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Most aggressive thyroid cancers are commonly associated with a BRAF  V600E mutation. Preclinical and clinical data in BRAF  V600E cancers suggest that combined BRAF and MEK inhibitor treatment results in a response, but resistance is common. One mechanism of acquired resistance is through persistent activation of tyrosine kinase (TK) signaling by alternate pathways. We hypothesized that combination therapy with BRAF and multitargeting TK inhibitors (MTKI) might be more effective in BRAF  V600E thyroid cancer than in single-agent or BRAF and MEK inhibitors.

A Combinatorial Strategy for Targeting BRAFV600E-Mutant Cancers with BRAFV600E Inhibitor (PLX4720) and Tyrosine Kinase Inhibitor (Ponatinib)