , Submitted for publication","Cardenes, H.; Indiana University Sch. of Medicine; Radiation Oncology Department; 525 Barnhill Dr Indianapolis, IN 46202, United States",,,,,,,,03784835,,ONCIE,,"English","Oncologia",Review,Scopus "Husain J., Jarial M.S., Muller J., Kocoshis T.A.","Giant-cell tumor of bone arising from the falx cerebri. A case report",2002,"Journal of Submicroscopic Cytology and Pathology",34,1,,67,76,,2,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-0036366330&partnerID=40&rel=R8.0.0","Department of Pathology, Ball Memorial Hospital, Muncie, IN, United States; Muncie Center for Medical Education, Ball State University, Muncie, IN, United States; Department of Pathology, Indiana University, School of Medicine, Indianapolis, IN, United States; Department of Pathology, Winona Memorial Hospital, 3232 N. Meridian St., Indianapolis, IN 46208, United States","The histological and ultrastructural features of a giant-cell tumor of bone arising in the falx cerebri of a 27 year-old man are described. The tumor was embedded in the medial aspect of the left frontal lobe and was not attached to any of the bones of the skull. At surgery, the tumor was lightly adherent to the falx and was easily extracted. Histologically, the tumor was composed of mononuclear spindle-shaped and ovoid stromal cells, multinuclear giant cells containing 20-30 nuclei, and foci of osteoid and bone production. Hemorrhagic and cystic areas were also present within the tumor. Ultrastructurally, the spindle-shaped cells resembled fibroblasts and were surrounded by small bundles of collagen fibrils. The ovoid cells contained numerous mitochondria, abundant rough endoplasmic reticulum, vesicles, lysosomes, phagosomes and osseous material in the cytoplasm suggesting their monocyte-macrophage lineage. These cells were closely apposed and displayed evidence of fusion in the form of focal and linear subplasmalemmal densities to form multinucleated giant cells with similar organelles and multiple nuclei. It is suggested that the primary giant cell tumor of the bone arose from the metaplastic ossification of the falx. To our knowledge, a giant-cell tumor of bone arising from the falx cerebri has not been previously described.","Falx cerebri; Giant cells; Lysosomes; Mononuclear cells; Phagosomes; Subplasmalemmal densities","collagen fibril; adult; article; bone tumor; brain; brain falx; cancer surgery; case report; cell density; cell fusion; cell lineage; cell nucleus; cell organelle; cell shape; cell ultrastructure; cell vacuole; cytoplasm; fibroblast; frontal lobe; giant cell; giant cell tumor; histology; human; human tissue; lysosome; macrophage; male; mitochondrion; monocyte; mononuclear cell; ossification; osteoid; phagosome; rough endoplasmic reticulum; skull; differential diagnosis; dura mater; heterotopic ossification; meningioma; osteoclastoma; pathology; ultrastructure; Adult; Diagnosis, Differential; Dura Mater; Frontal Lobe; Giant Cell Tumor of Bone; Humans; Male; Meningeal Neoplasms; Ossification, Heterotopic",,,,,"Batnitzky, S., Powers, J.M., Schechter, M.M., Falx 'calcification' - Does this exist? (1974) Neuroradiology, 7 (5), pp. 255-260; Campanacci, M., Baldini, N., Boriani, S., Sudanese, A., Giant-cell tumor of bone (1987) J. Bone Joint Surg. (Am), 69 A, pp. 106-114; Dahlin, D.C., (1967) Bone Tumors. General Aspects and Data on 3,987 Cases, pp. 78-89. , Charles C. Thomas, Springfield; Dahlin, D.C., Cupps, R.E., Johnson, E.W., Giant-cell tumor: A study of 195 cases (1970) Cancer, 25, pp. 1061-1070; Eyden, B., Yamazaki, K., Banerjee, S.S., Giant-cell fibroblastoma: A case report emphasizing the presence of hyperplastic subplasmalemmal linear densities in continuity with granular matrices in the extracellular space (2000) J. Submicrosc. Cytol. Pathol., 32 (4), pp. 509-514; Findlay, J.M., Chiasson, D., Hudson, A.R., Chui, M., Giant-cell tumor of the middle cranial fossa (1987) J. Neurosurg., 66, pp. 924-928; Hutter, R.V.P., Worcester Jr., J.N., Francis, K.C., Foote Jr., F.W., Stewart, F.W., Benign and malignant giant cell tumors of bone: A clinicopathological analysis of the natural history of the disease (1962) Cancer, 15, pp. 653-690; McDonald, D.J., Sim, F.H., McLeod, R.A., Dahlin, D.C., Giant-cell tumor of bone (1986) J. Bone Joint Surg. (Am), 68, pp. 235-242; McGrath, P.J., Giant-cell tumour of bone. An analysis of fifty-two cases (1972) J. Bone Joint Surg. (Br), 54, pp. 216-229; Medeiros, M.D., Beckstead, J.H., Rosenberg, A.E., Wernke, R.A., Wood, G.S., Giant cells and mononuclear cells of giant cell tumor of bone resemble histiocytes (1993) Appl. Immunocytochem., 1 (2), pp. 115-122; Picci, P., Giant cell reparative granuloma and other giant cell lesions of the bones of the hands and feet (1986) Skeletal. Radiol., 15 (6), pp. 415-421; Van Der Rhee, H.J., Van Der Burg-De Winter, C.P.M., Daems, W.Th., The differentiation of monocytes into macrophages, epithelioid cells and multinucleated giant cells in subcutaneous granulomas I. Fine Structure (1979) Cell Tissue Res., 179, pp. 355-378; Rosai, J., (1989) Ackerman's Surgical Pathology, pp. 1494-1499. , C.V. Mosby, St. Louis; Ruge, R.R., Russell, E.J., Levy, R.M., Mineralization of the falx cerebri simulating interhemispheric vascular anomalies on MR imaging (1990) J. Neurosurg., 72, pp. 971-974; Spjut, H.J., Dorfman, H.D., Fechner, R.E., Ackerman, L.V., Tumors of Bone and Cartilage (1971) Atlas of Tumor Pathology, Series 2, 5. , Armed Forces Institute of Pathology, Washington D.C; Steiner, G.C., Ghosh, L., Dorfman, H.D., Ultrastructure of giant cell tumors of bone (1972) Hum. Pathol., 3 (4), pp. 569-586","Husain, J.; Department of Pathology; Winona Memorial Hospital; 3232 N. Meridian St. Indianapolis, IN 46208, United States; email: jugnoo@iquest.net",,,,,,,,11229497,,JSCPE,,"English","Journal of Submicroscopic Cytology and Pathology",Article,Scopus "Dropcho E.J.","Novel chemotherapeutic approaches to brain tumors",2001,"Hematology/Oncology Clinics of North America",15,6,,1027,1052,,8,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-0035209004&partnerID=40&rel=R8.0.0","Department of Neurology, Indiana University Medical Center, Indianapolis Veterans Affairs Medical Center, Indianapolis, IN, United States","In reviewing the numerous investigational drug trials for patients with anaplastic gliomas over the past 20 years, it would be fair to say that there have been more than a few disappointments and that the real impact of many of these therapies on patients' duration and quality of survival has been minor at best. It is also fair to state that there has been progress in developing new types of chemotherapy and other agents, in devising new treatment strategies, and in gaining a deeper understanding of the problems that must be overcome to treat patients with anaplastic gliomas successfully. The past several years have seen the realization that oligodendroglioma, primary CNS lymphoma, and medulloblastoma are sensitive to chemotherapy treatments. It is hoped that future studies will delineate better the optimal use of chemotherapy for these tumors.",,"carboplatin; carmustine; chlormethine; cisplatin; cyclophosphamide; cytarabine; dexamethasone; doxorubicin; etoposide; fluorouracil; hydroxyurea; ifosfamide; mercaptopurine; methotrexate; mitolactol; paclitaxel; prednisone; procarbazine; temozolomide; tioguanine; topotecan; vincristine; astrocytoma; brain tumor; cancer chemotherapy; cancer survival; clinical trial; dose response; drug efficacy; drug indication; glioblastoma; human; medulloblastoma; meningioma; oligodendroglioma; priority journal; quality of life; review; Antineoplastic Agents; Antineoplastic Combined Chemotherapy Protocols; Blood-Brain Barrier; Brain Neoplasms; Glioma; Humans; Infusions, Intra-Arterial; Injections, Intralesional; Lymphoma; Medulloblastoma; Meningioma; Oligodendroglioma",,"Antineoplastic Agents",,,"Abrey, L.E., DeAngelis, L.M., Yahalom, J., Long-term survival in primary CNS lymphoma (1998) J Clin Oncol, 16, pp. 859-863; 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cisplatin; etoposide; ifosfamide; vinblastine; adult; aspiration biopsy; brain metastasis; cancer combination chemotherapy; cancer surgery; case report; clinical feature; computer assisted tomography; germ cell tumor; human; letter; lymph node dissection; male; mediastinum tumor; priority journal; salvage therapy; thorax radiography; treatment failure; treatment outcome; tumor diagnosis; Adult; alpha-Fetoproteins; Antineoplastic Combined Chemotherapy Protocols; Chorionic Gonadotropin, beta Subunit, Human; Germinoma; Gynecomastia; Humans; Male; Mediastinal Neoplasms; Neoplasm Metastasis",,"alpha-Fetoproteins; Chorionic Gonadotropin, beta Subunit, Human",,,"International germ cell consensus classification: A prognostic factor-based staging system for metastatic germ cell cancers (1997) J Clin Oncol, 15, pp. 594-603; Baniel, J., Foster, R., Gonin, R., Late relapse of testicular cancer (1995) J Clin Oncol, 13, pp. 1170-1176; Horwich, A., Sarcoid-like lymphadenopathy in malignant teratoma (1983) Post Grad Med J, 59, pp. 108-110; 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Indiana University Indianapolis, IN, United States",,,,,,,,0732183X,,JCOND,,"English","Journal of Clinical Oncology",Letter,Scopus "Woodburn R.T., Azzarelli B., Montebello J.F., Goss I.E.","Intense p53 staining is a valuable prognostic indicator for poor prognosis in medulloblastoma/central nervous system primitive neuroectodermal tumors",2001,"Journal of Neuro-Oncology",52,1,,57,62,,25,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-0034972938&partnerID=40&rel=R8.0.0","Department of Radiation Oncology, Indiana University Medical Center, Indianapolis, IN, United States; Department of Neuropathology, Indiana University Medical Center, Indianapolis, IN, United States","Intense p53 immunostaining may predict for a poor prognosis in central nervous system primitive neuroectodermal tumor of childhood. Background: Medulloblastoma is a common childhood primary brain tumor. Potential prognostic indicators for patients with local disease are age, extent of resection, and gender. However, none of these are well established. Immunohistologic staining is a potentially useful means to identify high-risk patients. The purpose of this clinical pathologic study was to investigate the prognostic significance of GFAP, synaptophysin, Ki-67, and p53 immunostaining in medulloblastoma/central nervous system primitive neuroectodermal tumors (CNS PNETs). Materials and methods: The records of 40 patients with CNS PNETs were reviewed. Their surgical specimens were immunostained for p53, glial fibrillary acidic protein (GFAP), synaptophysin, and Ki-67. The p53 specimens were scored blindly for the intensity of staining of nuclei (intense vs weak) and the quantity of cells stained. The Ki-67, GFAP, and synaptophysin specimens were analyzed for quantity of cells stained. Results: Ten patients' specimens stained intensely for the p53 protein. Eleven had weakly staining nuclei. Nineteen specimens had no staining. The patients with specimens that stained intensely had a statistically significant decreased disease free survival (P = 0.03). Mere presence or quantity of p53 nuclear staining did not correlate with disease free survival. Immunohistochemical staining for Ki-67, GFAP, and synaptophysin did not correlate with disease free survival. Clinical parameters of age, gender, and extent of resection also did not approach statistical significance for disease free survival. Conclusion: Intense nuclear staining for p53 was the only variable in this clinical pathologic study that reached statistical significance for disease free survival. This suggests that intense staining for p53 may be the most important prognostic indicator for non-metastatic CNS PNETs. p53 Immunostaining with antibodies against p53 in CNS PNETs should be studied in a multi-institutional setting with larger numbers of patients.","Glial fibrillary acidic protein; Immunostaining; Ki-67; Medulloblastoma; p53; Synaptophysin","glial fibrillary acidic protein; Ki 67 antigen; protein antibody; protein p53; synaptophysin; adolescent; adult; article; cancer growth; cancer localization; cancer survival; central nervous system tumor; child; childhood disease; clinical article; correlation function; disease marker; female; high risk patient; human; immunohistochemistry; male; medulloblastoma; neuroectoderm tumor; prediction; prognosis; statistical analysis; Adolescent; Brain Neoplasms; Cerebellar Neoplasms; Child; Child, Preschool; Female; Glial Fibrillary Acidic Protein; Humans; Infant; Ki-67 Antigen; Male; Medulloblastoma; Neuroectodermal Tumors, Primitive; Prognosis; 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Michigan Street, Indianapolis, IN 46202-5132, United States; Lilly Research Laboratories, Eli Lilly and Company, Lilly Corporate Center, Indianapolis, IN 46285, United States; Indiana Molecular Biology Institute, Bloomington, IN, United States; Cancer Center, Indiana University, School of Medicine","With the complete sequence of the human genome expected by winter 2001, genomic-based drug discovery efforts of the pharmaceutical industry are focusing on finding the relatively few therapeutically useful genes from among the total gene set. Methods to rapidly elucidate gene function will have increasing value in these investigations. The use of model organisms in functional genomics has begun to be recognized and exploited and is one example of the emerging use of the tools of developmental biology in recent drug discovery efforts. The use of protein products expressed during embryogenesis and the use of certain pluripotent cell populations (stem cells) as candidate therapeutics are other applications of developmental biology to the treatment of human diseases. These agents may be used to repair damaged or diseased tissues by inducing or directing developmental programs that recapitulate embryonic processes to replace specialized cells. The activation or silencing of embryonic genes in the disease state, particularly those encoding transcription factors, is another avenue of exploitation. 