Selective activation of p53-mediated tumour suppression in high-grade tumours

Melissa R. Junttila, Anthony N. Karnezis, Daniel Garcia, Francesc Madriles, Roderik M. Kortlever, Fanya Rostker, Lamorna Brown Swigart, David M. Pham, Youngho Seo, Gerard I. Evan () and Carla P. Martins
Additional contact information
Melissa R. Junttila: University of California San Francisco
Anthony N. Karnezis: University of California San Francisco
Daniel Garcia: University of California San Francisco
Francesc Madriles: Cancer Research UK Cambridge Research Institute, Li Ka Shing Centre
Roderik M. Kortlever: University of California San Francisco
Fanya Rostker: University of California San Francisco
Lamorna Brown Swigart: University of California San Francisco
David M. Pham: University of California San Francisco
Youngho Seo: University of California San Francisco
Gerard I. Evan: University of California San Francisco
Carla P. Martins: University of California San Francisco

Nature, 2010, vol. 468, issue 7323, 567-571

Abstract: Limits to antitumour effect of p53 restoration Inactivation of the p53 tumour-suppressor pathway is a common feature of human cancers, prompting suggestions that restoring p53 function in established tumours might be an effective therapy. However, two papers in this week's Nature highlight a practical limitation of p53-directed cancer therapeutics. They show in a K-Ras-driven lung-cancer model that p53-mediated tumour suppression is engaged only at a late stage of tumour progression, when the K-Ras oncogenic signal reaches a threshold that is sufficient to activate the ARF-p53 pathway. This means that p53 re-expression fails to restrict the early stages of tumorigenesis, although it does induce regression of more aggressive tumours.

Date: 2010
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DOI: 10.1038/nature09526

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