Abstract
Therapy for melanoma is making remarkable progress. Only 8 years after the initial discovery of mutations in the BRAF oncogene, a new small-molecule inhibitor specific for mutant BRAF, PLX4032 (also known as RG7204), induced tumor shrinkage in more than 80% of patients with cutaneous melanoma containing BRAF mutations and extended progression-free survival by an average of 7 months.1,2 Although BRAF-targeted therapy is not curative, it is possible that its combination with immunotherapy to potentiate antitumor T-cell responses may lead to durable responses.3 The mutant BRAF amino acid that is targeted by PLX4032 is present in 50% of cutaneous melanomas . . .
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