Abstract
Mutations in BRAF at the 600th codon have proven sensitive to combination BRAF and MEK inhibition. Mutations outside this codon, however, are approximately as common but do not have approved targeted therapy approaches. Herein, we discuss targeting these non-V600 mutation and fusions in BRAF with MEK inhibitors.
Highlights
Developing active, molecularly targeted agents against mutated BRAF has been a major success story of the precision-cancer movement
Mutations affecting the 600th codon may be targeted by several approaches, including mutant-specific BRAF inhibitors, blockers of downstream signal partners MEK1/2, or the combination of both
The management of BRAF V600mutant melanoma, lung cancer, hairy cell leukemia, and thyroid cancer has been transformed by these agents, which produce high response rates, occasionally resulting in durable responses [1,2,3,4,5]
Summary
Developing active, molecularly targeted agents against mutated BRAF has been a major success story of the precision-cancer movement. Mutations affecting the 600th codon may be targeted by several approaches, including mutant-specific BRAF inhibitors, blockers of downstream signal partners MEK1/2, or the combination of both. In contrast to the high-profile success of pharmacologic blockade of mutant BRAF V600, approaches to targeting other mutations in BRAF outside of the 600th codon have been less active.
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