Targeted therapies for metastatic melanoma such as PLX4032 (vemurafenib) have shown dramatic effects in patients. However, resistance to BRAF inhibitors such as PLX4032 soon develops. The result is a need to understand how resistance occurs due to cross talk and how to overcome this through a rational drug combination strategy.
Sally Church on Pharma Strategy Blog delves into the topic of BRAF resistance with demonstrable enthusiasm. In her insightful post she discusses data presented in the plenary session at the recent annual meeting of the American Association for Cancer Research (AACR) by Levi Garraway from Dana Farber.
As Sally discusses in some detail, the research identified a novel mutation in the downstream kinase MEK1 that may be the reason why patients become resistant to PLX4032.