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Cell Signal. 2011 Jan;23(1):6-13. doi: 10.1016/j.cellsig.2010.07.004. Epub 2010 Jul 13.

Jailbreak: oncogene-induced senescence and its evasion.

Author information

1
Division of Molecular Histopathology, Department of Pathology, University of Cambridge, Lab Block Level 3, Addenbrooke's Hospital, Cambridge, UK. fkem3@cam.ac.uk

Abstract

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.

PMID:
20633638
DOI:
10.1016/j.cellsig.2010.07.004
[Indexed for MEDLINE]

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