BRAF-Directed Therapy in Metastatic Colorectal Cancer

Abstract

Activating BRAF (V-raf murine sarcoma viral oncogene homolog B) mutations occur in approximately 5% to 10% of patients with metastatic colorectal cancer, mostly V600E mutation, and it is associated with distinct clinical and pathological features. To date, there are no approved treatments to target this mutation. BRAF inhibitor monotherapy has limited efficacy, in contrast to metastatic melanoma. Combination strategies that block not only BRAF mutated kinase but other alternative pathways are ongoing and have demonstrated improved activity. This review aims to provide data about new strategies to target to BRAF gene mutation in metastatic colorectal cancer.

Conflict of interest statement

Conflict of interest: The authors have declared that no conflict of interest exists

Figures

Figure 1

The combination treatment strategies in BRAF mutant CRC CRC=colorectal cancer; EGFR=epidermal growth factor receptor; BRAF= V-raf murine sarcoma viral oncogene homolog B; MEK=mitogen-activated extracellular signaling kinase; PIK3CA= phosphatidylinositol 3-kinase, catalytic subunit alpha; Bcl-2= B-cell lymphoma 2; i, inh.= inhibitor

Figure 2

Actionable drugs in proliferation pathway that have been evaluated in BRAFmut CRC