692 Using a novel p300 HAT inhibitor as epigenetic therapy to treat BRAF inhibitor-resistant melanoma cells

Abstract

Despite initial response to targeted therapy in many patients with advanced melanoma, innate and acquired resistance to BRAF inhibitor treatment limits the long-term success of monotherapy with these agents. Reactivation of the mitogen activated protein kinase (MAPK) pathway in melanoma cells is a crucial mechanism in the development of resistance to targeted therapy and usually does not occur through new genetic mutations. Therefore, epigenetic alterations such as histone modifications have emerged as key mediators of the ability of melanoma cells to achieve resistance.