- Solid Tumors
- Pipeline Molecules
- Alliance Partners
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Gene expression is controlled through access to DNA, which is mediated by epigenetic modifications to histones.1,2 Bromodomain and extra-terminal motif (BET) proteins are epigenetic “readers” that bind to acetylated lysine residues on histone tails.3,4 BET proteins regulate initiation and continuation of transcription of key cell cycle control genes by recruiting and interacting with transcription factors and RNA polymerase II.5-7 Additionally, BET proteins can “bookmark” genes by remaining bound to chromatin during mitosis, thereby speeding reinitiation of transcription.5 Superenhancers, which are noncoding regions of DNA critical to oncogene transcription and maintenance of cancer cell identity, are observed to have high densities of BET binding.8
Preclinical studies suggest that inhibition of BET may result in the downregulation of key cell cycle regulatory genes, cell cycle arrest, and apoptosis of tumor cells.4,9
Celgene is investigating BET inhibitors, including CC-90010 and FT-1101, for the treatment of solid tumors and hematologic malignancies.