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- W2149662085 abstract "We describe a mechanism of tumorigenesis mediated by kinase-dead BRAF in the presence of oncogenic RAS. We show that drugs that selectively inhibit BRAF drive RAS-dependent BRAF binding to CRAF, CRAF activation, and MEK–ERK signaling. This does not occur when oncogenic BRAF is inhibited, demonstrating that BRAF inhibition per se does not drive pathway activation; it only occurs when BRAF is inhibited in the presence of oncogenic RAS. Kinase-dead BRAF mimics the effects of the BRAF-selective drugs and kinase-dead Braf and oncogenic Ras cooperate to induce melanoma in mice. Our data reveal another paradigm of BRAF-mediated signaling that promotes tumor progression. They highlight the importance of understanding pathway signaling in clinical practice and of genotyping tumors prior to administering BRAF-selective drugs, to identify patients who are likely to respond and also to identify patients who may experience adverse effects.PaperClip/cms/asset/c43bc943-8c0c-498e-ac81-22a535857d2a/mmc3.mp3Loading ...(mp3, 3.03 MB) Download audio" @default.
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- W2149662085 date "2010-01-01" @default.
- W2149662085 modified "2023-10-18" @default.
- W2149662085 title "Kinase-Dead BRAF and Oncogenic RAS Cooperate to Drive Tumor Progression through CRAF" @default.
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- W2149662085 doi "https://doi.org/10.1016/j.cell.2009.12.040" @default.
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