Abstract

Personalized medicine has long been a mainstay of the treatment of localized melanoma, involving surgical decisions that are individualized on the basis of measured differences as small as 0.01 mm, as well as other biomarkers of metastatic potential, such as the presence of ulceration or mitoses.1 Once melanoma spreads beyond the regional nodes, however, the lack of validated molecular targets hampers efforts to individualize therapy. In this issue of the Journal, Flaherty and coworkers2 provide clinical proof that mutations in the gene encoding the serine–threonine protein kinase B-RAF (BRAF) are bona fide therapeutic targets in melanoma. A remarkable . . .

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