Modelling Myc inhibition as a cancer therapy

Laura Soucek, Jonathan Whitfield, Carla P. Martins, Andrew J. Finch, Daniel J. Murphy, Nicole M. Sodir, Anthony N. Karnezis, Lamorna Brown Swigart, Sergio Nasi and Gerard I. Evan ()
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Laura Soucek: University of California, San Francisco, California 94143-0875, USA
Jonathan Whitfield: University of California, San Francisco, California 94143-0875, USA
Carla P. Martins: University of California, San Francisco, California 94143-0875, USA
Andrew J. Finch: University of California, San Francisco, California 94143-0875, USA
Daniel J. Murphy: University of California, San Francisco, California 94143-0875, USA
Nicole M. Sodir: University of California, San Francisco, California 94143-0875, USA
Anthony N. Karnezis: University of California, San Francisco, California 94143-0875, USA
Lamorna Brown Swigart: University of California, San Francisco, California 94143-0875, USA
Sergio Nasi: Istituto di Biologia e Patologia Molecolari, C.N.R., University La Sapienza
Gerard I. Evan: University of California, San Francisco, California 94143-0875, USA

Nature, 2008, vol. 455, issue 7213, 679-683

Abstract: Myc back in the limelight The Myc gene encodes for a transcription factor that is central to gene regulation in normal cells. It is also an oncogene, overexpressed or amplified in many different types of tumour. Though this makes it a candidate target for antitumour drugs, its involvement in many normal cell functions, lack of evidence of therapeutic efficacy and the difficulty of targeting it mean that it is not top of many lists of potential targets. That could change. Using a mouse model of Ras-dependent lung cancer in which Myc function can in effect be turned on and off, Soucek et al. show that inhibition of endogenous Myc triggers tumour regression. Significantly, although systemic inhibition of Myc has effects in other tissues, these were readily reversible, suggesting that Myc might be a valid anticancer target.

Date: 2008
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DOI: 10.1038/nature07260

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