期刊
JOURNAL OF PATHOLOGY
卷 223, 期 2, 页码 127-136出版社
WILEY
DOI: 10.1002/path.2783
关键词
apoptosis; cell cycle arrest; senescence; genotoxic stress; radiation; mouse
资金
- NCI NIH HHS [P30 CA016672] Funding Source: Medline
- NATIONAL CANCER INSTITUTE [P30CA016672] Funding Source: NIH RePORTER
The tumour suppressor p53 pathway is often inactivated by multiple mechanisms in the genesis of human cancers. Aberrant cellular proliferation, DNA damage, hypoxia, and ribosomal stress cause activation of the p53 tumour suppressor with multiple possible consequences to the cell: cell death, cell cycle arrest, or senescence. These mechanisms ultimately ensure that the cell does not replicate, and are thus potent tumour suppressor mechanisms. An important question that has eluded the field is how p53 makes these cell fate decisions. This review summarizes the current status of knowledge regarding p53-mediated stress and tissue-dependent cell fate decisions in mouse models and human tumours. Copyright. (C) 2010 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
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