BRAF/MEK Inhibition in Melanoma: An Update
Lisa A. Kottschade, APRN, MSN, CNP, and Kathleen M. Madden, RN, MSN, FNP-BC, AOCNP®, APHN
Mayo Clinic, Rochester, Minnesota; and Laura and Isaac Perlmutter Clinical Cancer Center at NYU Langone Medical Center, New York City, New York
Authors’ disclosures of conflicts of interest are found at the end of this article.
Lisa A. Kottschade, APRN, MSN, CNP, Mayo Clinic, Department of Oncology, 200 First Street SW, Rochester, MN 55905.
J Adv Pract Oncol 2018;9(suppl 1):31–38 |
© 2018 Harborside™
Melanoma accounts for significant mortality, and its incidence continues to rise. Extensive research regarding the molecular basis of melanoma has identified a critical role for the aberrantly activated MAPK pathway in its pathogenesis, which is now the basis for targeted therapy. While BRAF inhibitors were initially associated with improved outcomes in BRAF-mutant melanoma, acquired resistance is known to cause relapse and refractory disease. Combining BRAF inhibitors with MEK inhibitors has now emerged as a standard of care for treating both metastatic and adjuvant melanoma patients whose tumors harbor BRAF V600 mutations. This review article outlines the role of the MAPK pathway and BRAF mutations in melanoma and examines the efficacy of BRAF and MEK inhibitors in overcoming current challenges in the treatment of patients with melanoma. The safety and effectiveness of newly approved BRAF/MEK combinations is also reviewed.
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