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First published online December 11, 2006
doi: 10.1242/10.1242/jcs.03293
Commentary |
Beatson Institute for Cancer Research, Garscube Estate, Switchback Road, Bearsden, Glasgow G61 1BD, UK
e-mail: k.vousden{at}beatson.gla.ac.uk
Accepted 20 September 2006
The p53 tumour suppressor protein can efficiently inhibit tumour development. This activity reflects its ability to induce a number of different responses, including cell cycle arrest and apoptosis. Recent studies have revealed some interesting insights into how the choice of response to p53 is regulated, highlighting a correlation between the activation of cell cycle arrest and survival with the ability of p53 to reduce oxidative stress and protect cells from genotoxic damage. Understanding the molecular mechanisms that determine which response is selected may allow us to modulate these pathways so that therapeutic reactivation of p53 favours apoptotic cell death in tumour cells, but a reversible - and therefore far less toxic - induction of cell cycle arrest in normal cells.
Key words: p53, Apoptosis, Survival
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