Finding cancer’s weakest link
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1 Department of Pathology and Helen Diller Family Comprehensive Cancer Center, University of California San Francisco, CA 94143, USA
2Department of Biochemistry, University of Cambridge, Cambridge CB2 1GA, UK
Received: December 20, 2011; Accepted: December 20, 2011; Published: December 22, 2011;
Keywords: Myc inhibition, tumor, microenvironment, cancer therapeutics
Gerard I. Evan, email:
The biological programs of vertebrates exhibit a remarkable degree of functional degeneracy, adaptive compensation and robustness, to preserve homeostasis and generate reproducible phenotypic outputs irrespective of variations in signal strength, noise and quality. Cancers are difficult to treat not only because they are so mechanistically diverse but also because they adapt or evolve in response to any pharmacological elective pressure we impose upon them. Hence, an ideal cancer drug target would exert a function both necessary for cancer cell survival and functionally non-redundant, rendering it impossible for tumor cells to compensate for, or evolve independence from, the inhibitory effect of any drug aimed at that target. In this review, we discuss the unique, non-degenerate and highly pleiotropic role played by Myc in coordinating, engaging and maintaining the diverse intracellular and extracellular programs required for cell proliferation in vivo. These properties make Myc a compelling candidate cancer drug target, at least in principle: an assertion recently reinforced by new in vivo genetic data.
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