Journal
SCIENCE SIGNALING
Volume 4, Issue 166, Pages -Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/scisignal.2001946
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Funding
- National Institutes of Health
- U.S. Department of Defense
- New Jersey Commission on Cancer Research
- Triple-Negative Breast Cancer Foundation
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Dysregulation of c-MYC plays a critical role in the development of many human cancers. New evidence has uncovered a previously unknown mechanism whereby increased abundance of c-MYC can promote poly(ADP-ribose) polymerase (PARP)-dependent DNA repair pathways and induce relative chemoresistance. The adaptor protein BIN1, whose expression is regulated by c-MYC, interacts with PARP1 and inhibits its enzymatic activity. A model has been proposed in which increased abundance of c-MYC indirectly leads to decreased BIN1 expression, in turn leading to increased PARP activity and resistance to DNA-damaging agents. The clinical implications of these findings are discussed.
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