title: Treatment of BRAF-mutated advanced cutaneous melanoma.
abstract: The field of melanoma oncology has recently awakened with groundbreaking scientific advances and innovative therapeutic strategies. New groups of small-molecule kinase inhibitors targeting the aberrant mitogen-activated protein kinase (MAPK) pathway activation mediating tumor growth and survival have revolutionized the therapeutic approach to advanced melanoma. BRAF and MEK inhibitors are the first groups of agents that improved all clinical efficacy endpoints, including response rate, progression-free survival (PFS) and overall survival (OS), in patients with BRAF-mutated advanced melanoma when compared with standard chemotherapy in randomized phase III studies. However, despite the impressive clinical responses in patients with BRAF mutant advanced melanoma, duration of response to MAPK pathway-targeted therapy remains limited, implicating rapid emergence of drug resistance. Diverse strategies to overcome tumor resistance to MAPK inhibitors, the focus of today's translational and clinical research, will further improve the clinical outcome for patients with BRAF-mutated advanced melanoma in the near future.
authors.affiliation: Pharmacy Clinical Programs, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
authors.forename: Van Anh
authors.initials: VA
authors.lastname: Trinh
authors.affiliation: The Third Affiliated Hospital of Harbin Medical University, Harbin 150081, China.
authors.forename: Yan
authors.initials: Y
authors.lastname: You
authors.affiliation: Department of Melanoma Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA. wenjhwu@mdanderson.org.
authors.forename: Wen-Jen
authors.initials: WJ
authors.lastname: Hwu
keywords: Advanced melanoma; BRAF inhibitor; BRAF inhibitor resistance; BRAF mutation; LGX818; MEK inhibitor; MEK162; cobimetinib; dabrafenib; dual mitogen-activated protein kinase (MAPK) blockade; selumetinib; trametinib; vemurafenib