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Michigan Street Indianapolis, IN 46202-5132, United States",,,,,,,,0071786X,,FAZMA,,"English","Progress in Drug Research",Review,Scopus "Sweeney C.J., Williams S.D., Finch D.E., Bihrle R., Foster R.S., Collins M., Fox S., Roth B.J.","A phase II study of paclitaxel and ifosfamide for patients with advanced refractory carcinoma of the urothelium",1999,"Cancer",86,3,,514,518,,35,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-0033178774&partnerID=40&rel=R8.0.0","Division of Hematology/Oncology, Department of Medicine, Indiana University Medical Center, Indianapolis, IN, United States; Department of Urology, Indiana University Medical Center, Indianapolis, IN, United States; Indiana University, Indiana Cancer Pavilion, 535 Barnhill Drive, Indianapolis, IN 46202, United States","BACKGROUND. Cisplatin-based combination chemotherapy for patients with advanced transitional cell carcinoma (TCC) of the urothelium has limitations, and new therapies need to be evaluated. METHODS. Ifosfamide 1.0 gm/m2 on Days 1-4 and paclitaxel 135 mg/m2 by 24-hour infusion on Day 4 were administered to 26 patients with locally unresectable or metastatic TCC. Cycles were repeated every 21 days for a maximum of 6 cycles; dose escalation was dependent on whether Grade 3 or 4 toxicities occurred. RESULTS. There were 24 males and 2 females, with a median age of 66 years and a median Eastern Cooperative Oncology Group performance status of 0. The median number of cycles administered was 3. Twelve patients had Grade 3 or 4 hematologic toxicities, including 1 patient who died of a gastrointestinal hemorrhage while pancytopenic. There were no episodes of neutropenic fever. Two patients each had a complete response (CR) that lasted 5 and 28 months, respectively (response rate: 15%; 95% CI: 2-45%), among the 13 patients who had received prior chemotherapy. Of the 13 patients without prior chemotherapy, there were 3 with complete responses and 1 with a partial response ranging from 8 to 25+ months (RR: 30.7%; 95% CI: 9-61%). CONCLUSIONS. The combination of ifosfamide and paclitaxel is well tolerated and can produce objective responses in patients who are chemonaive or have had prior therapy. For previously untreated patients, the addition of ifosfamide does not appear to result in a better response rate than single agent paclitaxel; and for previously treated patients, the addition of paclitaxel does not appear to result in a better response rate than single agent ifosfamide.","Ifosfamide; Paclitaxel; Phase II study; Urothelial carcinoma","cisplatin; doxorubicin; gallium nitrate; gemcitabine; ifosfamide; mesna; methotrexate; paclitaxel; recombinant granulocyte colony stimulating factor; vinblastine; adult; aged; antineoplastic activity; article; blood toxicity; brain disease; cancer combination chemotherapy; cancer regression; clinical article; clinical trial; controlled clinical trial; controlled study; drug efficacy; drug potentiation; drug tolerability; female; gastrointestinal symptom; human; male; myalgia; nephrotoxicity; phase 2 clinical trial; priority journal; transitional cell carcinoma; treatment outcome; Adult; Aged; Antineoplastic Combined Chemotherapy Protocols; Carcinoma, Transitional Cell; Drug Administration Schedule; Drug Evaluation; Female; Humans; Ifosfamide; Male; Middle Aged; Paclitaxel; Survival Analysis; Urologic Neoplasms; Urothelium",,"Ifosfamide, 3778-73-2; Paclitaxel, 33069-62-4",,,"Yagoda, A., Chemotherapy for advanced urothelial cancer (1983) Semin Urol, 1, pp. 60-74; Loehrer P.J., Sr., Einhorn, L.H., Elson, P.J., Crawford, E.D., Kuebler, P., Tannock, I., A randomized comparison of cisplatin alone or in combination with methotrexate, vinblastine, and doxorubicin in patients with metastatic urothelial carcinoma: A cooperative group study (1992) J Clin Oncol, 10, pp. 1066-1073. , published erratum appears in J Clin Oncol 1993;11:384; Logothetis, C.J., Dexeus, F.H., Finn, L., Sella, A., Amato, R.J., Ayala, A.G., A prospective randomized trial comparing MVAC and CISCA chemotherapy for patients with metastatic urothelial tumors (1990) J Clin Oncol, 8, pp. 1050-1055; Saxman, S.B., Propert, K.J., Einhorn, L.H., Crawford, E.D., Tannock, I., Raghavan, D., Long-term follow-up of a phase III intergroup study of cisplatin alone or in combination with methotrexate, vinblastine, and doxorubicin in patients with metastatic urothelial carcinoma: A cooperative group study (1997) J Clin Oncol, 15, pp. 2564-2569; Loehrer P.J., Sr., Elson, P., Dreicer, R., Hahn, R., Nichols, C.R., Williams, R., Escalated dosages of methotrexate, vinblastine, doxorubicin, and cisplatin plus recombinant human granulocyte colony-stimulating factor in advanced urothelial carcinoma: An Eastern Cooperative Oncology Group trial (1994) J Clin Oncol, 12, pp. 483-488; Seidman, A.D., Scher, H.I., Gabrilove, J.L., Bajorin, D.F., Motzer, R.J., O'Dell, M., Dose-intensification of MVAC with recombinant granulocyte colony-stimulating factor as initial therapy in advanced urothelial cancer (1993) J Clin Oncol, 11, pp. 408-414; Gabrilove, J.L., Jakubowski, A., Scher, H., Sternberg, C., Wong, G., Grous, J., Effect of granulocyte colony-stimulating factor on neutropenia and associated morbidity due to chemotherapy for transitional-cell carcinoma of the urothelium (1988) N Engl J Med, 318, pp. 1414-1422; Small, E.J., Fippin, L.J., Ernest, M.L., Carroll, P.R., A carboplatin-based regimen for the treatment of patients with advanced transitional cell carcinoma of the urothelium (1996) Cancer, 78, pp. 1775-1780; Roth, B.J., Dreicer, R., Einhorn, L.H., Neuberg, D., Johnson, D.H., Smith, J.L., Significant activity of paclitaxel in advanced transitional-cell carcinoma of the urothelium: A phase II trial of the Eastern Cooperative Oncology Group (1994) J Clin Oncol, 12, pp. 2264-2270; Moore, M.J., Tannock, I.F., Ernst, D.S., Huan, S., Murray, N., Gemcitabine: A promising new agent in the treatment of advanced urothelial cancer (1997) J Clin Oncol, 15, pp. 3441-3445; Seligman, P.A., Crawford, E.D., Treatment of advanced transitional cell carcinoma of the bladder with continuous-infusion gallium nitrate (1991) J Natl Cancer Inst, 83, pp. 1582-1584; Witte, R.S., Elson, P., Bono, B., Knop, R., Richardson, R.R., Dreicer, R., Eastern Cooperative Oncology Group phase II trial of ifosfamide in the treatment of previously treated advanced urothelial carcinoma (1997) J Clin Oncol, 15, pp. 589-593; Dieicer, R., Gustin, D.M., See, W.A., Williams, R.D., Paclitaxel in advanced urothelial carcinoma: Its role in patients with renal insufficiency and as salvage therapy (1996) J Urol, 156, pp. 1606-1608; Zielinski, C.C., Schnack, B., Grbovic, M., Brodowicz, T., Wiltschke, C., Steger, G., Paclitaxel and carboplatin in patients with metastatic urothelial cancer: Results of a phase II trial (1998) Br J Cancer, 78, pp. 370-374; Redman, B.G., Smith, D.C., Flaherty, L., Du, W., Hussain, M., Phase II trial of paclitaxel and carboplatin in the treatment of advanced urothelial carcinoma (1998) J Clin Oncol, 16, pp. 1844-1848; Vaughn, D.J., Malkowicz, S.B., Zoltick, B., Mick, R., Ramchandani, P., Holroyde, C., Paclitaxel plus carboplatin in advanced carcinoma of the urothelium: An active and tolerable outpatient regimen (1998) J Clin Oncol, 16, pp. 255-260; Schnack, B., Grbovic, M., Brodowicz, T., Wiltischke, C., Zielinski, C.C., High effectivity of a combination of taxol with carboplatin in the treatment of metastatic urothelial cancer (1997) Proc Am Assoc Clin Oncol, 16, p. 325; Burch, P.A., Richardson, R.L., Cha, S.S., Camoriano, J.K., Combination paclitaxel and cisplatin is active in advanced urothelial carcinoma (1997) Proc Am Assoc Clin Oncol, 16, p. 329; Dreicer, R., Roth, B., Lipsitz, S., Cohen, M., See, W., Wilding, G., E2895 cisplatin and paclitaxel in advanced carcinoma of the urothelium: A phase II trial of the Eastern Cooperative Oncology Group (1998) Proc Am Assoc Soc Clin Oncol, 17, p. 320; Einhorn, L.H., Roth, B.J., Ansari, R., Dreicer, R., Gonin, R., Loehrer, P.J., Phase II trial of vinblastine, ifosfamide, and gallium combination chemotherapy in metastatic urothelial carcinoma (1994) J Clin Oncol, 12, pp. 2271-2276; Dreicer, R., Propert, K.J., Roth, B.J., Einhorn, L.H., Loehrer, P.J., Vinblastine, ifosfamide, and gallium nitrate - An active new regimen in patients with advanced carcinoma of the urothelium. A phase II trial of the Eastern Cooperative Oncology Group (E5892) (1997) Cancer, 79, pp. 110-114; Bajorin, D.F., McCaffrey, J.A., Hilton, S., Mazumdar, M., Kelly, W.K., Scher, H.I., Treatment of patients with transitional cell carcinoma of the urothelial tract with ifosfamide, paclitaxel, and cisplatin: A phase II trial (1998) J Clin Oncol, 16, pp. 2722-2727; Forastiere, A.A., Urba, S.G., Single-agent paclitaxel and paclitaxel plus ifosfamide in the treatment of head and neck cancer (1995) Semin Oncol, 22 (3 SUPPL. 6), pp. 24-27","Roth, B.J.; Indiana University; Indiana Cancer Pavilion; 535 Barnhill Drive Indianapolis, IN 46202, United States",,,,,,,,0008543X,,CANCA,10.1002/(SICI)1097-0142(19990801)86:3<514::AID-CNCR21>3.0.CO;2-9,"English","Cancer",Article,Scopus "Bell B.B., Tognoni P.G., Bihrle R.","Limbic encephalitis as a paraneoplastic manifestation of renal cell carcinoma",1998,"Journal of Urology",160,3 I,,828,,,6,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-0032323399&partnerID=40&rel=R8.0.0","Indiana University Cancer Pavillion, Indianapolis, IN, United States",[No abstract available],"Carcinoma; Encephalitis; Paraneoplastic syndromes; Renal cell","adult; article; autopsy; brain disease; cancer survival; cancer therapy; case report; computer assisted tomography; disease association; electroencephalogram; encephalitis; female; human; kidney carcinoma; nuclear magnetic resonance imaging; paraneoplastic syndrome; priority journal; prognosis; Carcinoma, Renal Cell; Encephalitis; Female; Humans; Kidney Neoplasms; Limbic System; Middle Aged; Paraneoplastic Syndromes",,,,,,"Bell, B.B.; Indiana University Cancer Pavillion Indianapolis, IN, United States",,,,,,,,00225347,,JOURA,10.1016/S0022-5347(01)62798-8,"English","Journal of Urology",Article,Scopus "Opitz J.M., Weaver D.W., Reynolds Jr. J.F.","The syndromes of Sotos and Weaver: Reports and review",1998,"American Journal of Medical Genetics",79,4,,294,304,,56,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-0032475886&partnerID=40&rel=R8.0.0","Departments of Pediatrics, Human Genetics and Obstetrics and Gynecology, University of Utah, Salt Lake City, UT, United States; Department of Medical and Molecular Genetics, Indiana University, School of Medicine, Indianapolis, IN, United States; Shodair Hospital, Helena, MT, United States; Primary Children's Medical Center, 100 No. Medical Drive, Salt Lake City, UT 84113, United States","The syndromes of Sotos and Weaver are paradigmatic of the daily nosologic difficulties faced by clinical geneticists attempting to diagnose and counsel, and to give accurate prognoses in cases of extensive phenotypic overlap between molecularly undefined entities. Vertebrate development is constrained into only very few final or common developmental paths; therefore, no developmental anomaly seen in humans is unique to ('pathognomonic' of) one syndrome. Thus, it is not surprising that prenatal overgrowth occurs in several syndromes, including the Sotos and Weaver syndromes. Are they sufficiently different in other respects to allow the postulation of locus (rather than allele) heterogeneity? Phenotypic data in both conditions are biased because of ascertainment of propositi, and the apparent differences between them may be entirely artificial as they were between the G and BBB syndromes. On the other hand, the Sotos syndrome may be a cancer syndrome, the Weaver syndrome not (though a neuroblastoma was reported in the latter); in the former there is also remarkably advanced dental maturation rarely commented on in the latter. In Weaver syndrome there are more conspicuous contractures and a facial appearance that experts find convincingly different from that of Sotos individuals. Nevertheless, the hypothesis of locus heterogeneity is testable; at the moment we are inclined to favor the hypothesis of allele heterogeneity. An international effort is required to map, isolate, and sequence the causal gene or genes.","Autosomal dominant inheritance; Heterogeneity; Nosology; Sotos syndrome; Weaver syndrome","autosomal dominant inheritance; case report; child; conference paper; disease classification; genetic counseling; genetic disorder; human; multiple malformation syndrome; phenotype; priority journal; sotos syndrome; syndrome delineation; weaver syndrome; Brain; Female; Fetal Macrosomia; Genes, Dominant; Genetic Counseling; Growth Disorders; Humans; Infant; Male; Syndrome; Vertebrata",,,,,"Allanson, J.E., Cole, T.R.P., Sotos syndrome: Evolution of facial phenotype. Subjective and objective assessment (1996) Am J Med Genet, 65, pp. 13-20; Amir, N., Gross-Kieselstein, E., Hirsch, H., Lax, E., Silverberg-Shale, V.R., Weaver-Smith syndrome: A case study with long-term follow-up (1984) AJDC, 138, pp. 1113-1117; Ardinger, H.H., Hanson, J.W., Harrod, M.J.E., Cohen Jr., M.M., Tibbles, J.A.R., Welch, J.P., Young-Wee, T., Hoyme, H.E., Further delineation of Weaver syndrome (1986) J Pediatr, 108, pp. 228-235; Bale, A.E., Drum, M.A., Parry, D.M., Mulvihill, J.J., Familial Sotos syndrome (cerebral gigantism): Craniofacial and psychological characteristics (1985) Am J Med Genet, 20, pp. 613-624; Bayley-Wilson, J.E., Shapira, E., Blitzer, M.G., Braverman, N., An unusual case of early overgrowth and congenital anomalies - The Weaver syndrome (1983) Am J Hum Genet, 35, pp. 75A. , abstract 222; Beemer, F.A., Veenema, H., De Pater, J.M., Cerebral gigantism (Sotos syndrome) in two patients with fragile (X) syndrome (1986) Am J Med Genet, 23, pp. 221-226; Beighton, P., (1988) ""Inherited Disorders of the Skeleton."" 2nd Ed., , London: Churchill Livingstone; Bejar, R.L., Smith, G.F., Park, S.M., Spellacy, W.N., Wolfson, S.L., Nyhan, W.L., Cerebral gigantism: Concentrations of amino acids in plasma and muscle (1970) J Pediatr, 76, pp. 105-111; Boman, H., Nilsson, D., Sotos syndrome in two brothers (1980) Clin Genet, 18, pp. 421-427; Bosch-Banyeras, J.M., Salcedo, S., Lucaya, J., Laverde, R., Boronat, M., Marti-Henneberg, C., Accélération du developpement postnatal (1978) Arch Fr Pédiatr, 35, pp. 177-183; Butler, M.G., Meany, F.J., Kittur, S., Hersh, J.H., Hornstein, L., Metacarpophalangeal pattern profile analysis in Sotos syndrome (1985) Am J Med Genet, 20, pp. 625-629; Cohen Jr., M.M., A comprehensive and critical assessment of overgrowth and overgrowth syndromes (1989) Adv Hum Genet, 18, pp. 181-303; Cole, T.R.P., Hughes, H.E., Syndrome of the Month: Sotos syndrome (1990) J Med Genet, 27, pp. 571-576; Cole, T.R.P., Hughes, H.E., Sotos syndrome: A study of the diagnostic criteria and natural history (1994) J Med Genet, 31, pp. 20-32; Cole, T.R.P., Dennis, N.R., Hughes, H.E., Weaver syndrome (1992) J Med Genet, 29, pp. 332-337; Cole, T.R.P., Hughes, H.E., Jeffreys, M.J., Williams, G.T., Arnold, M.M., Small cell lung carcinoma in a patient with Sotos syndrome: Are genes at 3p21 involved in both conditions? (1992) J Med Genet, 29, pp. 338-341; Dawood, A.A., Machado, G.T., Winship, W.S., Weaver's syndrome - Primordial excessive growth velocity: A case report (1985) S Afr Med J, 67, pp. 646-648; DiLiberti, J.H., Inherited macrocephaly-hamartoma syndromes (1998) Am J Med Genet, 79, pp. 284-290; Dodge, P.R., Holmes, S.J., Sotos, J.F., Cerebral gigantism (1983) Dev Med Child Neurol, 25, pp. 248-252; Dumić, M., Vuković, J., Cvitković, M., Medica, I., Twins and their mildly affected mother with Weaver syndrome (1993) Clin Genet, 44, pp. 338-340; Dumić, M., Vukelić, D., Plavšić, V., Cviko, A., Sokolić, L., Filipović-Grčić, Nevo syndrome (1998) Am J Med Genet, 76, pp. 67-70; Farrell, S.A., Hughes, H.E., Brief clinical report: Weaver syndrome with pes cavus (1985) Am J Med Genet, 21, pp. 737-739; Fitch, N., Update on the Marshall-Smith-Weaver controversy (1985) Am J Med Genet, 20, pp. 559-562; Fretzayas, A., Papanicolaou, A., Tzanetakos, K., Theodoridis, C., Karpathios, T., Retarded skeletal maturation in Weaver syndrome (1988) Acta Paediatr Scand, 77, pp. 930-932; Fryer, A., Smith, C., Rosenbloom, L., Cole, T., Autosomal dominant inheritance of the Weaver