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Vemurafenib in Multiple Nonmelanoma Cancers with BRAF V600 Mutations
Vemurafenib in Multiple Nonmelanoma Cancers with BRAF V600 Mutations
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Vemurafenib in Multiple Nonmelanoma Cancers with BRAF V600 Mutations
Vemurafenib in Multiple Nonmelanoma Cancers with BRAF V600 Mutations

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Vemurafenib in Multiple Nonmelanoma Cancers with BRAF V600 Mutations
Vemurafenib in Multiple Nonmelanoma Cancers with BRAF V600 Mutations
Journal Article

Vemurafenib in Multiple Nonmelanoma Cancers with BRAF V600 Mutations

2015
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Overview
In a basket trial that included patients with a variety of cancers, all of which contained a BRAF V600 mutation, the rate of response to vemurafenib was highly variable. The histologic context influences the response to BRAF inhibition. BRAF V600 mutations occur in approximately 50% of cutaneous melanomas and result in constitutive activation of downstream signaling through the mitogen-activated protein kinase (MAPK) pathway. 1 , 2 Vemurafenib (Zelboraf, F. Hoffmann–La Roche/Genentech) is a selective oral inhibitor of the BRAF V600 kinase and is associated with a response rate of approximately 50% and improved survival among patients with BRAF V600E mutation–positive metastatic melanoma. 3 Efforts by the Cancer Genome Atlas 4 and other initiatives to characterize the genetic landscape of most tumor types have identified BRAF V600 mutations in nonmelanoma cancers, including colorectal cancer, 5 , 6 non–small-cell lung cancer, 7 papillary thyroid cancer, 8 diffuse gliomas, . . .