Identification of genes that are modulated by BET inhibitors in cancer cells to identify robust pharmacodynamic marker for monitoring target engagement of BET family bromodomain inhibitors in tumors and surrogate tissue. Homo sapiens

Competitive inhibitors of acetyl-lysine binding to the bromodomains of the BET (bromodomain and extra terminal) family are being developed for the treatment of solid and heme malignancies. BET family member BRD4 function at enhancers/super-enhancers has been shown to sustain signal-dependent or pathogenic gene expression programs. Overall design: Microarray study which included biological triplicates of the DMSO (Vehicle), MS417 (BETi) and C1 3 and 6 hr treated MiaPaCa-2 and NCI-H1299 cell line samples (n=36). C1 treatment is included as a inactive compound for the BETi.