syndrome (1997) J Med Genet, 34, pp. 418-419; Gemme, G., Bonioli, E., Ruffa, G., Lagorio, V., The Weaver-Smith syndrome (1980) J Pediatr, 97, pp. 962-964; Gorlin, R.J., Cohen Jr., M.M., Levin, L.S., (1990) ""Syndromes of the Head and Neck."" 3rd Ed., pp. 332-336. , New York: Oxford University Press; Greenberg, F., Wasiewski, W., McCabe, E.R.B., Brief clinical report: Weaver syndrome: The changing phenotype in an adult (1989) Am J Med Genet, 33, pp. 127-129; Halal, F., Male to male transmission of cerebral gigantism (1982) Am J Med Genet, 12, pp. 411-419; Halal, F., Letter to the editor: Cerebral gigantism, intestinal polyposis, and pigmentary spotting of the genitalia (1983) Am J Med Genet, 15, p. 161; Hall, B.D., Weaver syndrome: Expanded natural history (1985) Prog Clin Biol Res, 200, pp. 123-144; Hansen, F.J., Friis, B., Familial occurrence of cerebral gigantism, Sotos' syndrome (1976) Acta Paediatr Scand, 65, pp. 387-389; Hooft, C., Schotte, H., Van Hooren, G., Gigantisme cérébral familial (1968) Acta Paediatr Belg, 22, pp. 173-186; Hook, E.B., Reynolds, J.W., Cerebral gigantism: Endocrinological and clinical observations of six patients including a congenital giant, concordant monozygotic twins, and a child who achieved adult gigantic size (1967) J Pediatr, 70, pp. 900-914; Hoyme, H.E., West, B.R., Welsh, G.W., The Weaver syndrome: Natural history through adulthood (1984) Proc Greenwood Genet Ctr, 3, p. 86; Jalaguier, J., Montoya, F., Germain, M., Bonnet, H., Advance de la maturation osseuse et syndrome dysmorphique chez deux germains (syndrome de Marshall-Weaver) (1983) J Genet Hum, 31, pp. 385-395; Kajii, T., Tsukahara, M., The Golabi-Rosen syndrome (1984) Am J Med Genet, 19, p. 819. , Letter to the editor; Kaneko, H., Tsukahara, M., Tachibana, H., Kurashige, H., Kuwano, A., Kajii, T., Congenital heart defects in Sotos sequence (1987) Am J Med Genet, 26, pp. 569-576; Kelly, T., Stelling, M., Wilson, T., Weaver-like syndrome with hyperprogesteronemia and maternal luteoma (1983) Proc Greenwood Genet Ctr, 2, pp. 128-129; Kondo, I., Mori, Y., Kuwajima, K., A Japanese male infant with the Weaver syndrome (1990) J Hum Genet, 35, pp. 257-262; Kondo, I., Mori, Y., Kuwajima, K., Weaver syndrome in two Japanese children (1991) Am J Med Genet, 41, pp. 221-224; Majewski, F., Ranke, M., Kemperdick, H., Schmidt, E., The Weaver syndrome: A rare type of primordial overgrowth (1981) Eur J Pediatr, 137, pp. 277-282; Maroun, C., Schmerler, S., Hutcheon, R.G., Child with Sotos phenotype and a 5:15 translocation (1994) Am J Med Genet, 50, pp. 291-293; Marsh, D.J., Dahia, P.L.M., Zheng, Z., Liaw, D., Parsons, R., Gorlin, R.J., Eng, C., Germline mutations in PTEN are present in Bannayan-Zonana syndrome (1997) Nat Genet, 16, pp. 333-334; McKusick, V.A., (1997) Cerebral Gigantism: OMIM 117550, , http://www3.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim; McKusick, V.A., (1996) Weaver Syndrome: OMIM277590, , http://www3.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim; Meinecke, P., Schaefer, E., Engelbrecht, R., The Weaver syndrome in a girl (1983) Eur J Pediatr, 141, pp. 58-59; Moreno, H.C., Zachai, E.H., Kaufman, H.G., Mellman, W.J., Case report 18 (1974) Syndrome Identification, 2, pp. 22-25; Muhonen, M.G., Menezes, A.H., Weaver syndrome and instability of the upper cervical spine (1990) J Pediatr, 116, pp. 596-599; Nance, M.A., Neglia, J.P., Talwar, D., Berry, S.A., Neuroblastoma in a patient with Sotos' syndrome (1990) J Med Genet, 27, pp. 130-132; Nevo, S., Zeltzer, M., Benderly, A., Levy, J., Evidence for autosomal recessive inheritance in cerebral gigantism (1974) J Med Genet, 11, pp. 158-165; Nishimura, G., Hasegawa, T., Nagai, T., Propositus with Weaver syndrome and his mildly-affected mother: Implication of nontraditional inheritance (1996) Am J Med Genet, 65, pp. 249-251; Proud, V.K., Braddock, S.R., Cook, L., Weaver, D.D., Weaver syndrome: Autosomal dominant inheritance of the disorder (1998) Am J Med Genet, 79, pp. 305-310; Ramos-Arroyo, M.A., Weaver, D.D., Banks, E.R., Weaver syndrome: A case without early overgrowth and review of the literature (1991) Pediatrics, 88, pp. 1106-1111; Rojas-Martínez, A., Sánchez-Corona, J., García-Cruz, M.O., Gonzáles-Martínez, A., Nazará, Z., García-Cruz, D., A sporadic case of Weaver syndrome in a female (1991) Dysmorphol Clin Genet, 5, pp. 23-26; Roussounis, S., Crawford, M., Siblings with the Weaver syndrome (1983) J Pediatr, 10, pp. 595-597; Ruvalcaba, R.H.A., Myhre, S., Smith, D.W., Sotos syndrome with intestinal polyposis and pigmentary spotting of the genitalia (1980) Clin Genet, 18, pp. 413-416; Scarano, G., Della Monica, M., Leonardo, F., Neri, G., Novel findings in a patient with Weaver or a Weaver-like syndrome (1996) Am J Med Genet, 63, pp. 378-381; Schlesinger, B., Gigantism (acromegalic in type) (1931) Proc R Soc Med, 24, p. 1352; Schrander-Stumpel, C.T., Fryns, J.P., Hamers, G.G., Sotos syndrome and de novo balanced autosomal translocation [t(3;6)(p21;p21)] (1990) Clin Genet, 37, pp. 226-229; Smith, A., Farrar, J.R., Silink, M., Judzewitsch, R., Investigations in dominant Sotos syndrome (1981) Ann Genet, 24, pp. 226-228; Smith, M., Fullwood, P., Qi, Y., Palmer, S., Upadhyaya, M., Cole, T., No evidence for uniparental disomy as a common cause of Sotos syndrome (1997) J Med Genet, 34, pp. 10-12; Sotos, J.F., Dodge, P.R., Muirhead, D., Crawford, J.D., Talbot, N.B., Cerebral gigantism in childhood: A syndrome of excessively rapid growth with acromelic features and a non-progressive neurologic disorder (1964) N Engl J Med, 271, pp. 109-116; Stephenson, J.N., Mellinger, R.C., Manson, G., Cerebral gigantism (1968) Pediatrics, 41, pp. 130-138; Stoll, C., Talon, P., Mengus, L., Roth, M.P., Dott, B., A Weaver-like syndrome with endocrinological abnormalities in a boy and his mother (1985) Clin Genet, 28, pp. 255-259; Teebi, A.S., Sundaresham, T.S., Hammouri, M.Y., Al-Awadi, S.A., Al-Saleh, Q.A., A new autosomal recessive disorder resembling Weaver syndrome (1989) Am J Med Genet, 33, pp. 479-482; Thompson, E.M., Hill, S., Leonard, J.V., Pembrey, M.E., A girl with the Weaver syndrome (1987) J Med Genet, 24, pp. 232-234; Trabelsi, M., Ben Hariz, M.B., Monastiri, K., Taktak, M., Bennaceur, B., Le syndrome de Weaver: A propos d'un nouveau cas (1990) Ann Pédiatr, 37, pp. 327-330. , Paris; Tsukahara, M., Tanaka, S., Kajii, T., A Weaver-like syndrome in a Japanese boy (1984) Clin Genet, 25, pp. 73-78; Turner, D.R., Downing, J.W., Anesthetic problems associated with Weaver's syndrome (1985) Br J Anaesth, 57, pp. 1260-1263; Wajntal, A., Koiffman, C.P., Chromosome aberrations in Sotos syndrome (1991) Clin Genet, 40, p. 472; Weaver, D.D., Graham, C.B., Thomas, I.T., Smith, D.W., A new overgrowth syndrome with accelerated skeletal maturation, unusual facies, and camptodactyly (1974) J Pediatr, 84, pp. 547-552; Weisswichert, P.H., Knapp, G., Willich, E., Accelerated bone maturation syndrome of the Weaver type (1981) Eur J Pediatr, 137, pp. 329-333; Wilkins, L., (1965) ""The Diagnosis and Treatment of Endocrine Disorders in Childhood and Adolescence."" 3rd Ed., p. 181. , Springfield, IL: C.C. Thomas; Winship, I.M., Sotos syndrome - Autosomal dominant inheritance substantiated (1985) Clin Genet, 28, pp. 243-246; Zonana, J., Rimoin, D.L., Fisher, D.A., Cerebral gigantism - Apparent dominant inheritance (1976) Birth Defects, 12 (6), pp. 63-69; Zonana, J., Sotos, J.F., Romshe, C.A., Fischer, D.A., Elders, M.J., Rimoin, D.L., Dominant inheritance of cerebral gigantism (1977) J Pediatr, 91, pp. 251-256","Opitz, J.M.; Primary Children's Medical Center; 100 No. Medical Drive Salt Lake City, UT 84113, United States; email: AJMG@hsc.utah.edu",,,,,,,,01487299,,AJMGD,10.1002/(SICI)1096-8628(19981002)79:4<294::AID-AJMG12>3.0.CO;2-M,"English","American Journal of Medical Genetics",Conference Paper,Scopus "Yang H., Shen F., Herenyiova M., Weber G.","Phospholipase C (EC 3.1.4.11): A malignancy linked signal transduction enzyme",1998,"Anticancer Research",18,3 A,,1399,1404,,12,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-0031876257&partnerID=40&rel=R8.0.0","Laboratory for Experimental Oncology, Indiana University, School of Medicine, Indianapolis, IN 46202-5119, United States; Laboratory for Experimental Oncology, Indiana University, School of Medicine, 699 West Drive, Indianapolis, IN 46202-5119, United States","Aim: To elucidate the relationship between phospholipase C, phosphatidylinositol-4,5-bisphosphate (PIP2) phosphodiesterase, EC 3.1.4.11 (PLC) and transformation, progression and proliferation, steady-state activity was determined in a spectrum of transplantable solid rat hepatomas of different growth rates, and in a variety of normal rat organs. Methods. To measure PLC activity in the plasma membrane fraction a standard isotopic method was developed using exogenous PIP2 as substrate. PLC activity was linear with time for 2.5 min and proportional with protein concentrations over a range of 5 to 29 μg per 50 μl reaction mixture. Results. The apparent K(m) for PIP2 was 0.3 mM in both normal liver and rapidly growing hepatoma 3924A. PLC activity in adult rat liver was 747 and 986 nmol/h/mg protein; it increased 1.7- to 2.1-fold in hepatomas of slow an intermediate growth rates and 3.7-fold in rapidly growing hepatoma 3924A. By contrast, no significant difference was observed between 24 hours regenerating and sham-operated livers. PLC activity was high in thymus, spleen, testis, bone marrow, lung, brain, heart and renal cortex, but in the same range in skeletal muscle and liver. PLC has a relatively long half-life as there were no significant changes in PLC specific activity in bone marrow during the 9 hour period after intraperitoneal injection of the protein biosynthetic inhibitor, cycloheximide. PLC was subject to nutritional regulation because at 3 days' starvation the specific activity in rat bone marrow decreased to 78% of control values and recovered after 1-day refeeding. Conclusion: The results indicate that PLC is a transformation- and progression-linked signal transduction enzyme. This work and recent studies showing increased 1-phosphatidylinositol 4-kinase (EC 2.7.1.67) and 1-phosphatidylinositol 4-phosphate-5-kinase (EC 2.7.1.68) provide evidence of a gain in function for a markedly elevated capacity of signal transduction sequence in transplantable rat hepatomas of different growth rates. Inhibition of the activities of kinases and PLC may provide sensitive targets for selective cancer therapy by down-regulating the up-regulated signal transduction cascade.","Enzyme half-life; Hepatomas; Phospholipase C; Regenerating liver","cycloheximide; phosphatidylinositol 4 phosphate kinase; phosphatidylinositol 4,5 bisphosphate; phosphatidylinositol kinase; phosphodiesterase; phospholipase c; protein synthesis inhibitor; animal experiment; animal tissue; article; bone marrow; brain; cancer chemotherapy; cancer growth; cancer transplantation; cell membrane; cell proliferation; cell transformation; controlled study; enzyme activity; enzyme kinetics; enzyme localization; enzyme substrate; half life time; heart; kidney cortex; liver cell carcinoma; liver regeneration; lung; male; nonhuman; priority journal; rat; signal transduction; skeletal muscle; spleen; starvation; testis; thymus; Animals; Bone Marrow; Cell Division; Cycloheximide; Liver; Liver Neoplasms, Experimental; Liver Regeneration; Male; Organ Specificity; Phosphatidylinositol Diacylglycerol-Lyase; Phospholipase C; Phosphoric Diester Hydrolases; Phosphotransferases (Alcohol Group Acceptor); Rats; Rats, Inbred ACI; Rats, Inbred BUF; Rats, Wistar; Signal Transduction",,"1-phosphatidylinositol-4,5-bisphosphate phosphodiesterase, EC 3.1.4.11; 1-phosphatidylinositol-4-phosphate 5-kinase, EC 2.7.1.68; Cycloheximide, 66-81-9; Phosphatidylinositol Diacylglycerol-Lyase, EC 4.6.1.13; Phospholipase C, EC 3.1.4.3; Phosphoric Diester Hydrolases, EC 3.1.4.-; Phosphotransferases (Alcohol Group Acceptor), EC 2.7.1.-",,,"Weber, G., Biochemical strategy of cancer cells and the design of chemotherapy: GHA Clowes Memorial Lecture (1983) Cancer Res, 43, pp. 3466-3492; Tricot, G., Jayaram, H.N., Weber, G., Huffman, R., Tiazofurin: Biological effects and clinical uses (1990) Intl J Cell Cloning, 8, pp. 161-170; Tricot, G., Weber, G., Biochemically targeted therapy of refractory leukemia and myeloid blast crisis of chronic granulocytic leukemia with tiazofurin. A selective blocker of inosine 5'-phosphate dehydrogenase activity (1996) Anticancer Res, 16, pp. 3341-3348; Berridge, M.J., Inositol trisphosphate and calcium signaling (1993) Nature, 361, pp. 315-325; Rana, R.S., Hokin, L.E., Role of phosphoinositides in transmembrane signaling (1990) Physiol Rev, 70, pp. 115-164; Manzoli, L., Billi, A.M., Gilmour, R.S., Martelli, A.M., Matteucci, A., Rubbini, S., Weber, G., Cocco, L., Phosphoinositide signaling in nuclei of Friend cells: Tiazofurin down-regulates phospholipase C β1 (1995) Cancer Res, 55, pp. 2978-2980; Rizzo, M.T., Weber, G., 1-Phosphatidylinositol 4-kinase: An enzyme linked with proliferation and malignancy (1994) Cancer Res, 54, pp. 2611-2614; S Singhal, R.L., Prajda, N., Yeh, Y.A., Weber, G., 1-Phosphatidylinositol 4-phosphate 5-kinase (EC 2.7.1.68): A proliferation- and malignancy-linked signal transduction enzyme (1994) Cancer Res., 54, pp. 5574-5578; Olah, E., Weber, G., Giemsa-banding karyotype of rat hepatomas of different growth rates (1979) Cancer Res, 39, pp. 1708-1717; Higgins, G.M., Anderson, R.M., Experimental pathology of the liver. I. Restoration of the liver of the white rat following partial surgical removal (1931) Arch Path, 12, pp. 186-202; Prajda, N., Natsumeda, Y., Ikegami, T., Reardon, M.A., Szondy, S., Hashimoto, Y., Emrani, J., Weber, G., Enzymic programs of rat bone marrow and the impact of acivicin and tiazofurin (1988) Biochem Pharm, 37, pp. 875-880; Bradford, M.M., A rapid and sensitive method for the quantification of microgram quantities of protein utilizing the principle of protein-dye binding (1976) Analytical Biochem, 72, pp. 248-254; Rhee, S.G., Suh, P.G., Ryu, S.H., Lee, S.Y., Studies of inositol phospholipid-specific phospholipase C (1989) Sci, 244, pp. 546-550; Cockcroft, S., Thomas, G.M.H., Inositol-lipid-specific phospholipase C isozymes and their differential regulation by receptors (1992) Biochem J, 288, pp. 1-14; Melin, P.M., Sundler, R., Jergil, B., Phospholipase C in rat liver membranes. Phosphoinositide specificity and regulation by guanine nucleotides and calcium (1986) FEBS Letters, 198, pp. 85-88; Taylor, S.J., Exton, J.H., Guanine-nucleotide and hormone regulation of polyphosphoinositide phospholipase C activity of rat liver plasma membranes. Bivalent cation and phospholipid requirements (1987) Biochem J, 248, pp. 791-799; Rhee, S.G., Kim, H., Suh, P.