Taking on Challenging Targets: Making MYC Druggable #MMPMID24857145
Horiuchi D; Anderton B; Goga A
Am Soc Clin Oncol Educ Book 2014[]; ä (ä): e497-502 PMID24857145show ga
The transcription factor proto-oncogene c-MYC (hereafter MYC) was first identified more than three decades ago, and has since been found deregulated in a wide variety of the most aggressive human malignancies. As a pleiotropic transcription factor, MYC directly or indirectly controls expression of hundreds of coding as well as non-coding genes, which affect cell cycle entry, proliferation, differentiation, metabolism, and death / survival decisions of normal and cancer cells. Tumors with elevated MYC expression often exhibit highly proliferative, aggressive phenotypes and elevated MYC expression has been correlated with diminished disease-free survival for a variety of human cancers. The use of MYC overexpression or MYC-dependent transcriptional gene signatures as clinical biomarkers is currently being investigated. Furthermore, pre-clinical animal and cell-based model systems have been extensively utilized in an effort to uncover the mechanisms of MYC-dependent tumorigenesis and tumor maintenance. Despite our ever-growing understanding of MYC biology, currently no targeted therapeutic strategy is clinically available to treat tumors that have acquired elevated MYC expression. Here we summarize the progresses being made to discover and implement new therapies to kill MYC over-expressing tumors, a target that was once deemed undruggable.
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Am+Soc+Clin+Oncol+Educ+Book 2014 ; ä (ä): e497-502
