Health & Medical Cancer & Oncology

New Targeted Therapies in Melanoma

New Targeted Therapies in Melanoma

Biology of BRAF


The discovery in 2002 of activating mutations in the serine/threonine kinase gene BRAF in approximately 50% of melanomas led to efforts to develop agents to block this kinase. An understanding of the rat sarcoma (RAS)/rapidly accelerated fibrosarcoma/mitogen-activated protein kinase (MEK/MAPK)/extracellular signal-regulated kinase signal transduction pathway was important for the development of drugs to fight melanoma. Mutations have been described at a number of sites in the BRAF gene. All mutations lead to constitutive activity of the MAPK pathway without the need for upstream activation signals, thus resulting in increased proliferation. Approximately 80% of mutations result from the substitution of glutamic acid (E) for valine (V) in codon 600, the BRAF V600E mutation. Other common BRAF mutations in melanoma are V600K (about 16% of mutations in melanoma) and V600D/R (3% of all mutations). These less common variants are found at slightly higher rates in melanomas arising in older patients. A total of 80% of benign and dysplastic nevi harbor the mutation, leading researchers to conclude that the BRAF mutation is necessary for melanoma development but by itself does not cause melanoma development.

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