-G., Choi, W.C., Multiple forms of phosphoinositide-specific phospbolipase C and different modes of activation (1991) Intracellular Phospholipases, 19, pp. 337-341; Bresnick, E., Williams, S.S., Mosse, H., Rates of turnover of deoxythymidine kinase and its template RNA in regenerating and control liver (1967) Cancer Res, 27, pp. 469-475; Weber, G., Prajda, N., Yang, H., Yeh, Y.A., Shen, F., Singhal, R.L., Herenyiova, M., Look, K.Y., Current issues in the regulation of signal transduction (1996) Advan Enzyme Regul, 36, pp. 33-55; Lalwani, N.D., Hylemon, P.B., Strom, S.C., Altered levels of phosphoinositide metabolites and activation of guanine-nucleotide dependent phospholipase C in rat hepatic tumors (1991) J Cell Physiol, 147, pp. 354-361; Homma, M.K., Homma, Y., Namba, M., Yuasa, Y., Enhanced phosphoinositide metabolism in colorectal carcinoma cells derived from familial adenomatous polyposis patients (1994) J Cell Biochem, 55, pp. 477-485; Nomoto, K., Tomita, N., Miyake, M., Xhu, D.-B., LoGerfo, P.R., Weinstein, I.B., Expression of phospholipase γ1, β1, and δ1 in primary human colon carcinomas and colon carcinoma cell lines (1995) Molec Carcinogenesis, 12, pp. 146-152; Noh, D.-Y., Lee, Y.H., Kim, S.S., Kim, Y.I., Ryu, S.-H., Suh, P.-G., Park, J.-G., Elevated content of phospholipase C-γ-1 in colorectal cancer tissues (1994) Cancer, 73, pp. 36-41; Arteaga, C.L., Johnson, M.D., Todderud, G., Coffey, R.J., Carpenter, G., Page, D.L., Elevated content of the tyrosine kinase substrate phospholipase C-γ1 in primary human breast carcinomas (1991) Proc Natl Acad Sci USA, 88, pp. 10435-10439","Weber, G.; Laboratory for Experimental Oncology; Indiana University School Medicine; 699 West Drive Indianapolis, IN 46202-5119, United States",,,,,,,,02507005,,ANTRD,,"English","Anticancer Research",Article,Scopus "Dropcho E.J., Rosenfeld S.S., Vitek J., Guthrie B.L., Morawetz R.B.","Phase II study of intracarotid or selective intracerebral infusion of cisplatin for treatment of recurrent anaplastic gliomas",1998,"Journal of Neuro-Oncology",36,2,,191,198,,12,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-0031881748&partnerID=40&rel=R8.0.0","Department of Neurology, Indiana University Medical Center, Indianapolis, IN, United States; Department of Neurology, University of Alabama, Birmingham, AL, United States; Department of Radiology, University of Alabama, Birmingham, AL, United States; Department of Surgery (Neurosurgery), University of Alabama, Birmingham, AL, United States; Department of Neurology CL 365, Indiana University Medical Center, Indianapolis, IN, United States; Richard Roudebush Vet. Aff. Med. C., Indianapolis, IN, United States","Purpose: To assess the response of patients with recurrent malignant gliomas to intra-arterial (IA) cisplatin. Methods: Eligibility criteria included patients with recurrent supratentorial malignant gliomas and measurable, unilateral contrast-enhancing tumor located within the territory of one or two major cerebral arteries. Patients received 75 mg/m2 IA cisplatin every four weeks. Depending on individual patients' tumor topography, cisplatin was infused either into the cervical internal carotid artery (ICA) (15 patients), or into one or two major cerebral arteries (26 patients), most often the M1 segment of the middle cerebral artery. Results: Of 40 patients evaluable for tumor response, four patients (10%) were responders and nine patients (22%) had disease stabilization. The median time to tumor progression among the 13 patients with tumor response or stable disease was 23.7 weeks. The response rate did not significantly differ between patients receiving ICA versus selective intracerebral infusion, although the latter group contained a higher proportion of glioblastoma. Tumor progression occurred solely as local failure in 33 patients (82%), with all enhancing tumor still located within the vascular territory infused with IA cisplatin. Ipsilateral vision loss occurred in two patients after ICA cisplatin but in none of the selective infusion patients. Seizures and/or transient or permanent neurologic deterioration occurred in four patients (27%) after ICA cisplatin and in 11 patients (44%) after selective intracerebral infusion. Conclusions: Although this was not a randomized comparison, selective intracerebral artery cisplatin infusion in this group of patients reduced the risk of eye toxicity, but did not produce a better tumor response rate, and carried a higher risk of neurotoxicity relative to ICA infusion.","Cisplatin; Glioma","antineoplastic agent; cisplatin; adult; article; blood toxicity; brain artery; cancer recurrence; clinical article; clinical trial; drug efficacy; glioblastoma; human; internal carotid artery; intraarterial drug administration; intracerebral drug administration; neurologic disease; neurotoxicity; phase 2 clinical trial; seizure; visual impairment; Adult; Carotid Arteries; Cerebral Arteries; Cisplatin; Glioma; Humans; Infusions, Intra-Arterial; Injections, Intra-Arterial; Middle Aged; Neoplasm Recurrence, Local; Supratentorial Neoplasms; Treatment Outcome",,"Cisplatin, 15663-27-1",,"bristol","Dropcho, E.J., Intra-arterial chemotherapy for malignant gliomas Textbook of Gliomas, , Berger MS, Wilson CB (eds) W.B. Saunders, Cambridge, MA, in press; Mahaley, M.S., Hipp, S.W., Dropcho, E.J., Bertsch, L., Cush, S., Tirey, T., Gillespie, G.Y., Intracarotid cisplatin chemotherapy for recurrent gliomas (1989) J Neurosurg, 70, pp. 371-378; Dropcho, E.J., Rosenfeld, S.S., Morawetz, R.B., Vitek, J., Brothers, M., Gorum, T., Bell, S., Schold, S.C., Pre-radiation intracarotid cisplatin treatment of newly diagnosed anaplastic gliomas (1992) J Clin Oncol, 10, pp. 452-458; Burger, P.C., Malignant astrocytic neoplasms: Classification, pathologic anatomy, and response to treatment (1986) Semin Oncol, 13 (MARCH), pp. 16-26; Mahaley, M.S., Gillespie, G.Y., Hammett, R., Computerized tomography brain scan tumor volume determinations (1990) J Neurosurg, 72, pp. 872-878; Newton, H.B., Page, M.A., Junck, L., Greenberg, H.S., Intra-arterial cisplatin for the treatment of malignant gliomas (1989) J Neuro-Oncol, 7, pp. 39-45; Stewart, D.J., Belanger, J.M., Grahovac, Z., Curuvija, S., Phase I study of intracarotid administration of carboplatin (1992) Neurosurgery, 30, pp. 512-517; Feun, L.G., Wallace, S., Stewart, D.J., Intracarotid infusion of cis-diamminedichloroplatinum in the treatment of recurrent malignant brain tumors (1984) Cancer, 54, pp. 794-799; Bobo, H., Kapp, J.P., Vance, R., Effect of intra-arterial cisplatin and BCNU dosage on radiographic response and regional toxicity in malignant glioma patients: Proposal of a new method of intra-arterial dosage calculation (1992) J Neuro-Oncol, 13, pp. 291-299; Nakagawa, H., Fujita, T., Kubo, S., Tsuruzono, K., Yamada, M., Selective intra-arterial chemotherapy with a combination of etoposide and cisplatin for malignant gliomas: Preliminary report (1994) Surg Neurol, 41, pp. 19-27; Recht, L., Fram, R.J., Strauss, G., Fitzgerald, T.J., Preirradiation chemotherapy of supratentorial malignant primary brain tumors with intracarotid cis-platinum and IV BCNU (1990) Am J Clin Oncol, 13, pp. 125-131; Junck, L., Koeppe, R.A., Greenberg, H.S., Mixing in the human carotid artery during carotid drug infusion studied with PET (1989) J Cerebral Blood Flow Metab, 9, pp. 681-689; Saris, S.C., Blasberg, R.G., Carson, R.E., De Vroom, H.L., Intravascular streaming during carotid artery infusions: Demonstration in humans and reduction using diastole-pulsatile administration (1991) J Neurosurg, 74, pp. 763-772; Aoki, S., Terada, H., Kosuda, S., Shitara, N., Fujii, H., Supraophthalmic chemotherapy with long tapered catheter: Distribution evaluated with intraarterial and intravenous Tc-99m HMPAO (1993) Radiology, 188, pp. 347-350","Dropcho, E.J.; Department of Neurology; CL 365; Indiana University Medical Center Indianapolis IN, United States",,,,,,,,0167594X,,JNODD,10.1023/A:1005871721697,"English","Journal of Neuro-Oncology",Article,Scopus "Sokol D.K., Azzarelli B., Smith R.R., Kassing L.C., Roos K.L., Pascuzzi R.M., Blinkhorn Jr. R.J.","Primary intravascular lymphomatosis associated with Mycobacterium marinum",1998,"Journal of Neuroimaging",8,1,,47,49,,5,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-0031942591&partnerID=40&rel=R8.0.0","Department of Neurology, Indiana University Medical Center, Indianapolis, IN, United States; Department of Neuropathology, Indiana University Medical Center; Department of Neuroradiology, Indiana University Medical Center; Department of Neurology, Indiana University Medical Center; Department of Neurology, Indiana University Medical Center, 1050 Walnut St., Indianapolis, IN 46202, United States; Department of Internal Medicine, Metro-Health Medical Center, Cleveland, OH, United States","Intravascular lymphomatosis (IVL) is a rare condition in which neoplastic cells preferentially infiltrate blood vessels of the central nervous system. Nonspecific symptoms associated with IVL include dementia, seizures, and multifocal cerebrovascular events. IVL was discovered at autopsy of a patient whose neurological deficits were predated by a particularly aggressive form of Mycobacterium marinum soft-tissue infection. It is speculated that IVL may have had an occult effect on the patient's cell-mediated immunity that predisposed him to this normally innocuous mycobacteria.",,"adult; article; brain angiography; brain blood vessel; cancer infiltration; case report; cellular immunodeficiency; dementia; disease association; disease predisposition; human; human tissue; lymphomatosis; male; mycobacterium marinum; nuclear magnetic resonance imaging; seizure; soft tissue infection; Blood Vessels; Brain; Brain Neoplasms; Humans; Lymphoma, B-Cell; Male; Middle Aged; Mycobacterium Infections, Atypical; Mycobacterium marinum; Soft Tissue Infections",,,,,"Demirer, T., Dail, D.H., Aboulafia, D.M., Four varied cases of intravascular lymphomatosis and a literature review (1994) Cancer, 73, pp. 17738-17745; Daniel, S.E., Rudge, P., Scaravilli, F., Malignant angioendotheliosis involving the nervous system: Support for a lymphoid origin of the neoplastic cells (1987) J Neurol Neurosurg Psychiatry, 50, pp. 1173-1177; Torenbeek, R., Scheltens, P., Van Schijndel Strack, R.J.M., Angiotropic intravascular large-cell lymphoma with massive cerebral extension (1993) J Neurol Neurosurg Psychiatry, 56, pp. 917-919; Bergmann, M., Terzija-Wessel, U., Blasius, S., Intravascular lymphomatosis of the CNS: Clinicopathologic study and search for expression of oncoproteins and Epstein-Barr virus (1994) Clin Neurol Neurosurg, 96, pp. 236-243; Glas, J., Hochberg, F.H., Miller, D.C., Intravascular lymphomatosis. A systemic disease with neurological manifestations (1993) Cancer, 71, pp. 31156-31164; Clark, W.C., Dohan, F.C., Moss, T., Schweitzer, J.B., Immunocytochemical evidence of lymphocytic derivation of neoplastic cells in malignant angioendotheliomatosis (1991) J Neurosurg, 74, pp. 757-762; Liszka, U., Drlicek, M., Hitzenberger, P., Intravascular lymphomatosis: A clinicopathologic study of three cases (1994) J Cancer Res Clin Oncol, 120, pp. 164-168; Reinglass, J.L., Muller, J., Wissman, S., Wellman, H., Central nervous system angioendotheliosis: A treatable multiple infarct dementia (1977) Stroke, 8, pp. 218-221; Stahl, R.L., Chan, W., Duncan, A., Corley Jr., C.C., Malignant angioendotheliomatosis presenting as disseminated intravascular coagulopathy (1991) Cancer, 68, pp. 2319-2323; Ontaka, A., Muroi, K., Izumi, T., Severe bleeding in a case of factor V inhibitor associated with intravascular lymphomatosis (Japanese) (1993) Jpn J Clin Hematol, 34, pp. 194-199; Smadja, D., Mas, J.L., Fallet Biannco, C., Intravascular lymphomatosis (neoplastic angioendotheliosis) of the central nervous system: Case report and literature review (1991) J Neurooncol, 11, pp. 171-180; Petito, C.K., Gottlieb, G.J., Dougherty, J.H., Petito, F.A., Neoplastic angioendotheliosis: Ultrastructural study and review of literature (1978) Ann Neurol, 3, pp. 393-399; Kleinschmidt-DeMasters, M.D., Filley, C.M., Bitter, M.A., Central nervous system angiocentric, angiodestructive T-cell lymphoma (lymphomatoid granulomatosis) (1992) Surg Neurol, 37, pp. 130-137; Sanqueza, O., Hyder, D.M., Sangueza, P., Intravascular lymphomatosis: Report of an unusual case with T-cell pheno-type occurring in an adolescent male (1991) J Cutan Pathol, 19, pp. 226-231; Tateyama, H., Eimoto, T., Tada, T., Congenital angiotropic lymphoma (intravascular lymphomatosis) of the T-cell type (1991) Cancer, 67, pp. 2131-2136","Pascuzzi, R.M.; Department of Neurology; Indiana University Medical Center; 100 Walnut St. Indianapolis, IN 46202, United States",,,,,,,,10512284,,JNERE,,"English","Journal of Neuroimaging",Article,Scopus "Bindal R.K., Bindal A.K., Sawaya R.","Outcome of surgical therapy for metastatic cancer to the brain.",1997,"Advances in surgery",31,,,351,373,,5,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-0031310025&partnerID=40&rel=R8.0.0","Indiana University School of Medicine, Indianapolis, USA.",[No abstract available],,"brain tumor; human; metastasis; mortality; multimodality cancer therapy; radiosurgery; randomized controlled trial; recurrent disease; review; survival; tumor recurrence; Brain Neoplasms; Combined Modality Therapy; Humans; Neoplasm Recurrence, Local; Radiosurgery; Randomized Controlled Trials; Recurrence; Survival Analysis",,,,,,"Bindal, R.K.",,,,,,,,00653411,,,,"English","Advances in surgery",Review,Scopus "Del Rosario M., Werlin S.L., Lauer S.J.","Hyperammonemic encephalopathy after chemotherapy: Survival after treatment with sodium benzoate and sodium phenylacetate",1997,"Journal of Clinical Gastroenterology",25,4,,682,684,,8,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-0031460362&partnerID=40&rel=R8.0.0","Department of Pediatrics, Divisions of Gastroenterology and Hematology, Oncology and Transplant, Childrens Hospital of Wisconsin, Milwaukee, WI, United States; Department of Pediatrics, University of Indiana, School of Medicine, Indianapolis, IN, United States; Department of Pediatrics, Emory University, School of Medicine, Atlanta, GA, United States; Department of Pediatrics, Medical College of Wisconsin, 8701 Watertown Plank Road, Milwaukee, WI 53226, United States","A 16-year-old boy had hyperammonemia and encephalopathy develop after high-dose chemotherapy for acute lymphoblastic leukemia. He was treated successfully with the ammonia-trapping agents sodium benzoate and sodium phenylacetate.",,"amsacrine; antineoplaston as2-1; asparaginase; benzoic acid; cyclophosphamide; cytarabine; daunorubicin; etoposide; lactulose; neomycin; vincristine; acute lymphoblastic leukemia; adolescent; article; brain disease; cancer chemotherapy; case report; disease association; dose response; human; hyperammonemia; male; mortality; priority journal; protein restriction; prothrombin time; urea cycle; Adolescent; Ammonia; Antimetabolites; Benzoates; Benzoic Acid; Brain Diseases; Drug Therapy; Humans; Male; Phenylacetates",,"Ammonia, 7664-41-7; Antimetabolites; Benzoates; Benzoic Acid, 65-85-0; Phenylacetates; phenylacetic acid, 103-82-2",,"bristol, United States","Watson, A.J., Chambers, T., Karp, J.E., Risch, V.R., Walker, W.G., Brusilow, S.W., Transient idiopathic hyperammonemia in adults (1985) Lancet, 2, pp. 1271-1274; Leonard, J.V., Kay, J.D., Acute encephalopathy and hyperammonemia complicating treatment of acute lymphoblastic leukemia with asparaginase (1986) Lancet, 1, pp. 162-163; Sharp, R.A., Lang, C.C., Hyperammonemic encephalopathy in chronic myelomonocytic leukemia (1987) Lancet, 4, p. 805; Mitchell, R.B., Wagner, J.E., Karp, J.E., Syndrome of idiopathic hyperammonemia after high-dose chemotherapy: Review of nine