Journal
CELLULAR SIGNALLING
Volume 23, Issue 1, Pages 6-13Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.cellsig.2010.07.004
Keywords
Oncogene-induced senescence; Tumourigenesis; p53; Rb
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Funding
- Leukaemia and Lymphoma Research
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Aberrant oncogenic signals are typically counteracted by anti-proliferative mechanisms governed principally by the p53 and Rb tumour-suppressor proteins. Apoptosis is firmly established as a potent anti-proliferative mechanism to prevent tumour growth but it is only in recent years that oncogene-induced senescence has achieved similar recognition. Senescence is defined as an irreversible cell-cycle arrest suggesting that entry of oncogene-expressing cells into this static yet viable state is permanent. However, tumours do develop and express the very same oncogenes that landed them in jail. We ask whether this is because rogue incipient cancer cells find ways to escape this imposed imprisonment or otherwise entirely avoid capture by senescence gate-keepers. (C) 2010 Elsevier Inc. All rights reserved.
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