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    BRAFV600E: implications for carcinogenesis and molecular therapy.

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    Authors
    Cantwell-Dorris, Emma R
    O'Leary, John J
    Sheils, Orla M
    Affiliation
    Department of Histopathology, Trinity College, Sir Patrick Dun Research, Laboratory, Pathology Building, St. James' Hospital, Dublin 8, Ireland., cantweer@tcd.ie
    Issue Date
    2012-02-01T10:44:54Z
    MeSH
    Animals
    Cell Transformation, Neoplastic/*genetics
    Extracellular Signal-Regulated MAP Kinases/genetics/metabolism
    Humans
    Mice
    Mitogen-Activated Protein Kinases/*genetics/metabolism
    *Molecular Targeted Therapy
    *Mutation
    Proto-Oncogene Proteins B-raf/*genetics
    
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    Citation
    Mol Cancer Ther. 2011 Mar;10(3):385-94.
    Journal
    Molecular cancer therapeutics
    URI
    http://hdl.handle.net/10147/207794
    DOI
    10.1158/1535-7163.MCT-10-0799
    PubMed ID
    21388974
    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.
    Language
    eng
    ISSN
    1538-8514 (Electronic)
    1535-7163 (Linking)
    ae974a485f413a2113503eed53cd6c53
    10.1158/1535-7163.MCT-10-0799
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