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The p53 gene and its role in human brain tumors
Author(s) -
Bögler Oliver,
Su Huang H.J.,
Kleihues Paul,
Cavenee Webster K.
Publication year - 1995
Publication title -
glia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.954
H-Index - 164
eISSN - 1098-1136
pISSN - 0894-1491
DOI - 10.1002/glia.440150311
Subject(s) - biology , allele , tumor suppressor gene , gene , mutation , germline , mutant , glioma , genetics , suppressor , germline mutation , cancer research , carcinogenesis
Mutation of the p53 gene is among the most common lesions in a variety of human tumors, including those of the central nervous system. In most instances, mutation of one p53 allele is followed by loss of the remaining wild‐type allele, resulting in cells with a complete absence of functional wild‐type p53 protein. However, in some situations, such as at initiation of spontaneously arising gliomas or as the germline configuration of patients with the Li‐Fraumeni syndrome, cells clearly carry both wild‐type and mutant p53 alleles. These observations lead to the hypothesis that p53 mutations can give rise to loss of tumor suppressor functions as well as to gain of oncogenic transformation capabilities. In this review, we define the types of mutations that occur in the p53 gene in various glial tumors, contrast that with the spectra described in other human tumor types, and discuss the biochemistry and physiology of the p53 protein and its ability to regulate and be regulated by other gene products. We use this information to propose roles for p53 in the initiation and progression of human gliomas. © 1995 Wiley‐Liss, Inc.