cases (1988) Am J Med, 85, pp. 662-667; Fine, P., Adler, K., Gerstenfeld, D., Idiopathic hyperammonemia after high-dose chemotherapy (1989) Am J Med, 86, p. 629; Tse, N., Cederbaum, S., Glaspy, J.A., Hyperammonemia following allogeneic bone marrow transplantation (1991) Am J Hematol, 38, pp. 140-141; Liaw, C.C., Liaw, S.J., Wang, C.H., Chiu, M.C., Huang, J.S., Transient hyperammonemia related to chemotherapy with continuous infusion of high dose 5-fluorouracil (1993) Anti-Cancer Drugs, 4, pp. 311-315; Batshaw, M.L., Monahan, P.S., Treatment of urea cycle disorders (1987) Enzyme, 38, pp. 242-250; Hines, J.D., Fay, J.W., Philips, G.L., Herzig, R.H., Lazarus, H.M., Herzig, G.P., Central nervous system toxicity with high dose cytosine arabinoside (1985) Semin Oncol, 12, pp. 233-236; Batshaw, M.L., Inborn errors of urea synthesis (1994) Ann Neurol, 35, pp. 133-141","Werlin, S.L.; Department of Pediatrics; Medical College of Wisconsin; 8701 Watertown Plank Road Milwaukee, WI 53226, United States",,,,,,,,01920790,,JCGAD,10.1097/00004836-199712000-00026,"English","Journal of Clinical Gastroenterology",Article,Scopus "Burgett R.A., Purvin V.A., Kawasaki A.","Lumboperitoneal shunting for pseudotumor cerebri",1997,"Neurology",49,3,,734,739,,59,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-0030833207&partnerID=40&rel=R8.0.0","Department of Ophthalmology, Indiana University Medical Center, Indianapolis, IN, United States; Department of Neurology, Indiana University Medical Center, Indianapolis, IN, United States; Midwest Eye Institute, Methodist Hospital of Indiana, Indianapolis, IN, United States; Midwest Eye Institute, 201 Pennsylvania Parkway, Indianapolis, IN 46280, United States","To clarify the appropriate role of lumboperitoneal (LP) shunting in the surgical management of pseudotumor cerebri (PTC), we retrospectively analyzed the clinical data from 30 patients who underwent this procedure. We found LP shunting to be an effective means of acutely lowering intracranial pressure. Symptoms of increased intracranial pressure improved in 82% of patients. Among 14 eyes with impaired visual acuity, 10 (71%) improved by at least two lines. Worsening of vision occurred in only one eye. Of 28 eyes with abnormal Goldmann perimetry, 18 (64%) improved and none worsened. The incidence of serious complications was low. The major drawback of LP shunting was the need for frequent revisions in a few patients. The reason for poor shunt tolerance in certain individuals is unclear. In PTC, LP shunting should be considered as the first surgical procedure for patients with severe visual loss at presentation or with intractable headache (with or without visual loss). After shunting it is important to identify patients who are shunt intolerant.",,"adolescent; adult; aged; article; brain pseudotumor; cancer incidence; data analysis; human; intracranial pressure; major clinical study; priority journal; retrospective study; school child; shunting; surgical technique; visual impairment; Adolescent; Adult; Aged; Anastomosis, Surgical; Cerebrospinal Fluid; Cerebrospinal Fluid Pressure; Cerebrospinal Fluid Shunts; Child; Female; Headache; Humans; Male; Meninges; Middle Aged; Optic Nerve; Papilledema; Perimetry; Peritoneum; Pseudotumor Cerebri; Reoperation; Subarachnoid Space; Vision Disorders; Visual Acuity; Visual Fields",,,,,"Eggenberger, E.R., Miller, N.R., Vitale, S., Lumboperitoneal shunt for the treatment of pseudotumor cerebri (1996) Neurology, 46, pp. 1524-1530; Johnston, I., Besser, M., Morgan, M.K., Cerebrospinal fluid diversion in the treatment of pseudotumor cerebri (1988) J Neurosurg, 69, pp. 195-202; Cornblath, W.T., Miller, N.R., Pseudotumor cerebri treated with lumboperitoneal shunt (1989) Ann Neurol, 26, p. 183; Rosenberg, M.L., Corbett, J.J., Smith, C., Cerebrospinal fluid diversion procedures in pseudotumor cerebri (1993) Neurology, 43, pp. 1071-1072; Sugerman, H.J., Felton, W.L., Salvant, J.B., Sismanis, A., Kellum, J.M., Effects of surgically induced weight loss on idiopathic intracranial hypertension in morbid obesity (1995) Neurology, 45, pp. 1655-1659; Sergott, R.C., Savino, P.J., Bosley, T.M., Modified optic nerve sheath decompression provides long-term visual improvement for pseudotumor cerebn (1988) Arch Ophthalmol, 106, pp. 1384-1390; Corbett, J.J., Nerad, J.A., Tse, D.T., Anderson, R.L., Results of optic nerve fenestration for pseudotumor cerebri: The lateral orbitotomy approach (1988) Arch Ophthalmol, 106, pp. 1391-1397; Brourman, N.D., Spoor, T.C., Ramocki, J.M., Optic nerve sheath decompression for pseudotumor cerebri (1988) Arch Ophthalmol, 106, pp. 1378-1383; Rizzo, J., Lessell, S., Choroidal infarction after optic nerve sheath fenestration (1994) Ophthalmology, 101, pp. 1622-1626; Plotnik, J., Kosmorsky, G., Operative complications of optic nerve sheath decompression (1993) Ophthalmology, 100, pp. 683-690; Spoor, T.C., McHenry, J.G., Complications of optic nerve sheath decompression (1993) Ophthalmology, 100, p. 1432; Kelman, S.E., Sergott, R.C., Cioffi, G.A., Savino, P.J., Bosley, T.M., Elman, M.J., Modified optic nerve sheath decompression in patients with functioning lumboperitoneal shunts and progressive visual loss (1991) Ophthalmology, 98, pp. 1449-1453","Purvin, V.A.; Midwest Eye Institute; 201 Pennsylvania Parkway Indianapolis, IN 46280, United States",,,,,,,,00283878,,NEURA,,"English","Neurology",Article,Scopus "Nichols C.R.","Early utilization of high-dose chemotherapy in germ cell tumors",1996,"Bone Marrow Transplantation",18,SUPPL. 1,,,,,,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-0029864481&partnerID=40&rel=R8.0.0","Indiana University, Indianapolis, IN, United States",[No abstract available],,"antineoplastic agent; bleomycin; carboplatin; cisplatin; cyclophosphamide; etoposide; ifosfamide; vinblastine; vincristine; autologous bone marrow transplantation; blood toxicity; brain disease; cancer regression; cancer survival; clinical trial; conference paper; germ cell tumor; human; male; meta analysis; nephrotoxicity; oral drug administration; priority journal; treatment outcome; Antineoplastic Combined Chemotherapy Protocols; Carboplatin; Clinical Protocols; Etoposide; Germinoma; Hematopoietic Stem Cell Transplantation; Humans; Ifosfamide; Male; Testicular Neoplasms",,"Carboplatin, 41575-94-4; Etoposide, 33419-42-0; Ifosfamide, 3778-73-2","vp 16",,,"Nichols, C.R.; Indiana University Indianapolis, IN, United States",,,,,,,,02683369,,BMTRE,,"English","Bone Marrow Transplantation",Conference Paper,Scopus "Dropcho E.J., Soong S.-J.","The prognostic impact of prior low grade histology in patients with anaplastic gliomas: A case-control study",1996,"Neurology",47,3,,684,690,,36,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-0029843049&partnerID=40&rel=R8.0.0","Department of Neurology, Indiana University Medical Center, Richard Roudebush Veterans Affairs Medical Center, Indianapolis, IN, United States; Biostatistics Unit, University of Alabama, Birmingham Comprehensive Cancer Center, Birmingham, AL, United States; Department of Neurology, Indiana University Medical Center, 541 Clinical Drive, Indianapolis, IN 46202-5111, United States","At the time of recurrence, the majority of low grade cerebral gliomas transform to a higher grade of histologic malignancy. The purpose of this study was to determine the survival outcome for patients whose anaplastic gliomas began as low-grade tumors compared with patients with de novo high- grade gliomas. Seventy-seven (11.5%) of 667 patients with anaplastic gliomas consecutively treated at the University of Alabama at Birmingham had histologically proven prior low-grade tumors. As a group, the patients with prior low-grade tumors would be expected to have a relatively favorable outcome, as they were younger and had a lower proportion of glioblastoma multiforme than the patients with de novo anaplastic gliomas. To provide a valid comparison, we performed a matched case-control study. We matched 68 patients from the prior low-grade group one-to-one with patients from the de hove group for tumor histology, age, Karnofsky performance scores, and type of surgery, without knowledge of outcome. The two groups received comparable radiotherapy and chemotherapy. For the 68 patients with prior low-grade tumor, median actuarial survival from the time of diagnosis of malignant degeneration was 19.7 months and the 5-year survival rate was 22%, compared with 22.0 months and 28% for the 68 matched de novo patients. Kaplan-Meier survival curves for the two groups did not significantly differ (p = 0.24 by logrank test). There were no significant survival differences between the patient subsets of prior low-grade versus de hove with glioblastoma, anaplastic astrocytoma, or anaplastic oligodendroglioma/mixed anaplastic glioma. These data indicate that with currently available treatment options, the survival outlook for patients with anaplastic gliomas, whose tumors arose from transformation of low-grade gliomas, is equivalent to the prognosis for patients with de hove anaplastic gliomas.",,"antineoplastic agent; carmustine; cisplatin; diaziquone; hydroxyurea; lomustine; mercaptopurine; nitrosourea; procarbazine; vincristine; adult; aged; article; astrocytoma; cancer grading; cancer survival; case control study; central nervous system tumor; glioblastoma; glioma; histology; human; intraarterial drug administration; major clinical study; malignant transformation; oligodendroglioma; priority journal; prognosis; Adolescent; Adult; Brain Neoplasms; Case-Control Studies; Glioblastoma; Humans; Middle Aged; Prognosis; Survival Analysis",,,,,"Muller, W., Afra, D., Schröder, R., Supratentorial recurrences of gliomas: Morphological studies in relation to time intervals with astrocytomas (1977) Acta Neurochir (Wien), 37, pp. 75-91; Afra, D., Muller, W., Benoist, G., Schröder, R., Supratentorial recurrences of gliomas: Results of reoperations on astrocytomas and oligodendrogliomas (1978) Acta Neurochir (Wien), 43, pp. 217-227; Laws, E.R., Taylor, W.F., Clifton, M.B., Okazaki, H., Neurosurgical management of low-grade astrocytoma of the cerebral hemispheres (1984) J Neurosurg, 61, pp. 665-673; Vertosick, F.T., Selker, R.G., Arena, V.C., Survival of patients with well-differentiated astrocytomas diagnosed in the era of computed tomography (1991) Neurosurgery, 28, pp. 496-501; Scherer, H.J., Cerebral astrocytomas and their derivatives (1940) Am J Cancer, 40, pp. 159-198; Burger, P.C., Kleihues, P., Cytologie composition of the untreated glioblastoma with implications for evaluation of needle biopsies (1989) Cancer, 63, pp. 2014-2023; Winger, M.J., Macdonald, D.R., Cairncross, J.G., Supratentorial anaplastic gliomas: The prognostic importance of extent of resection and prior low-grade glioma (1989) J Neurosurg, 71, pp. 487-493; Kleihues, P., Burger, P.C., Scheithauer, B.W., The new WHO classification of brain tumors (1993) Brain Pathol, 3, pp. 255-268; Kaplan, E.L., Meier, P., Nonparametric estimation from incomplete observations (1958) J Am Stat Assoc, 53, pp. 457-481; Mantel, N., Evaluation of survival data and two new rank order statistics arising from its consideration (1966) Cancer Chemother Rep, 50, pp. 163-170; Shaw, E.G., Scheithauer, B.W., Gilbertson, D.T., Postoperative radiotherapy of supratentorial low-grade gliomas (1989) Int J Radiât Oncol Biol Phys, 16, pp. 663-668; Shaw, E.G., Scheithauer, B., O'Fallon, J., Astrocytomas, oligoastrocytomas, and oligodendrogliomas: A comparative study (1992) Neurology, 42 (3 SUPPL.), p. 342; Whitton, A.C., Bloom, H.J., Low grade glioma of the cerebral hemispheres in adults: A retrospective analysis of 88 cases (1990) Int J Radiât Oncol Biol Phys, 18, pp. 783-786; Byar, D.P., Green, S.B., Strike, T.A., Prognostic factors for malignant gliomas (1983) Oncology of the Nervous System, pp. 379-395. , Walker MD, ed. Boston: Martinus Nijhoff; Wood, J.R., Green, S.B., Shapiro, W.R., The prognostic importance of tumor size in malignant gliomas: A computed tomographic scan study by the Brain Tumor Cooperative Group (1988) J Clin Oncol, 6, pp. 338-343; Simpson, J.R., Horton, J., Scott, C., Influence of location and extent of surgical resection on survival of patients with glioblastoma multiforme: Results of three consecutive Radiation Therapy Oncology Group (RTOG) clinical trials (1993) Int J Radiât Oncol Biol Phys, 26, pp. 239-244; Nazzaro, J.M., Neuwelt, E.A., The role of surgery in the manage- Ment of supratentorial intermediate and high-grade astrocytomas in adults (1990) J Neurosurg, 73, pp. 331-344; Walker, M.D., Alexander, E., Hunt, W.E., Evaluation of BCNU and/or radiotherapy in the treatment of anaplastic gliomas: A cooperative clinical trial (1978) J Neurosurg, 49, pp. 333-343; Walker, M.D., Green, S.B., Byar, D.P., Randomized comparison of radiotherapy and nitrosoureas for the treatment of malignant glioma after surgery (1980) New Engl J Med, 303, pp. 1323-1329; Von Deimling, A., Von Ammon, K., Schoenfeld, D., Wiestler, O.D., Seizinger, B.R., Louis, D.N., Subsets of glioblastoma multiforme defined by molecular genetic analysis (1993) Brain Pathol, 3, pp. 19-26; Chozick, B.S., Weicker, E., Pezzullo, J.C., Pattern of mutant p53 expression in human astrocytomas suggests the existence of alternate pathways of tumorigenesis (1994) Cancer, 73, pp. 406-415; Lang, F.F., Miller, D.C., Koslow, M., Newcomb, E.W., Pathways leading to glioblastoma multiforme: A molecular analysis of genetic alterations in 65 astrocytic tumors (1994) J Neurosurg, 81, pp. 427-436; Bello, M.J., Leone, P.E., Nebreda, P., Allelic status of chromosome 1 in neoplasms of the nervous system (1995) Cancer Genet Cytogenet, 83, pp. 160-164; Von Deimling, A., Nagel, J., Bender, B., Deletion mapping of chromosome 19 in human gliomas (1994) Int J Cancer, 57, pp. 676-680","Dropcho, E.J.; Department of Neurology; Indiana University Medical Center; 541 Clinical Drive Indianapolis, IN 46202-5111, United States",,,,,,,,00283878,,NEURA,,"English","Neurology",Article,Scopus "Dropcho E.J.","Antiamphiphysin antibodies with small-cell lung carcinoma and paraneoplastic encephalomyelitis",1996,"Annals of Neurology",39,5,,659,667,,93,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-0030003801&partnerID=40&rel=R8.0.0","Department of Neurology, Indiana University Medical Center, Richard Roudebush Vet. Aff. Med. C., Indianapolis, IN, United States; Department of Neurology CL 365, 541 Clinical Drive, Indianapolis, IN 46202-5111, United States","Paraneoplastic encephalomyelitis developed as the presenting feature of small-cell lung carcinoma in 3 patients. Two patients with paraneoplastic encephalomyelitis manifested predominantly as subacute sensory neuronopathy did not improve after prednisone treatment and chemotherapy. The third patient had severe axial and limb rigidity and myoclonus, which partially improved after chemotherapy and treatment with intravenous immunoglobulin and prednisone. Serum from each patient immunocytochemically stained the neuropil and to a lesser degree the neuronal cytoplasm in human cerebral and cerebellar cortex. On immunoblots of human neuronal extracts, each patient's serum contained high-titer IgG antibodies reacting with a protein band of apparent molecular mass 125 kd. This autoantibody pattern is indistinguishable