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Daniel L. Peterson, Peter J. Sheridan and Willis E. Brown Jr.

trauma. The murine GFAP promoter was fused to the bacterial reporter gene β-galactosidase. The β-galactosidase activity can be readily detected in tissue sections and has no harmful effects in vivo . This model showed baseline GFAP activity in the hippocampus, glial limitans, and along white-matter tracts including the optic nerves, and GFAP expression was proven to be induced within 1 hour of focal injury (needlestick in right frontal lobe). Our laboratory is currently developing transgenic lines that express the temperature-sensitive mutant p53 tumor suppressor gene

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Steffen Albrecht, J. Clay Goodman, Sri Rajagopolan, Moise Levy, David A. Cech and Linda D. Cooley

This case shows structural abnormalities of both copies of chromosome 22 and, in addition to the t(5;9), has other translocations. This complex karyotype is consistent with the malignant nature of the tumor. Mutations of the p53 tumor suppressor gene are now recognized as the most frequent genetic lesion in human malignancies. 3 They occur in all major classes of cancers, including carcinomas, sarcomas, lymphomas, and gliomas. In one study, only one of eight meningiomas had a p53 mutation, but the meningiomas studied were apparently all benign. 20 We therefore

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Frederick F. Lang, Douglas C. Miller, Maxim Koslow and Elizabeth W. Newcomb

combinations of genetic alterations in proto-oncogenes and known or putative tumor suppressor genes. 11, 40 For astrocytic tumors, the genetic alterations most often reported are mutation or alteration of the p53 tumor suppressor gene; 3, 4, 7, 12, 13, 21, 24–28, 34, 37, 41, 46 loss of heterozygosity for chromosome 17p, 4, 7, 10–12, 15, 22, 25, 28, 37, 41, 44, 46, 49 for chromosome 10, 2, 8, 10, 12, 15, 22, 44, 47, 49, 51 for chromosome 9p, 16, 22, 31 or for chromosome 19q; 48 amplification and rearrangement of the epidermal growth factor receptor (EGFR) gene (c- erb B

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Kalman Kovacs, Lucia Stefaneanu, Eva Horvath, Michael Buchfelder, Rudolph Fahlbusch and Wolfgang Becker

proliferating cells in microwave-processed formalin-fixed paraffin sections. J Pathol 168: 357–363, 1992 7. Chang F , Syrjänen S , Tervahauta A , et al : Tumourigenesis associated with the p53 tumour suppressor gene. Br J Cancer 68 : 653 – 661 , 1993 Chang F, Syrjänen S, Tervahauta A, et al: Tumourigenesis associated with the p53 tumour suppressor gene. Br J Cancer 68: 653–661, 1993 8. Davis JRE , Sheppard MC , Heath DA : Giant invasive prolactinoma: a case report and review of nine further

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Julie M. Cunningham, David W. Kimmel, Bernd W. Scheithauer, Judith R. O'Fallon and Paul J. Novotny

70 : 379 – 384 , 1989 Nishizaki T, Orita T, Furutani Y, et al: Flow-cytometric DNA analysis and immunohistochemical measurement of Ki-67 and BUdR labeling indices in human brain tumors. J Neurosurg 70: 379–384, 1989 53. Ohgaki H , Eibl RH , Schwab M , et al : Mutations of the p53 tumor suppressor gene in neoplasms of the human nervous system. Mol Carcinog 8 : 74 – 80 , 1993 Ohgaki H, Eibl RH, Schwab M, et al: Mutations of the p53 tumor suppressor gene in neoplasms of the human nervous system. Mol

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David Y. Eng, Franco DeMonte, Lawrence Ginsberg, Gregory N. Fuller and Kurt Jaeckle

neoplasm was strongly positive for the neuronal marker synaptophysin ( Fig. 1C ) and immunonegative for glial fibrillary acidic protein (GFAP) and for S-100 protein, confirming the diagnosis of a central neurocytoma. Mitotic figures were rare (< 1/10 high-power fields). The MIB-1 (Ki-67 antigen) tumor labeling index was 3.3%. Immunostaining for the p53 tumor suppressor gene was negative. Case 2 Tissue sections from the initial biopsy specimen showed the typical morphological features of central neurocytoma: round tumor cells with perinuclear halos mimicking the

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Christine Decaestecker, Isabelle Salmon, Olivier Dewitte, Isabelle Camby, Philippe Van Ham, Jean-Lambert Pasteels, Jacques Brotchi and Robert Kiss

tumor suppressor gene mutations 5, 10 are helpful in characterizing astrocytic tumor aggressiveness. The computer-assisted microscopic analysis of Feulgen-stained nuclei can also contribute significant prognosis information. 19, 20 In our previous studies we observed that conventional univariate statistical analyses (such as oneway analysis of variance) were not sufficiently powerful to overcome the problem of biological heterogeneity. In fact, multivariate statistical analysis techniques are required to exploit the information contributed by each of the cytometry

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N. Scott Litofsky and Lawrence D. Recht

The tumor suppressor gene, p53, is important in glioma biology. The authors of this paper review its role in cell physiology, epidemiology, glioma progression, prognosis, and therapeutic advances.

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following aneurysmal subarachnoid hemorrhage Jeffrey E. Thomas M.D. 9 1997 3 3 E5 10.3171/foc.1997.3.3.6 FOC.1997.3.3.6 The impact of p53 tumor suppressor gene on glioma biology N. Scott Litofsky M.D. Lawrence D. Recht M.D. 9 1997 3 3 E6 10.3171/foc.1997.3.3.7 FOC.1997.3.3.7 Growth factors in central nervous system development and tumorigenesis Barbara E. Lazio M.D. Lawrence S. Chin M.D. 9 1997 3 3 E7 10.3171/foc.1997.3.3.8 FOC.1997.3.3.8 Current concepts of apoptosis David H. Harter M.D. Patrick F. Doherty M.D. Lawrence S. Chin M.D. 9 1997 3 3 E8 10

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Oliver Dorigo, Sally T. Turla, Svetlana Lebedeva and Ruth A. Gjerset

the poor responsiveness of glioblastoma multiforme to therapy appears to lie in the disease process itself. Genetic changes such as loss of expression of the p53 tumor suppressor gene can result in failure of apoptosis and acquisition of therapy resistance. One of the key modulators of apoptosis in cells that have sustained DNA damage is the p53 nuclear phosphoprotein. 11, 20, 30, 33 Loss of p53 function arising as a result of gene deletion or mutation is common in cancer cells and occurs in some 35 to 60% of glioblastomas multiforme. 1, 10, 31 Recently we have