About MYC Driven Cancers
The MYC gene is a critical regulator of cell growth, division, and metabolism. However, when MYC becomes dysregulated, it can drive the development and progression of cancer. Abnormal MYC activity—through gene amplification, chromosomal rearrangements, overexpression or increased protein stability—has been identified in up to 70% of human cancers. This dysregulation contributes to the growth of a wide range of solid tumors, including pancreatic, lung, breast, ovarian, endometrial, colorectal, prostate, and kidney cancers.
BET Inhibitors and MYC Driven Cancers
BET inhibitors have been shown to downregulate the expression of the MYC oncogene by directly disrupting the interaction of BRD4 with regulatory regions called super-enhancers of the MYC chromatin. The combination of BET inhibitors with HDAC inhibitors may have a synergistic effect that could be harnessed to treat patients with MYC-driven cancers. An NCI sponsored trial (NCT05053971) is evaluating the combination of ZEN-3694 and HDAC inhibitor, entinostat, in solid tumors including pancreatic cancer.