from antibodies recently identified in several women with breast carcinoma and stiff-man syndrome. Screening of a human brain complementary DNA expression library with patient serum yielded clones whose sequence is identical to that of the synaptic vesicle-related protein amphiphysin. Reverse transcriptase-polymerase chain reaction demonstrated expression of amphiphysin in 8 of 10 small-cell lung carcinomas and in 5 of 14 breast carcinomas. These observations highlight the clinical and serological heterogeneity of paraneoplastic central nervous system disorders: Patients with a given clinical syndrome may have different antineuronal antibodies, and patients with a given autoantibody specificity have differing clinical presentations.",,"amphiphysin; autoantibody; cell protein; immunoglobulin; immunoglobulin g antibody; prednisone; unclassified drug; adult; antibody specificity; article; case report; encephalomyelitis; female; human; lung small cell cancer; muscle rigidity; myoclonus; paraneoplastic syndrome; priority journal; sensory neuropathy; sequence homology; serology; synapse vesicle; Aged; Antibodies, Antinuclear; Base Sequence; Blotting, Northern; Blotting, Southern; Carcinoma, Small Cell; Cloning, Molecular; DNA, Complementary; Encephalomyelitis; Female; Humans; Immunohistochemistry; Lung Neoplasms; Male; Middle Aged; Molecular Sequence Data; Nerve Tissue Proteins; Paraneoplastic Syndromes; Polymerase Chain Reaction; Stiff-Person Syndrome",,"amphiphysin, 147954-52-7; Antibodies, Antinuclear; DNA, Complementary; Nerve Tissue Proteins",,,"Dropcho, E.J., Autoimmune CNS paraneoplastic disorders: Mechanisms, diagnosis, and therapeutic options (1995) Ann Neurol, 37 (1 SUPPL.), pp. S102-S113; Dalmau, J., Graus, F., Rosenblum, M.K., Anti-Hu-associated paraneoplastic encephalomyelitis/sensory neuronopathy: A clinical study of 71 patients (1992) Medicine, 71, pp. 59-72; De Camilli, P., Thomas, A., Cofiell, R., The synaptic vesicle-associated protein amphiphysin is the 128-kD autoantigen of stiff-man syndrome with breast cancer (1993) J Exp Med, 178, pp. 2219-2223; Folli, F., Solimena, M., Cofiell, R., Autoantibodies to a 128-kd synaptic protein in three women with the stiff-man syndrome and breast cancer (1993) N Engl J Med, 328, pp. 546-551; Shi, S.R., Key, M.E., Kalra, K.L., Antigen retrieval in formalin-fixed, paraffin-embedded tissues: An enhancement method for immunohistochemical staining based on microwave oven heating of tissue sections (1991) J Histochem Cytochem, 39, pp. 741-748; Cunningham, J., Graus, F., Anderson, N.E., Partial characterization of Purkinje cell antigens in paraneoplastic cerebellar degeneration (1986) Neurology, 36, pp. 1163-1168; Laemmli, U.K., Cleavage of structural protein during the assembly of the head of bacteriophage T4 (1970) Nature, 227, pp. 680-685; Towbin, H., Staehelin, T., Gordon, J., Electrophoretic transfer of proteins from polyacrylamide gels to nitrocellulose sheets: Procedure and some applications (1979) Proc Natl Acad Sci USA, 76, pp. 4350-4354; Dropcho, E.J., Chen, Y.T., Posner, J.B., Cloning of a brain protein identified by autoantibodies from a patient with paraneoplastic cerebellar degeneration (1987) Proc Natl Acad Sci USA, 84, pp. 4552-4556; Chonczynski, P., Sacchi, N., Single-step method of RNA isolation by acid guanidium thiocyanate-phenol-chloroform extraction (1987) Anal Biochem, 162, pp. 156-159; Sambrook, J., Fritsch, E.F., Maniatis, T., (1989) Molecular Cloning: A Laboratory Manual. 2nd Ed., , Cold Spring Harbor: Cold Spring Harbor Laboratory Press; Feinberg, A.P., Vogelstein, B., A technique for radiolabeling DNA restriction endonuclease fragments to high specific activity (1983) Anal Biochem, 132, pp. 6-13; Maier, C.C., Marchetti, B., LeBoeuf, R.D., Thymocytes express a mRNA that is identical to hypothalamic luteinizing hormone-releasing hormone mRNA (1992) Cell Mol Neurobiol, 12, pp. 447-454; Graus, F., Cordon-Cardo, C., Posner, J.B., Neuronal antinuclear antibody in sensory neuronopathy from lung cancer (1985) Neurology, 35, pp. 538-543; Dropcho, E.J., King, P.H., Auroantibodies against the Hel-N1 RNA-binding protein among patients with lung carcinoma: An association with type I anti-neuronal nuclear antibodies (1994) Ann Neurol, 36, pp. 200-205; David, C., Solimena, M., De Camilli, P., Autoimmunity in stiff-man syndrome with breast cancer is targeted to the C-terminal region of human amphiphysin, a protein similar to the yeast proteins, Rvs167 and Rvs161 (1994) FEBS Lett, 351, pp. 73-79; Grimaldi, L.M., Martino, G., Braghi, S., Heterogeneity of autoantibodies in stiff-man syndrome (1993) Ann Neurol, 34, pp. 57-64; Lichte, B., Veh, R.W., Meyer, H.E., Amphiphysin, a novel protein associated with synaptic vesicles (1992) EMBO J, 11, pp. 2521-2530; Jahn, R., Sudhof, T.C., Synaptic vesicles and exocytosis (1994) Annu Rev Neurosci, 17, pp. 219-246; Wendland, B., Scheller, R.H., Molecular mechanisms of synaptic vesicle docking and membrane fusion (1994) Semin Neurosci, 6, pp. 167-176; Koyama, S., Yu, H., Dalgarno, D.C., Structure of the PI3K domain and analysis of the SH3 family (1993) Cell, 72, pp. 945-952; Roobol, T.H., Kazzaz, B.A., Vecht, C.J., Segmental rigidity and spinal myoclonus as a paraneoplastic syndrome (1987) J Neurol Neurosurg Psychiatry, 50, pp. 628-631; Bateman, D.E., Weller, R.O., Kennedy, P., Stiffman syndrome: A rare paraneoplastic disorder? (1990) J Neurol Neurosurg Psychiatry, 53, pp. 695-696; Piccolo, G., Martino, G., Moglia, A., Autoimmune myasthenia gravis with thymoma following the spontaneous remission of stiff-man syndrome (1990) Ital J Neurol Sci, 11, pp. 177-180; Nicholas, A.P., Chatterjee, A., Dropcho, E.J., Stiff-man syndrome associated with thymoma (1994) Ann Neurol, 36, p. 294. , Abstract; Horwich, M.S., Cho, L., Porro, R.S., Subacute sensory neuropathy: A remote effect of carcinoma (1977) Ann Neurol, 2, pp. 7-19; Chalk, C.H., Windebank, A.J., Kimmel, D.W., The distinctive clinical features of paraneoplastic sensory neuronopathy (1992) Can J Neurol Sci, 19, pp. 346-351","Dropcho, E.J.; Department of Neurology; 541 Clinical Drive Indianapolis, IN 46202-5111, United States",,,,,,,,03645134,,ANNED,10.1002/ana.410390516,"English","Annals of Neurology",Article,Scopus "Einhorn L.H.","The case against prophylactic cranial irradiation in limited small cell lung cancer",1995,"Seminars in Radiation Oncology",5,1,,57,60,,10,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-0028885346&partnerID=40&rel=R8.0.0","Indiana University Medical Center, Univesity Hospital, 550 University Blvd, Indianapolis, IN 46202-5265, United States","There have been significant advances in the treatment of small cell lung cancer during the past two decades. Systemic chemotherapy for extensive disease and combined modality therapy for limited small cell lung cancer has improved both quality and quantity of survival. In extensive disease, although the median survival time is improved with chemotherapy, only rarely is a patient cured. However, in limited disease, over 50% of the patients will achieve a complete remission and the 5-year survival is approximately 20%. There has been significant controversy concerning the role of prophylactic cranial irradiation, especially in patients with limited small cell lung cancer who achieve a complete remission. This article addresses the currently available data concerning benefit, toxicity, and results from randomized clinical trials using prophylactic cranial irradiation in patients with small cell lung cancer.",,"antineoplastic agent; cyclophosphamide; doxorubicin; prednisone; vincristine; brain metastasis; brain protection; cancer combination chemotherapy; cancer radiotherapy; cancer regression; cancer survival; central nervous system metastasis; clinical trial; controlled clinical trial; controlled study; dementia; human; lung small cell cancer; multimodality cancer therapy; neurological complication; phase 2 clinical trial; phase 3 clinical trial; priority journal; randomized controlled trial; review; skull irradiation",,,,,,"Einhorn, L.H.; Indiana University Medical Center; Univesity Hospital; 550 University Blvd Indianapolis, IN 46202-5265, United States",,,,,,,,10534296,,SRONE,10.1016/S1053-4296(05)80011-6,"English","Seminars in Radiation Oncology",Review,Scopus "Caldemeyer K.S., Zimmerman R.A., Azzarelli B., Smith R.R., Moran C.C.","Gliofibroma: CT and MRI",1995,"Neuroradiology",37,6,,481,485,,8,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-0029084875&partnerID=40&rel=R8.0.0","Department of Radiology, Indiana University School Medicine, University Hospital, 550 N. University Blvd., Indianapolis, IN 46202-5253, United States","We describe CT and MRI appearances in two children with pathologically proven gliofibromas, in the cerebrum and cerebellum. A striking finding was lack of high signal on T2-weighted MRI.","Brain, neoplasms; Gliofibroma; Magnetic resonance imaging","article; brain tumor; cancer diagnosis; case report; cerebellum; child; computer assisted tomography; female; fibroma; glioma; human; infant; male; nuclear magnetic resonance imaging; priority journal; school child; Biopsy; Brain Neoplasms; Case Report; Cerebellar Neoplasms; Cerebellum; Child; Female; Fibroma; Glial Fibrillary Acidic Protein; Glioma; Human; Infant; Magnetic Resonance Imaging; Male; S100 Proteins; Temporal Lobe; Tomography, X-Ray Computed; Tumor Markers, Biological",,"Glial Fibrillary Acidic Protein; S100 Proteins; Tumor Markers, Biological",,,,"Caldemeyer, K.S.; Department of Radiology; Indiana University School Medicine; University Hospital; 550 N. University Blvd. Indianapolis, IN 46202-5253, United States",,,,,,,,00283940,,NRDYA,10.1007/s002340050141,"English","Neuroradiology",Article,Scopus "George J.C., Edwards M.K., Jakacki R.I., Kho-Duffin J.","Melanotic neuroectodermal tumor of infancy",1995,"American Journal of Neuroradiology",16,6,,1273,1275,,14,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-0029055889&partnerID=40&rel=R8.0.0","Department of Radiology, Indiana University Sch. of Medicine, J. Whitcomb Riley Hosp. for Children, 702 Barnhill Dr, Indianapolis, IN 46202-5200, United States","We present a case of malignant melanotic neuroectodermal tumor of infancy arising in the skull and secondarily invading brain. The central tumor was hyperintense to brain on T1-weighted images and hypointense to brain on T2- weighted images. This appearance corresponded to the surgical and histologic findings of melanin-containing tumor.","Brain, neoplasms; Children, neoplasms; Neuroectodermal tumor; Skull, neoplasms","article; case report; childhood cancer; diagnostic imaging; human; image analysis; male; neuroectoderm tumor; preschool child; skull; tumor localization; Brain Neoplasms; Case Report; Child, Preschool; Female; Follow-Up Studies; Human; Infant; Neoplasm Recurrence, Local; Neuroectodermal Tumor, Melanotic; Parietal Bone; Reoperation; Skull Neoplasms; Temporal Bone",,,,,,"George, J.C.; Department of Radiology; Indiana University Sch. of Medicine; J. Whitcomb Riley Hosp. for Children; 702 Barnhill Dr Indianapolis, IN 46202-5200, United States",,,,,,,,01956108,,AAJND,,"English","American Journal of Neuroradiology",Article,Scopus "Singhal R.L., Prajda N., Yeh Y.A., Weber G.","1-Phosphatidylinositol 4-phosphate 5-kinase (EC 2.7.1.68): A proliferation- and malignancy-linked signal transduction enzyme",1994,"Cancer Research",54,21,,5574,5578,,28,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-0028034551&partnerID=40&rel=R8.0.0","Laboratory for Experimental Oncology, Indiana University, School of Medicine, Indianapolis, IN 46202-5200, United States; National Institute of Oncology, Rath Gy. Utca, Budapest, Hungary; Laboratory for Experimental Oncology, Indiana University, School of Medicine, 702 Barnhill Drive, Indianapolis, IN 46202-5200, United States","The activity of PIP kinase (1-phosphatidylinositol 4-phosphate 5-kinase; EC 2.7.1.68), the second ATP-utilizing enzyme of 1,4,5-trisphosphate and diacylglycerol biosynthesis, was determined in the rat in a spectrum of transplantable solid hepatomas of different growth rates and in normal tissues of high and low cell renewal rates. In a standard isotopic method developed for the assay, the enzyme activity was linear with time for 4 min and proportional with protein concentration over a range of 0.05 to 1 mg per 0.135-ml reaction mixture. The apparent K(m) for the substrate PIP (phosphatidylinositol 4-phosphate) and for ATP and Mg2+ in normal liver were 0.06, 0.5, and 4.2 mM, respectively, and in rapidly growing hepatoma 3924A, 0.08, 0.7, and 7.1 mM. The kinase activity in adult Wistar rat liver was 0.046 ± 0.003 nmol/h/mg protein. In hepatomas of slow and intermediate growth rates, PIP kinase activity increased 3.3-9.7-fold, and in hepatoma 3924A, it was elevated 45-fold over that of normal liver. When hepatoma 3924A cells were plated and expressed their proliferative program, enzyme activity increased 4.3-fold in mid-log phase. To further clarify the linkage between PIP kinase activity and proliferation, enzyme activity was determined in rat organs of high and low cell renewal capacity. The PIP kinase activity in rat thymus, bone marrow, spleen, and testes was 5.4-, 6.3-, 4.8- and 4.3-fold higher, respectively, than in normal rat liver; in lung, brain, skeletal muscle, renal cortex, and heart, the activities were low. In all tissues examined, the activity of PIP kinase was 4.6 to 18% of that of phosphatidylinositol kinase. Since enzymes of crucial significance frequently have short half-lives, the decay rates of PIP kinase were examined in liver, bone marrow, and hepatoma 3924A in rats injected with cycloheximide, which inhibits protein biosynthesis. In cycloheximide-treated animals, PIP kinase had the shortest decay rate (t( 1/2 ) = 0.12 h) in comparison with eight enzymes of purine and pyrimidine biosynthesis of rat bone marrow (t( 1/2 ) = 0.6 to 4.3 h). In liver and solid hepatoma 3924A, the activity of PIP kinase was degraded less rapidly (t( 1/2 ) = 5 h). The relationship of PIP kinase activity with proliferation and transformation is apparent in the high activity in thymus, bone marrow, spleen, and testes and in the increased activities in the rat hepatomas of different growth rates. The coordinate increases in phosphatidylinositol and PIP kinase activities suggest that the capacity for signal transduction is heightened in cancer cells. The elevated inositol 1,4,5-trisphosphate concentrations observed in the hepatomas support this conclusion. Since both kinase activities are linked with malignancy, these may well be sensitive targets for designing new chemotherapeutic agents.",,"adenosine triphosphate; cycloheximide; inositol 1,4,5 trisphosphate; magnesium; phosphatidylinositol 4 phosphate; phosphatidylinositol 4 phosphate kinase; phosphatidylinositol kinase; animal cell; animal model; animal tissue; article; cell proliferation; controlled study; enzyme analysis; enzyme assay; enzyme localization; enzyme synthesis; liver cell carcinoma; male; malignant transformation; nonhuman; priority journal; rat; signal transduction; Animal; Bone Marrow; Carcinoma, Hepatocellular; Diglycerides; Inositol 1,4,5-Trisphosphate; Liver Neoplasms; Male; Phosphatidylinositols; Phosphorylation; Phosphotransferases (Alcohol