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Mol Cancer Ther. 2011 Mar;10(3):385-94. doi: 10.1158/1535-7163.MCT-10-0799.

BRAFV600E: implications for carcinogenesis and molecular therapy.

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1
Department of Histopathology, Trinity College, Sir Patrick Dun Research Laboratory, Pathology Building, St. James' Hospital, Dublin 8, Ireland. cantweer@tcd.ie

Abstract

The mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK) pathway is frequently mutated in human cancer. This pathway consists of a small GTP protein of the RAS family that is activated in response to extracellular signaling to recruit a member of the RAF kinase family to the cell membrane. Active RAF signals through MAP/ERK kinase to activate ERK and its downstream effectors to regulate a wide range of biological activities including cell differentiation, proliferation, senescence, and survival. Mutations in the v-raf murine sarcoma viral oncogenes homolog B1 (BRAF) isoform of the RAF kinase or KRAS isoform of the RAS protein are found as activating mutations in approximately 30% of all human cancers. The BRAF pathway has become a target of interest for molecular therapy, with promising results emerging from clinical trials. Here, the role of the most common BRAF mutation BRAF(V600E) in human carcinogenesis is investigated through a review of the literature, with specific focus on its role in melanoma, colorectal, and thyroid cancers and its potential as a therapeutic target.

PMID:
21388974
DOI:
10.1158/1535-7163.MCT-10-0799
[Indexed for MEDLINE]
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