Super enhancers have been shown to regulate the expression ofoncogenes like Myc. These super enhancers can be targeted by smallmolecule inhibitors to histone readers like BRD4. Inhibitinghistone readers like BRD4 has been leveraged as a therapeuticstrategy to repress oncogene expression (i.e. Myc) in specifictumor types. Can you further explain the rationale behind thisapproach by addressing the following questions? A.) Does BRD4occupy super enhancers to a different extent than regularenhancers? If so, why does BRD4 bind to super enhancersdifferently? B.) Would BRD4 inhibition affect normal enhancers inthe patient’s body to the same extent as the active super enhancersin the patient’s tumor? If yes or no why? C.) Would BRD4 inhibitionin tumors of different origin (lymphoma vs neuroblastoma) affectthe expression of the same oncogenes? If yes or no why?