Group Acceptor); Rats; Rats, Inbred ACI; Rats, Inbred BUF; Rats, Wistar; Signal Transduction; Support, Non-U.S. Gov't; Support, U.S. Gov't, P.H.S.; Tumor Cells, Cultured",,"1-phosphatidylinositol-4-phosphate 5-kinase, EC 2.7.1.68; Diglycerides; Inositol 1,4,5-Trisphosphate, 85166-31-0; Phosphatidylinositols; Phosphotransferases (Alcohol Group Acceptor), EC 2.7.1",,"sigma, United States",,"Weber, G.; Laboratory for Experimental Oncology; Indiana Univ. School of Medicine; 702 Barnhill Drive Indianapolis, IN 46202-5200, United States",,,,,,,,00085472,,CNREA,,"English","Cancer Research",Article,Scopus "Singhal R.L., Weber G.","Deoxycytidine kinase and thymidine kinase activities in rat brain",1993,"Oncology Research",5,4-5,,191,195,,,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-0027384657&partnerID=40&rel=R8.0.0","Laboratory for Experimental Oncology, Indiana University Sch. of Medicine, 702 Barnhill Drive, Indianapolis, IN 46202-5200, United States","Deoxycytidine (CdR) kinase (E.C. 2.7.1.74) acts as a salvage enzyme in DNA biosynthesis, but little is known about this important nucleoside kinase in the brain. We report that CdR kinase activity in the 100,000 x g cytosolic fraction of normal adult rat brain cortex was 0.89 ± 0.04 nmol/hr/mg protein which is twice that of the liver enzyme. For brain CdR kinase the apparent K(m) for CdR, ATP and Mg++ were 0.22, 1.1 and 0.63 mM, respectively. When the cytosolic preparation was incubated at 37°C, CdR kinase activity rapidly decreased (t( 1/2 ) = 15 min); CdR (400 μM) protected the enzyme. Addition of DFDC (0 to 100 μM) competitively inhibited brain CdR kinase activity with K(i) = 17 μM. DFDC elevated the apparent K(m) for CdR of brain CdR kinase 3.5-fold, from 0.22 to 0.8 mM. DFDC did not inhibit brain TdR kinase. AZT, which competitively inhibited TdR kinase (K(i) = 0.6 μM), did not affect brain CdR kinase activity. These results indicate that the cytosol of rat brain contains CdR kinase which is inhibited by the deoxycytidine analog, DFDC. The enzyme is protected from thermal denaturation by CdR but not by TdR.",,"deoxycytidine; deoxycytidine kinase; thymidine kinase; zidovudine; animal tissue; article; brain cortex; cancer; cancer chemotherapy; drug mechanism; enzyme activity; enzyme assay; male; nonhuman; priority journal; pyrimidine synthesis; rat; Animal; Cerebral Cortex; Cytosol; Deoxycytidine; Deoxycytidine Kinase; Male; Rats; Rats, Wistar; Substrate Specificity; Support, U.S. Gov't, P.H.S.; Thymidine Kinase; Zidovudine",,"deoxycytidine kinase, 9039-45-6; deoxycytidine, 951-77-9; thymidine kinase, 9002-06-6, 9086-73-1; zidovudine, 30516-87-1; Deoxycytidine Kinase, EC 2.7.1.74; Deoxycytidine, 951-77-9; Thymidine Kinase, EC 2.7.1.21; Zidovudine, 30516-87-1",,"lilly, United States; moravek, United States; sigma, United States",,"Weber, G.; Laboratory for Experimental Oncology; Indiana University Sch. of Medicine; 702 Barnhill Drive Indianapolis, IN 46202-5200, United States",,,,,,,,09650407,,ONREE,,"English","Oncology Research",Article,Scopus "Shapiro S., Mealey Jr. J., Kay S.","Multimodal treatment of adult intracranial gliomas.",1991,"Indiana medicine : the journal of the Indiana State Medical Association",84,4,,246,250,,,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-0026146153&partnerID=40&rel=R8.0.0","Section of Neurosurgery, Indiana University School of Medicine, Indianapolis.","Recent advances, experimental treatments and future protocols of adult intracranial gliomas are discussed in this article. Adult intracranial gliomas are not benign, and most are incurable with poor prognosis, despite aggressive treatment. Breakthroughs will be found only through well-designed, experimental protocol evaluation on patients with intracranial gliomas.",,"adult; brain tumor; glioma; human; multimodality cancer therapy; review; Adult; Brain Neoplasms; Combined Modality Therapy; Glioma; Human",,,,,,"Shapiro, S.",,,,,,,,07468288,,,,"English","Indiana medicine : the journal of the Indiana State Medical Association",Review,Scopus "Fleck J.F., Einhorn L.H., Lauer R.C., Schultz S.M., Miller M.E.","Is prophylactic cranial irradiation indicated in small-cell lung cancer?",1990,"Journal of Clinical Oncology",8,2,,209,214,,33,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-0025164986&partnerID=40&rel=R8.0.0","Department of Medicine, Section of Hematology and Oncology, Indiana University, Indianapolis, IN 46223, United States","Although prophylactic cranial irradiation (PCI) is frequently used in the treatment of patients with limited-extent small-cell lung cancer (SCLC), its role remains controversial. One hundred fourteen SCLC patients with limited disease treated at Indiana University were retrospectively reviewed. Fifty-eight of 114 (51%) patients achieved a complete remission (CR) and were analyzed. Thirty-eight of these 58 CR patients received PCI (+PCI) and 20 of 58 CR patients did not receive PCI (-PCI). Twenty-six of 38 patients who received PCI subsequently relapsed. No patient initially relapsed in the CNS, although one patient had a brain metastasis following recurrence in the chest. Eleven of 38 patients who were treated with PCI survived for longer than 30 months and were considered long-term survivors. Seven of these 11 patients (63%) developed clinically significant neurological toxicity. Sixteen of 20 patients who did not receive PCI relapsed, but there was only one initial relapse in the CNS. Three additional patients who relapsed in the chest subsequently developed CNS metastasis. All responded to palliative radiation with improvement in their symptoms. The high incidence of CNS toxicity in the long-term survivors and the relatively infrequent incidence of isolated CNS recurrent in patients not subjected to PCI raise serious questions concerning the role, if any, of PCI in limited SCLC.",,"cisplatin; cyclophosphamide; doxorubicin; etoposide; vincristine; article; brain; brain metastasis; controlled study; intravenous drug administration; lung cancer; lung carcinoma; lung small cell cancer; major clinical study; priority journal; prophylaxis; skull irradiation; small cell carcinoma; Adult; Aged; Antineoplastic Combined Chemotherapy Protocols; Brain; Brain Neoplasms; Carcinoma, Small Cell; Female; Human; Lung Neoplasms; Male; Middle Age; Radiotherapy Dosage; Random Allocation; Remission Induction; Retrospective Studies; Support, Non-U.S. Gov't; Support, U.S. Gov't, P.H.S.; Survival Rate; Thorax",,"cisplatin, 15663-27-1, 26035-31-4, 96081-74-2; cyclophosphamide, 50-18-0; doxorubicin, 23214-92-8, 25316-40-9; etoposide, 33419-42-0; vincristine, 57-22-7; Antineoplastic Combined Chemotherapy Protocols","vp 16",,,"Einhorn, L.H.; Indiana University Hospital; 926 W Michigan Indianapolis, IN 46223, United States",,,,,,,,0732183X,,JCOND,,"English","Journal of Clinical Oncology",Article,Scopus "Mathews V.P., Broome D.R., Smith R.R., Bognanno J.R., Einhorn L.H., Edwards M.K.","Neuroimaging of disseminated germ cell neoplasms",1990,"American Journal of Roentgenology",154,6,,1299,1304,,,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-0025285148&partnerID=40&rel=R8.0.0","Department of Radiology, Indiana University, Medical Center, 926 W. Michigan St., Indianapolis, IN 46223, United States","The purpose of this study was to determine the role of neuroimaging in the management of patients with metastatic germ cell tumors. Retrospective evaluation of 299 patients treated in 1986 and 1987 for initial presentation or recurrence of testicular, retroperitoneal, and mediastinal germ cell tumors was performed to determine indications for neuroimaging, frequency and site of CNS metastases, and occurrence of other CNS abnormalities. Sixty-six patients required CNS imaging with myelography, CT, or MR. Studies were normal in 24 patients. Twenty patients had CNS metastases including 11 with intracranial metastases, eight with spine lesions, and one with both brain and spine involvement. Sixteen had cerebral or cerebellar atrophy of unclear origin and functional significance. Two patients had ventriculomegaly without symptoms of hydrocephalus. Four patients had questionable lesions that were never confirmed. None of the 25 asymptomatic patients with elevated serum tumor markers had brain metastases. Fifteen of 17 patients with focal neurologic deficits and three of six patients with seizures had CNS metastases. CNS imaging to detect germ cell tumor metastases is most useful in the presence of neurologic deficits or seizures but is not useful in patients with unexplained elevation of serum tumor markers in the absence of neurologic deficits.",,"adolescent; adult; aged; article; central nervous system; computer analysis; computer assisted tomography; diagnosis; germ cell tumor; human; male; metastasis; methodology; myelography; nuclear magnetic resonance imaging; priority journal; testis cancer; Adolescent; Adult; Brain Neoplasms; Diagnostic Imaging; Human; Magnetic Resonance Imaging; Male; Middle Age; Myelography; Neoplasms, Germ Cell and Embryonal; Radiographic Image Enhancement; Retrospective Studies; Spinal Neoplasms; Tomography, X-Ray Computed",,,,,,"Smith, R.R.; Department of Radiology; Indiana University; Medical Center; 926 W. Michigan St. Indianapolis, IN 46223, United States",,,,,,,,0361803X,,AJROA,,"English","American Journal of Roentgenology",Article,Scopus "Shapiro S., Mealey Jr. J.","Late anaplastic gliomas in children previously treated for acute lymphoblasic leukemia",1989,"Pediatric Neuroscience",15,4,,176,180,,7,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-0024842386&partnerID=40&rel=R8.0.0","Division of Neurosurgery, Indiana University Medical Center, Indianapolis, IN, United States",[No abstract available],,"methotrexate; acute lymphoblastic leukemia; anaplastic carcinoma; article; astrocytoma; brain radiation; child; clinical article; glioma; human; prognosis; risk; second cancer; Adolescent; Brain Neoplasms; Child; Child, Preschool; Combined Modality Therapy; Glioma; Human; Infant; Leukemia, Lymphocytic, Acute; Methotrexate; Neoplasms, Radiation-Induced; Radiotherapy",,"methotrexate, 15475-56-6, 59-05-2, 7413-34-5; Methotrexate, 59-05-2",,,,,,,,,,,,02557975,,PENEE,,"English","Pediatric Neuroscience",Article,Scopus "Vakili S.T., Muller J., Shidnia H., Campbell R.L.","Primary lymphoma of the central nervous system: A clinicopathologic analysis of 26 cases",1986,"Journal of Surgical Oncology",33,2,,95,102,,6,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-0023024155&partnerID=40&rel=R8.0.0","Department of Neuropathology, Indiana University School of Medicine, Indianapolis, IN, United States",[No abstract available],,"carmustine; cyclophosphamide; doxorubicin; methotrexate; prednisone; procarbazine; radioisotope; vincristine; brain tumor; cancer combination chemotherapy; central nervous system; diagnosis; drug efficacy; histology; human; immunoblastic lymphoma; intravenous drug administration; lymphatic system; major clinical study; methodology; microgliomatosis; oral drug administration; priority journal; sarcoma; therapy; Adolescent; Adult; Aged; Autopsy; Biopsy; Brain Neoplasms; Cerebellar Neoplasms; Child; Child, Preschool; Combined Modality Therapy; Craniotomy; Female; Frontal Lobe; Human; Lymphoma; Male; Middle Age; Spinal Cord Diseases",,"carmustine, 154-93-8; cyclophosphamide, 50-18-0; doxorubicin, 23214-92-8, 25316-40-9; methotrexate, 15475-56-6, 59-05-2, 7413-34-5; prednisone, 53-03-2; procarbazine, 366-70-1, 671-16-9; vincristine, 57-22-7",,,,,,,,,,,,00224790,,JSONA,,"English","Journal of Surgical Oncology",Article,Scopus "Edwards M.K., Terry J.G., Montebello J.F., Hornback N.B., Kuharik M.A.","Gliomas in children following radiation therapy for lymphoblastic leukemia.",1986,"Acta Radiologica, Supplement",369,,,651,653,,1,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-0022821312&partnerID=40&rel=R8.0.0","Department of Radiology, Indiana University Medical Center, Indianapolis.","Four children treated for acute lymphoblastic leukemia developed intracranial gliomas between 40 and 120 months following multiagent chemotherapy, prophylactic whole brain irradiation, and intrathecal Methotrexate. The diagnosis of glioma was confirmed in each case with biopsy or autopsy. These children were part of a larger series of 73 patients with acute lymphoblastic leukemia treated at Indiana University receiving 24 Gy as per the protocol guidelines of the Children's Cancer Study Group. Currently 42 patients of the original 73 children survive in continuous remission.",,"acute lymphocytic leukemia; article; brain tumor; case report; child; female; glioma; human; infant; male; preschool child; radiation injury; radiography; radiotherapy; tomography; Brain Neoplasms; Case Report; Child; Child, Preschool; Female; Glioma; Human; Infant; Leukemia, Lymphocytic, Acute; Male; Neoplasms, Radiation-Induced; Radiotherapy; Tomography, X-Ray Computed",,,,,,"Edwards, M.K.",,,,,,,,03655954,,,,"English","Acta Radiologica, Supplement",Article,Scopus "Shidnia H., Hornback N.B., Lingeman R., Barlow P.","Extranodal lymphoma of the head and neck area",1985,"American Journal of Clinical Oncology: Cancer Clinical Trials",8,3,,235,243,,7,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-0022187891&partnerID=40&rel=R8.0.0","Department of Radiation Oncology, Indiana University School of Medicine, Indianapolis, IN 46223, United States","Record of 64 patients with extranodal lymphoma of the head and neck area treated at this institution between 1965 and 1982 have been reviewed. Of these cases, 78% had Stage I-EA disease, 20% had Stage II-EA disease, and 2% had Stage III-EA disease. Excluded from this study were patients of the pediatric age, patients with previous chemotherapy and surgery, patients in whom extranodal involvement has been a terminal manifestation of wide-spread disease, and patients with nodal involvement with extension of disease outside the lymph nodes. Patients with a histiocytic histology accounted for 63%, 28% were of lymphocytic histologies, 4.5% were of mixed histologies, and in 4.5% a diagnosis of lymphoma or benign lymphocytic proliferation had been made. The paranasal sinuses, nasal cavity, and oral cavity were the most frequent sites of involvement, making up 39% of the cases - with the orbit, central nervous system, nasopharynx, salivary glands, thyroid, skin, and larynx following in that order of frequency. All patients received a definitive course of radiotherapy, except patients with CNS involvement. In no case was chemotherapy given concomitantly with the radiation therapy. One-third of the patients did require chemotherapy at a later time for progression of disease. No patients were lost to follow-up. Seven patients with primaries of the brain were inevaluable for response; however, all patients having visible or palpable tumors achieved a complete response (100%), and there was no recurrence or persistent disease in the field of therapy. The next area of disease involvement depended on the site of the primary. Nodal involvement following extranodal disease carried a poor prognosis.",,"chemotherapy; head and neck cancer; human; lymphatic system; lymphoma; major clinical study; priority journal; radiotherapy; therapy; Adult; Aged; Brain Neoplasms; Female; Head and Neck Neoplasms; Human; Lymphatic