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Carcinogenesis Advance Access originally published online on May 11, 2005
Carcinogenesis 2005 26(8):1317-1322; doi:10.1093/carcin/bgi122
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Carcinogenesis vol.26 no.8 © Oxford University Press 2005; all rights reserved.

REVIEW

Complicating the complexity of p53

Karen S. Yee and Karen H. Vousden *

The Beatson Institute for Cancer Research, Garscube Estate, Switchback Road, Bearsden, Glasgow G61 1BD, UK

* To whom correspondence should be addressed. Tel: +44 (0)141 330 2424; Fax: +44 (0)141 943 0372; Email: k.vousden{at}beatson.gla.ac.uk

Recent studies have suggested that the straightforward role of p53 as a transcription factor that functions by inducing apoptotic target genes to eliminate developing tumor cells is only part of a much more complicated story. There is now a firm body of evidence supporting a transcriptionally independent activity of p53 as a functional, if not structural, homologue of the BH3-only proteins. Although this information adds another nuance to the mechanism by which p53 can induce apoptosis, further studies indicate that the apoptotic function of p53 represents only a part of its tumor suppressive activity. Although complicating our understanding of p53, these new insights may also provide some exciting new targets for the design of therapeutics that can reactivate p53 in cancers.


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