MYC on the path to cancer

Chi V. Dang

Research output: Contribution to journalArticle

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 languageEnglish (US)
Pages (from-to)22-35
Number of pages14
JournalCell
Volume149
Issue number1
DOIs
StatePublished - Mar 30 2012
Externally publishedYes

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Tumors
Dimerization
Glutamine
MicroRNAs
Metabolism
Neoplasms
Biomass
Chemical activation
Glucose
Molecules
Pharmaceutical Preparations
Proteins
Oncogenes
Energy Metabolism
Therapeutics
Growth

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

Cite this

MYC on the path to cancer. / Dang, Chi V.

In: Cell, Vol. 149, No. 1, 30.03.2012, p. 22-35.

Research output: Contribution to journalArticle

Dang, CV 2012, 'MYC on the path to cancer', Cell, vol. 149, no. 1, pp. 22-35. https://doi.org/10.1016/j.cell.2012.03.003
Dang, Chi V. / MYC on the path to cancer. In: Cell. 2012 ; Vol. 149, No. 1. pp. 22-35.
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