Metastasis; Lymphoma; Male; Middle Age; Mouth Neoplasms; Nasopharyngeal Neoplasms; Nose Neoplasms; Orbital Neoplasms; Paranasal Sinus Neoplasms; Prognosis; Salivary Gland Neoplasms; Skin Neoplasms; Support, Non-U.S. Gov't",,,,,,,,,,,,,,02773732,,AJCOD,,"English","American Journal of Clinical Oncology: Cancer Clinical Trials",Article,Scopus "Lester S.G., Morphis II J.G., Hornback N.B.","Brain metastases and testicular tumors: Need for aggressive therapy",1984,"Journal of Clinical Oncology",2,12,,1397,1403,,15,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-0021677939&partnerID=40&rel=R8.0.0","Department of Radiation Oncology, Indiana University Medical Center, Indianapolis, IN 46223, United States","In late 1974, the combination of cisplatin, vinblastine, and bleomycin (PVB) became the standard chemotherapeutic regimen for treatment of disseminated nonseminomatous germ cell testicular tumors (NSGCT) at Indiana University Hospital. A retrospective analysis of the treatment records of all patients with brain metastases from NSGCTs treated at the Indiana University Radiation Oncology Department from 1975 through 1982 was undertaken. These 22 patients were divided into four groups. Group 1 (n = 5) consisted of those patients who presented initially with brain metastases and had no prior systemic treatment. Group 2 (n = 4) were referred to Indiana University after failing systemic therapy other than PVB chemotherapy. Group 3 (n = 5) consisted of those patients who after achieving a complete response with PVB developed a relapse confined to the brain. Group 4 (n = 8) consisted of those patients who were initially treated with PVB and eventually developed progressive disease and brain metastases. The survival by group is 80%, 0%, 60%, and 0%, respectively, with the overall survival for the entire group being 31.8%. All patients currently alive have a range of follow-up of 22 to 96 months from diagnosis and 12 to 83 months from whole brain irradiation (WBRT). Group 1 was treated with PVB+/- doxorubicin plus WBRT. Group 3 was treated with surgical excision, when feasible, followed by WBRT and platinum-containing chemotherapy. Group 2 and 4 were usually treated with palliative intent WBRT. The CNS is a site of sanctuary from PVB. Patients with brain metastases who may achieve a complete response should be treated with curative intent and receive aggressive WBRT (5,000 rad/25 fractions) with concomitant chemotherapy.",,"bleomycin; chlorambucil; cisplatin; cyclophosphamide; dactinomycin; doxorubicin; melphalan; methotrexate; mithramycin; vinblastine; vincristine; cancer chemotherapy; cancer combination chemotherapy; cancer radiotherapy; central nervous system; central nervous system metastasis; clinical article; diagnosis; germ cell tumor; human; male genital system; priority journal; testis cancer; therapy; Adult; Antineoplastic Combined Chemotherapy Protocols; Bleomycin; Brain Neoplasms; Choriocarcinoma; Cisplatin; Human; Male; Support, U.S. Gov't, P.H.S.; Teratoma; Testicular Neoplasms; Vinblastine",,"bleomycin, 11056-06-7; chlorambucil, 305-03-3; cisplatin, 15663-27-1, 26035-31-4, 96081-74-2; cyclophosphamide, 50-18-0; dactinomycin, 1402-38-6, 1402-58-0, 50-76-0; doxorubicin, 23214-92-8, 25316-40-9; melphalan, 148-82-3; methotrexate, 15475-56-6, 59-05-2, 7413-34-5; mithramycin, 18378-89-7; vinblastine, 865-21-4; vincristine, 57-22-7; Antineoplastic Combined Chemotherapy Protocols; Bleomycin, 11056-06-7; Cisplatin, 15663-27-1; PVB protocol; Vinblastine, 865-21-4","cytoxan; leukeran","burroughs wellcome, United States",,,,,,,,,,0732183X,,JCOND,,"English","Journal of Clinical Oncology",Article,Scopus "Tarver R.D., Richmond B.D., Klatte E.C.","Cerebral metastases from lung carcinoma: Neurological and CT correlation. Work in progress",1984,"Radiology",153,3 I,,689,692,,28,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-0021691547&partnerID=40&rel=R8.0.0","Department of Radiology, Indiana University Medical Center, Indianapolis, IN 46223, United States","To determine the role of brain CT in neurologically asymptomatic lung cancer patients, a review was made of the CT and clinical findings in 279 patients. Neurological status in these patients was categorized as (a) normal, (b) abnormal with specific signs and symptoms, and (c) abnormal with vague signs and symptoms. Brain metastases were found in 94.5% of patients (69/73) with specific abnormal neurological findings, 26.6% of patients (16/60) with vague neurological signs and symptoms, 11% of patients (10/92) with oat cell carcinoma and a normal neurological examination, and 40% of patients (8/20) with adenocarcinoma and a normal neurological examination. Brain metastasis was not seen on CT in the 29 patients with squamous cell carcinoma, and a normal neurological examination. It is concluded that brain CT is useful for the detection of occult brain metastases, particularly oat cell carcinoma and adenocarcinoma, in neurologically asymptomatic lung cancer patients.",,"central nervous system; central nervous system metastasis; computer analysis; computer assisted tomography; diagnosis; human; lung carcinoma; major clinical study; nervous system; neurology; priority journal; respiratory system; Adenocarcinoma; Brain Neoplasms; Carcinoma; Carcinoma, Bronchogenic; Carcinoma, Small Cell; Human; Lung Neoplasms; Neurologic Examination; Tomography, X-Ray Computed",,,,,,,,,,,,,,00338419,,RADLA,,"English","Radiology",Article,Scopus "Looper J.D., Hornback N.B.","The role of chest irradiation in limited small cell carcinoma of the lung treated with combination chemotherapy",1984,"International Journal of Radiation Oncology Biology Physics",10,10,,1855,1860,,,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-0021749132&partnerID=40&rel=R8.0.0","Department of Radiation Oncology, Indiana University School of Medicine, Indianapolis, IN 46223, United States","Between October 1974 and December 1980, 123 patients with limited small cell carcinoma were treated in the Indiana University Medical Center Department of Radiation Oncology. Of these, 115 were treated with preplanned combined modality therapy using irradiation and polychemotherapy (Adriamycin, Cytoxan and Oncovin). All patients received whole brain prophylactic irradiation and were followed a minimum of 2 years. Sixty-six patients were given chest irradiation with all but two receiving 3500-4000 rad while 49 did not receive this treatment. Sixty-five percent of those patients receiving chest irradiation had a complete response to therapy, as opposed to 33% who did not (p < 0.02). The median and overall survivals were significantly different between the 2 groups (423 days vs. 307 days). The overall and long-term survivals were higher in those receiving chest irradiation or resective surgery. Serial chest X rays (and port films, where applicable) were reviewed on all patients to determine sites of failure. Of relapsing patients who did not receive chest irradiation, failure always included the primary site. Of those who had chest irradiation, only 15% of evaluable patients did not relapse in the chest prior to death. This study demonstrates an increased response rate, median survival, and overall survival in patients receiving chest irradiation. The high rate of relapse in the chest suggests the need for more effective control of the primary. This may be accomplished by increasing the dose of chest irradiation or surgical removal when feasible.",,"adjuvant; altretamine; bcg vaccine; cyclophosphamide; doxorubicin; etoposide; lomustine; methotrexate; vincristine; vincristine sulfate; cancer chemotherapy; cancer combination chemotherapy; clinical article; human; lung cancer; lung carcinoma; priority journal; pyradine; radiotherapy; respiratory system; small cell carcinoma; therapy; Adult; Aged; Antineoplastic Combined Chemotherapy Protocols; Carcinoma, Small Cell; Clinical Trials; Combined Modality Therapy; Cyclophosphamide; Doxorubicin; Female; Follow-Up Studies; Human; Lung Neoplasms; Male; Middle Age; Prospective Studies; Random Allocation; Thorax; Vincristine",,"altretamine, 15468-34-5, 2975-00-0, 645-05-6; cyclophosphamide, 50-18-0; doxorubicin, 23214-92-8, 25316-40-9; etoposide, 33419-42-0; lomustine, 13010-47-4; methotrexate, 15475-56-6, 59-05-2, 7413-34-5; vincristine sulfate, 2068-78-2; vincristine, 57-22-7; Antineoplastic Combined Chemotherapy Protocols; CAV protocol; Cyclophosphamide, 50-18-0; Doxorubicin, 23214-92-8; Vincristine, 57-22-7","cytoxan; oncovin",,,,,,,,,,,03603016,,IOBPD,,"English","International Journal of Radiation Oncology Biology Physics",Article,Scopus "Natsumeda Y., Prajda N., Donohue J.P.","Enzymic capacities of purine de novo and salvage pathways for nucleotide synthesis in normal and neoplastic tissues",1984,"Cancer Research",44,6,,2475,2479,,26,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-0021136347&partnerID=40&rel=R8.0.0","Laboratory for Experimental Oncology, Indiana University School of Medicine, Indianapolis, IN 46223, United States","The enzymic capacities of the de novo and the salvage pathways for purine nucleotide synthesis were compared in rat in normal, differentiating, and regenerating liver, and in three hepatomas of widely different growth rates. The activities of the key de novo and salvage enzymes were also determined in mouse lung and Lewis lung carcinoma, in human kidney and liver, and in renal cell carcinoma and hepatocellular carcinomas. A precise and reproducible assay was worked out for measuring the activities of adenine phosphoribosyltransferase (EC 2.4.2.7) and hypoxanthine-guanine phosphoribosyltransferase (HGPRT; EC 2.4.2.8) in crude liver and hepatoma systems. Kinetic studies on the salvage enzymes were carried out in the crude 100,000 x g supernatant fluid from normal liver and rapidly growing hepatoma 3924A. In both tissue extracts, Michaelis-Menten kinetics was observed for adenine phosphoribosyltransferase and HGPRT. The reciprocal plots for 5-phosphoribosyl-1-pyrophosphate (PRPP) of liver and hepatoma enzymes gave apparent K(m)s of 2 μM for adenine phosphoribosyltransferase and 4 μM for HGPRT, showing two orders of magnitude higher affinities for PRPP than that of the rate-limiting enzyme of de novo purine synthesis, amidophosphoribosyltransferase (EC 2.4.2.14) (K(m) = 400 to 900 μM). The apparent K(m) values for adenine of liver and hepatoma adenine phosphoribosyltransferase were 0.6 to 0.9 μM, respectively. For both liver and hepatoma HGPRT, the reciprocal plots for hypoxanthine and guanine yielded the same K(m) of 3 μM. The specific activities of purine phosphoribosyltransferases were markedly higher than that of amidophosphoribosyltransferase in rat thymus, spleen, testis, bone marrow, colon, liver, kidney cortex, lung, heart, brain, and skeletal muscle, but were lower in the small intestine. In hepatomas and regenerating and differentiating liver, the activities of the salvage enzymes were 2.1- to 32-fold higher than that of amidophosphoribosyltransferase. The purine phosphoribosyltransferase activities were also higher than that of amidophosphoribosyltransferase in Lewis lung carcinoma (8.2- to 32-fold), human renal cell carcinoma (3.5 to 22-fold), and hepatocellular carcinoma (3.4- to 30-fold). The high activities and the high affinity to PRPP of the purine phosphoribosyltransferases might explain the lack of linkage of the behavior of these enzymic activities with proliferation in normal, regenerating, differentiating, or neoplastic tissues. In contrast, the specific activity of the amidophosphoribosyltransferase, which is lower than that of the salvage enzymes, is linked with transformation as it is increased in all examined tumors. The high activity and affinity to PRPP of the purine phosphoribosyltransferases indicate the important role which salvage enzymes might play in circumventing the action of inhibitors of de novo purine biosynthesis in cancer chemotherapy.",,"adenine phosphoribosyltransferase; hypoxanthine phosphoribosyltransferase; nucleotide; purine; radioisotope; animal cell; animal experiment; liver; liver cancer; nonhuman; rat; Adenine Phosphoribosyltransferase; Adult; Amidophosphoribosyltransferase; Animal; Carcinoma, Hepatocellular; Human; Hypoxanthine Phosphoribosyltransferase; Infant, Newborn; Kidney Neoplasms; Kinetics; Liver; Liver Neoplasms; Liver Regeneration; Lung Neoplasms; Mice; Nucleotides; Pentosyltransferases; Purine-Nucleoside Phosphorylase; Support, U.S. Gov't, P.H.S.; Tissue Distribution",,"adenine phosphoribosyltransferase, 9027-80-9; hypoxanthine phosphoribosyltransferase, 9016-12-0; purine, 120-73-0; Adenine Phosphoribosyltransferase, EC 2.4.2.7; Amidophosphoribosyltransferase, EC 2.4.2.14; Hypoxanthine Phosphoribosyltransferase, EC 2.4.2.8; Nucleotides; Pentosyltransferases, EC 2.4.2.; Purine-Nucleoside Phosphorylase, EC 2.4.2.1",,,,,,,,,,,,00085472,,CNREA,,"English","Cancer Research",Article,Scopus "Sebolt J.S., Weber G.","Negative correlation of L-glutamine concentration with proliferation rate in rat hepatomas",1984,"Life Sciences",34,3,,301,306,,7,"http://www.scopus.com/scopus/inward/record.url?eid=2-s2.0-0021332051&partnerID=40&rel=R8.0.0","Laboratory for Experimental Oncology, Indiana University School of Medicine, Indianapolis, IN 46223, United States","The concentration of L-glutamine was determined in freeze-clamp samples of normal liver of adult male fed rats (5.7-6.1 μmol/g) and in transplantable hepatomas of vastly different proliferative rates. The L-glutamine concentration in the slowly growing hepatomas was in the range of the normal liver and it decreased in relation to the increase of hepatoma growth rate, in the most rapidly growing tumors amounting to 12% of that of normal liver. In 24-hour regenerating liver, the glutamine content was slightly reduced (by 17%). In normal rat organs of high cell renewal, such as testis, intestinal mucosa, spleen, and thymus, the L-glutamine concentration was 18 to 46% of that of normal rat liver. The L-glutamine content was similar in rat brain and liver, but it was 1.6-fold higher in the heart, and low in the blood. Glutamine synthetase (EC 6.3.1.3) activity in normal adult liver of ACI/N strain rats was 1,000 nmol per hr per mg protein; the activity increased in the very slowly growing hepatoma 20, but decreased markedly in all the other hepatomas. Thus, glutamine synthetase activity was essentially transformation-linked. The negative correlation of glutamine content with growth rate in transplanted hepatomas appears to be more closely linked with the activities of enzymes that utilize glutamine. The low L-glutamine concentration in the rapidly growing hepatomas provides a potential marker for anti-glutamine chemotherapy selectively targeted against the glutamine-utilizing enzymes.",,"animal experiment; cancer growth; cell proliferation; levoglutamide; liver; liver cell carcinoma; nonhuman; rat; Animal; Cell Differentiation; Cell Division; Glutamate-Ammonia Ligase; Glutamine; Hepatectomy; Liver; Liver Neoplasms, Experimental; Liver Regeneration; Male; Rats; Rats, Inbred ACI; Rats, Inbred BUF; Support, U.S. Gov't, P.H.S.; Tissue Distribution",,"Glutamate-Ammonia Ligase, EC 6.3.1.2; Glutamine, 56-85-9",,,,,,,,,,,,00243205,,LIFSA,10.1016/0024-3205(84)90603-9,"English","Life Sciences",Article,Scopus