Melanoma Treatment (Professional) (cont.)
IN THIS ARTICLE
Cellular and Molecular Classification of Melanoma
Following is a list of clinicopathologic cellular subtypes of malignant melanoma. These should be considered descriptive terms of historic interest only as they do not have independent prognostic or therapeutic significance.
Molecular characterization of melanoma is an active area of research. Activating mutations in the BRAF (V-raf murine sarcoma viral oncogene homolog B1) gene, first reported in 2002, are the most frequent mutation in cutaneous melanoma. Approximately 40% to 60% of malignant melanomas harbor a single nucleotide transversion. The majority have a mutation that results in a substitution from valine to glutamic acid at position 600 BRAF (V600E); less frequent mutations include valine 600 to lysine or arginine residues (V600K/R). Drugs that target this mutation by inhibiting BRAF are under evaluation in clinical trials. One such drug, vemurafenib, was approved by the U.S. Food and Drug Administration (FDA) in 2011 for the treatment of unresectable or metastatic melanoma in patients who test positive for the BRAF mutation as detected by an FDA-approved test (e.g., cobas® 4800 BRAF V600 Mutation Test).
In smaller subsets of cutaneous melanoma, other activating mutations have been described, including NRAS [neuroblastoma RAS viral (v-ras) oncogene homolog], c-KIT, and CDK4 (cyclin-dependent kinase 4).
Drugs developed to target these mutations are currently in clinical trials. Additional oncogenes and tumor-suppressor gene candidates currently under evaluation include P13K, AKT, P53, PTEN, mTOR, Bcl-2, MITF.
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