Treatment of Advanced BRAF-Mutated Colorectal Cancer: Where We Are and Where We Are Going

In recent years, studies on the molecular typing of colorectal cancer have matured, and the V-raf murine sarcoma viral oncogene homolog B (BRAF) of the mitogen-activated protein kinase pathway has been shown to be an important effector molecule of this pathway and regulates the occurrence and development of colorectal cancer. Clinical observations indicate that colorectal cancer patients harboring the BRAF V600E mutation have a worse prognosis than BRAF wild type patients. Several resistance mechanisms have been identified that have led to the development of different treatment strategies, which have shown encouraging activity in early clinical trials. Therefore, a reasonable combination of targeted therapies is expected to further enhance the efficacy of selective BRAF inhibitors. Moreover, some CRC patients with high microsatellite instability or a mismatch repair deficiency seem to be susceptible to checkpoint inhibitors with objective and sustained clinical responses, providing new opportunities for patients with advanced disease. This article primarily explores 3 aspects of the treatment strategies for advanced BRAF-mutated colorectal cancer; chemotherapy, targeted therapy, and immunotherapy.