Abstract
Background: BRAF mutations are identified in many advanced cancers. Despite the curative approaches developed with targeted therapies (BRAF and/or MEK inhibitors (BRAFi and MEKi)) for patients with V600 (Class 1) BRAF mutant cancers, optimal strategies for oncogenic non-V600 BRAF mutant tumors have not been established. Class 2 BRAF mutations are oncogenic non-V600 mutations that signal as RAS-independent dimers. Clinical data supports efficacy of BRAFi+MEKi in some Class 2 BRAF mutant tumors – but this strategy may not be as effective as it is for Class 1 BRAF mutant tumors.
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