Promises from Trametinib in RAF Active Tumors

Progression of human cancer occurs through genetic changes in cancer cells that activate biochemical pathways governing hallmarks of cancer, including proliferation and tumor-cell survival,1 among others. Tumor growth factor receptors activate RAS oncoproteins, which subsequently activate a kinase cascade that includes RAF, MEK, and ERK kinases. This pathway is mutated to promote tumor growth in at least 20% of cancers.2 The RAS–MEK–ERK pathway is thus a focus of intense interest for the development of cancer drugs. First fruits from this quest have yielded drugs directed against growth factor receptors, including the monoclonal antibody trastuzumab and the small molecules erlotinib and . . .