BRAF Alterations as Therapeutic Targets in Non–Small-Cell Lung Cancer

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Presentation transcript:

BRAF Alterations as Therapeutic Targets in Non–Small-Cell Lung Cancer Tu Nguyen-Ngoc, MD, PhD, Hasna Bouchaab, MD, Alex A. Adjei, MD, PhD, Solange Peters, MD, PhD Journal of Thoracic Oncology Volume 10, Issue 10, Pages 1396-1403 (October 2015) DOI: 10.1097/JTO.0000000000000644 Copyright © 2015 International Association for the Study of Lung Cancer Terms and Conditions

FIGURE 1 Illustration of RAS–RAF–MEK–ERK MAP kinase signaling pathway. Current inhibitors targeting BRAF, MEK, and ERK are depicted. AKT, Ak strain transforming; ARAF, v-Raf murine sarcoma viral oncogene homolog A; BRAF, v-Raf murine sarcoma viral oncogene homolog B; CRAF, v-Raf murine sarcoma viral oncogene homolog C; ERK-1/2, extracellular signal-regulated kinase 1/2; GDP, guanosine diphosphate; GRB2, growth factor receptor-bound protein 2; GTP, guanosine triphosphate; MAP, mitogen-activated protein; MEK1/2, mitogen-activated protein/extracellular signal-regulated kinase kinase 1/2; mTOR, mammalian target of rapamycin; P, phosphate; PI3K, phosphatidylinositol 3-kinase; PLCγ, phospholipase Cγ; RAF, rapidly accelerated fibrosarcoma; RAS, rat sarcoma; RHEB, Ras homolog enriched in brain; RTK, receptor tyrosine kinase; SHC, Src homology 2 domain-containing-transforming protein; SOS, son of sevenless; TSC1/2, tuberous sclerosis protein 1/2. Journal of Thoracic Oncology 2015 10, 1396-1403DOI: (10.1097/JTO.0000000000000644) Copyright © 2015 International Association for the Study of Lung Cancer Terms and Conditions