Abstract：
:TP53 is mutated in most types of human cancers and is one of the most popular genes in cancer research. The p53 protein is a sensor of multiple forms of genotoxic, oncogenic and non-genotoxic stress. It suppresses growth and controls survival of stressed cells, and as such, is the focal point of selection pressures in tissues exposed to carcinogens or to oncogenic changes. Thus, the clonal expansion of cells with mutations in TP53 may be seen as the result of a selection process intrinsic to the natural history of cancer. In this review, we discuss the nature of these various forms of selection pressure. We present a hypothesis to explain why TP53 is often mutated as either an early or a late event in cancer. Furthermore, we also summarise current knowledge on the molecular consequences of mutation for loss of wild-type protein function, dominant-negative activity, and a possible gain of oncogenic function.
journal_name
Biochimiejournal_title
Biochimieauthors
Guimaraes DP,Hainaut Pdoi
10.1016/s0300-9084(01)01356-6keywords:
subject
Has Abstractpub_date
2002-01-01 00:00:00pages
83-93issue
1eissn
0300-9084issn
1638-6183pii
S0300908401013566journal_volume
84pub_type
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