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Comparative Study of p53 Gene and Protein Alterations in Human Astrocytic Tumors

Comparative Study of p53 Gene and Protein Alterations in Human Astrocytic Tumors Abstract The p53 gene is a tumor suppressor gene involved in many common malignancies, including astrocytomas. Genetic analysis of the p53 gene and immunohistochemistry of the p53 protein have each been used to screen astrocytomas. To compare these methods, we performed immunohistochemistry with the monoclonal antibody PAb 1801 and single-strand conformational polymorphism (SSCP) with sequence analysis on 34 astrocytic tumors (WHO grades II, HI and IV). Seven cases had detectable p53 protein and gene mutations, while twelve cases had neither detectable protein nor gene mutations. Four tumors had frameshift mutations in the p53 gene that were not revealed by immunohistochemistry. One tumor had a genetic polymorphism and no detectable p53 protein. Ten tumors had p53 protein accumulation but no mutations by SSCP; these cases may represent p53 mutations outside of the conserved exons or elevated levels of wild-type p53 protein. Thus, some p53 mutations are missed with PAb 1801 immunohistochemistry alone. p53 immunohistochemistry, however, may reveal p53 accumulation independent of mutations in the conserved portions of the gene. Finally, we suggest that glioblastomas with p53 mutations in the conserved region of the gene may be a subset that are more common in women and in younger patients. Age, Astrocytoma, Glioblastoma multiforme, Immunohistochemistry, p53 gene, p53 protein, Sex This content is only available as a PDF. Author notes DNL is supported by NIH CA 09144. AvD is supported by the Deutsche Forschungsgemeinschaft. RYC is a predoctoral trainee of the NIH Medical Scientist Training Program (T32 GMO 7753-12). M-PR is supported by the Government of Navarra, Spain. ADT is supported by NIH POI CA 44768. This work was supported by Faculty Research Award #CD 455 of the American Cancer Society to BRS and by a generous grant from the Preuss Foundation. © 1993 by the American Association of Neuropathologists http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Journal of Neuropathology & Experimental Neurology Oxford University Press

Comparative Study of p53 Gene and Protein Alterations in Human Astrocytic Tumors

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Publisher
Oxford University Press
Copyright
© 1993 by the American Association of Neuropathologists
ISSN
0022-3069
eISSN
1554-6578
DOI
10.1097/00005072-199301000-00005
Publisher site
See Article on Publisher Site

Abstract

Abstract The p53 gene is a tumor suppressor gene involved in many common malignancies, including astrocytomas. Genetic analysis of the p53 gene and immunohistochemistry of the p53 protein have each been used to screen astrocytomas. To compare these methods, we performed immunohistochemistry with the monoclonal antibody PAb 1801 and single-strand conformational polymorphism (SSCP) with sequence analysis on 34 astrocytic tumors (WHO grades II, HI and IV). Seven cases had detectable p53 protein and gene mutations, while twelve cases had neither detectable protein nor gene mutations. Four tumors had frameshift mutations in the p53 gene that were not revealed by immunohistochemistry. One tumor had a genetic polymorphism and no detectable p53 protein. Ten tumors had p53 protein accumulation but no mutations by SSCP; these cases may represent p53 mutations outside of the conserved exons or elevated levels of wild-type p53 protein. Thus, some p53 mutations are missed with PAb 1801 immunohistochemistry alone. p53 immunohistochemistry, however, may reveal p53 accumulation independent of mutations in the conserved portions of the gene. Finally, we suggest that glioblastomas with p53 mutations in the conserved region of the gene may be a subset that are more common in women and in younger patients. Age, Astrocytoma, Glioblastoma multiforme, Immunohistochemistry, p53 gene, p53 protein, Sex This content is only available as a PDF. Author notes DNL is supported by NIH CA 09144. AvD is supported by the Deutsche Forschungsgemeinschaft. RYC is a predoctoral trainee of the NIH Medical Scientist Training Program (T32 GMO 7753-12). M-PR is supported by the Government of Navarra, Spain. ADT is supported by NIH POI CA 44768. This work was supported by Faculty Research Award #CD 455 of the American Cancer Society to BRS and by a generous grant from the Preuss Foundation. © 1993 by the American Association of Neuropathologists

Journal

Journal of Neuropathology & Experimental Neurology – Oxford University Press

Published: Jan 1, 1993

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