Restoration of p53 function leads to tumour regression in vivo

Andrea Ventura, David G. Kirsch, Margaret E. McLaughlin, David A. Tuveson, Jan Grimm, Laura Lintault, Jamie Newman, Elizabeth E. Reczek, Ralph Weissleder and Tyler Jacks ()
Additional contact information
Andrea Ventura: Massachusetts Institute of Technology
David G. Kirsch: Massachusetts Institute of Technology
Margaret E. McLaughlin: Massachusetts Institute of Technology
David A. Tuveson: Massachusetts Institute of Technology
Jan Grimm: Massachusetts General Hospital
Laura Lintault: Massachusetts Institute of Technology
Jamie Newman: Massachusetts Institute of Technology
Elizabeth E. Reczek: Massachusetts Institute of Technology
Ralph Weissleder: Massachusetts General Hospital
Tyler Jacks: Massachusetts Institute of Technology

Nature, 2007, vol. 445, issue 7128, 661-665

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/nature05541

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