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Jailbreak: oncogene-induced senescence and its evasion.
MedLine Citation:
PMID:  20633638     Owner:  NLM     Status:  In-Process    
Abstract/OtherAbstract:
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.
Authors:
Fiona K E McDuff; Suzanne D Turner
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-07-13
Journal Detail:
Title:  Cellular signalling     Volume:  23     ISSN:  1873-3913     ISO Abbreviation:  Cell. Signal.     Publication Date:  2011 Jan 
Date Detail:
Created Date:  2010-10-18     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8904683     Medline TA:  Cell Signal     Country:  England    
Other Details:
Languages:  eng     Pagination:  6-13     Citation Subset:  IM    
Copyright Information:
Copyright © 2010 Elsevier Inc. All rights reserved.
Affiliation:
Division of Molecular Histopathology, Department of Pathology, University of Cambridge, Lab Block Level 3, Addenbrooke's Hospital, Cambridge, UK. fkem3@cam.ac.uk
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