MYC on the path to cancer

Chi V. Dang

doi:10.1016/j.cell.2012.03.003

MYC on the path to cancer

Chi V. Dang

Research output: Contribution to journal › Review article › peer-review

1641 Scopus citations

Abstract

The MYC oncogene contributes to the genesis of many human cancers. Recent insights into its expression and function have led to therapeutic opportunities. MYC's activation by bromodomain proteins could be inhibited by drug-like molecules, resulting in tumor inhibition in vivo. Tumor growth can also be curbed by pharmacologically uncoupling bioenergetic pathways involving glucose or glutamine metabolism from Myc-induced cellular biomass accumulation. Other approaches to halt Myc on the path to cancer involve targeting Myc-Max dimerization or Myc-induced microRNA expression. Here the richness of our understanding of MYC is reviewed, highlighting new biological insights and opportunities for cancer therapies.

Original language	English (US)
Pages (from-to)	22-35
Number of pages	14
Journal	Cell
Volume	149
Issue number	1
DOIs	https://doi.org/10.1016/j.cell.2012.03.003
State	Published - Mar 30 2012
Externally published	Yes

ASJC Scopus subject areas

General Biochemistry, Genetics and Molecular Biology

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10.1016/j.cell.2012.03.003

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title = "MYC on the path to cancer",

abstract = "The MYC oncogene contributes to the genesis of many human cancers. Recent insights into its expression and function have led to therapeutic opportunities. MYC's activation by bromodomain proteins could be inhibited by drug-like molecules, resulting in tumor inhibition in vivo. Tumor growth can also be curbed by pharmacologically uncoupling bioenergetic pathways involving glucose or glutamine metabolism from Myc-induced cellular biomass accumulation. Other approaches to halt Myc on the path to cancer involve targeting Myc-Max dimerization or Myc-induced microRNA expression. Here the richness of our understanding of MYC is reviewed, highlighting new biological insights and opportunities for cancer therapies.",

author = "Dang, {Chi V.}",

note = "Funding Information: I thank the reviewers for comments. Our primary work is supported in part by the Leukemia and Lymphoma Foundation, National Institutes of Health, National Cancer Institute, an AACR Stand-Up-to-Cancer translational grant, and the Abramson Family Cancer Research Institute. I apologize for omissions, which necessarily happen because of space limitation. C.V.D. is The John H. Glick, MD, Professor.",

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MYC on the path to cancer

Abstract

ASJC Scopus subject areas

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