Abstract
Nearly all melanomas harbor constitutive activity in the mitogen activated protein kinase pathway, which contributes to their growth and oncogenic behavior. This activity can arise as the result of the activating BRAF V600E, N-Ras and c-Kit mutations or through autocrine growth factor signaling. There is currently much interest in targeting two constituents of the pathway, BRAF and MEK, as a novel approach to melanoma therapy. In the current review we discuss the role of this pathway in melanoma progression and some of the issues that face the clinical translation of BRAF and MEK inhibitors as antagonists of mitogen activated protein kinase pathway in this disease.
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