Senescence and tumour clearance is triggered by p53 restoration in murine liver carcinomas

Wen Xue, Lars Zender, Cornelius Miething, Ross A. Dickins, Eva Hernando, Valery Krizhanovsky, Carlos Cordon-Cardo and Scott W. Lowe ()
Additional contact information
Wen Xue: Cold Spring Harbor Laboratory
Lars Zender: Cold Spring Harbor Laboratory
Cornelius Miething: Cold Spring Harbor Laboratory
Ross A. Dickins: Cold Spring Harbor Laboratory
Eva Hernando: Memorial Sloan-Kettering Cancer Center
Valery Krizhanovsky: Cold Spring Harbor Laboratory
Carlos Cordon-Cardo: Memorial Sloan-Kettering Cancer Center
Scott W. Lowe: Cold Spring Harbor Laboratory

Nature, 2007, vol. 445, issue 7128, 656-660

Abstract: p53 and tumour regression The p53 tumour suppressor is either mutated or inactivated by other alterations in most human cancers. Two papers in this issue show that even brief reactivation of the endogenous p53 genes in established tumours can cause cancer regression in some animal models. In some tumours, p53 reactivation causes cellular senescence associated with an innate immune response that contributes to tumour clearance. These experiments used gene manipulation to alter p53 levels, but they lend further support to the idea that p53-boosting drugs could be a useful form of cancer treatment.

Date: 2007
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DOI: 10.1038/nature05529

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