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Certain types of cancer can be pushed into regression by reactivating the tumour suppressor gene p53, suggest two papers published online by Nature. Although both studies used genetic tricks to achieve their effects, they lend support to the idea that p53-boosting drugs could be a useful form of cancer treatment.
p53, which is mutated or inactivated by other alterations in most human cancers, is one of the most studied genes in cancer. But we still don't know whether established tumours can survive and progress if p53 is re-activated. Groups led by Scott W. Lowe and Tyler Jacks now show that even brief reactivation of endogenous p53 can cause a variety of cancers to completely regress in a handful of animal models. The mechanism of regression appears tumour-specific. Jacks' team find that lymphoma cells are coaxed to commit suicide, whilst sarcoma cells start to senesce. Lowe's team report a novel mechanism in their liver carcinoma model whereby cell senescence appears linked to an innate immune response - certain inflammatory molecules are up-regulated, which then help to clear the cancer cells. CONTACT Scott W. Lowe (Cold Spring Harbor Laboratory, NY, USA)
E-mail: lowe@cshl.edu Tyler Jacks (Massachusetts Institute of Technology, Cambridge, MA, USA)
E-mail: tjacks@mit.edu Ronald A. DePinho (Harvard Medical School, Boston, MA, USA)
E-mail: ron_depinho@dfci.harvard.edu Abstracts available online:
Paper 1.
Paper 2. (C) Nature press release.
Message posted by: Trevor M. D'Souza
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