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Although BRAF inhibition has demonstrated activity in  BRAF   V600  –mutated brain tumors, ultimately these cancers grow resistant to BRAF inhibitor monotherapy. Parallel activation of the phosphatidylinositol 3-kinase-mammalian target of rapamycin pathway has been implicated as a mechanism of primary and secondary resistance to BRAF inhibition. Moreover, it has been shown specifically that mTOR signaling activation occurs in BRAF-mutant brain tumors. We therefore conducted phase 1 trials combining vemurafenib with everolimus, enrolling five pediatric and young adults with  BRAF   V600  -mutated brain tumors. None of the patients required treatment discontinuation as a result of adverse events. Overall, two patients (40%) had a partial response and one (20%) had 12 mo of stable disease as best response. Co-targeting BRAF and mTOR in molecularly selected brain cancers should be further investigated.

Dual inhibition of BRAF and mTOR in BRAFV600E-mutant pediatric, adolescent, and young adult brain tumors

Dual inhibition of BRAF and mTOR in BRAF^V600E-mutant pediatric, adolescent, and young adult brain tumors