Melanoma frequently harbors oncogenic mutations in the BRAF gene, which drives
melanoma growth. Therefore, BRAF kinase inhibitors (BRAFi) are developed and approved …

Purpose: Molecular targeted therapy using BRAF and/or MEK inhibitors has been applied to
BRAFV600E-mutant high-grade gliomas (HGG); however, the therapeutic effect is limited by …

Purpose: Dual MAPK pathway inhibition (dMAPKi) with BRAF and MEK inhibitors improves
survival in BRAF V600E/K mutant melanoma, but the efficacy of dMAPKi in non-V600 BRAF …

Background Treatment of metastatic malignant melanoma patients harboring BRAF (V600E)
has improved drastically after the discovery of the BRAF inhibitor, vemurafenib. However …

Summary BRAF (V600E) mutant melanomas treated with inhibitors of the BRAF and MEK
kinases almost invariably develop resistance that is frequently caused by reactivation of the …

The development of BRAF and MEK inhibitors (BRAFi/MEKi) has led to major advances in
melanoma treatment. However, the emergence of resistance mechanisms limits the benefit …

Purpose: Selective RAF-targeted therapy is effective in some patients with BRAFV600E-
mutated glioma, though emergent and adaptive resistance occurs through ill-defined …

Combined BRAF and MEK inhibition is a standard of care in patients with advanced BRAF-
mutant melanoma, but acquired resistance remains a challenge that limits response …

Glioblastoma (GBM) is the most common malignant primary brain tumor. 1 Despite
aggressive multimodality treatment, median overall survival (OS) is 14 to 18 months. 2 One …

The therapeutic benefit of approved BRAF and MEK inhibitors (BRAFi/MEKi) in patients with
brain metastatic BRAF V600E/K–mutated melanoma is limited and transient. Resistance …