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Accumulation of wild‐type p53 in meningiomas
Author(s) -
Ellison D. W.,
Lunec J.,
Gallagher P. J.,
Steart P. V.,
Jaros E.,
Gatter K. C.
Publication year - 1995
Publication title -
neuropathology and applied neurobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.538
H-Index - 95
eISSN - 1365-2990
pISSN - 0305-1846
DOI - 10.1111/j.1365-2990.1995.tb01040.x
Subject(s) - gene product , gene , exon , biology , mutation , tumor suppressor gene , p53 protein , cancer research , gene mutation , apoptosis , dna damage , dna , dna repair , microbiology and biotechnology , gene expression , genetics , carcinogenesis
The p53 tumour suppressor gene contributes to the regulation of DNA repair and the initiation of apoptosis. Mutations of this gene and nuclear accumulation of its protein product are features of a large variety of turnours. A histological spectrum of meningiomas, including anaplastic examples and a meningosarcoma. was analysed for accumulation of the p53 protein and mutations in exons 4–9 of the p53 gene. No mutations were found, but 9134 (26%) tumours showed accumulation of the p53 protein. The p53‐positive meningiomas came from across the histological spectrum and were not restricted to the anaplastic group. The accumulation of wild‐type p53 in a proportion of meningiomas may reflect this gene's role in DNA repair, or its enhanced stability when bound to cellular proteins such as the mdm‐2 gene product.