BRAF as a target for cancer therapy

Rodrigo Dienstmann, Josep Tabernero

    Research output: Contribution to journalReview articleResearchpeer-review

    48 Citations (Scopus)


    Tumors with mutations in the gene encoding the serine-threonine protein kinase BRAF are dependent on the MAPK signaling pathway for their growth, what offers an opportunity to test oncogene-targeted therapy. Mutations at the position V600 of BRAF were described in approximately 8% of all solid tumors, including 50% of melanomas, 30 to 70% of papillary thyroid carcinomas and 5 to 8% of colorectal adenocarcinomas. Specific BRAF kinase inhibitors are undergoing rapid clinical development and promising data on efficacy have been demonstrated in activated mutant BRAF V600 melanomas. This review article will address: (a) preclinical data on the antitumor activity of BRAF inhibitors in cell lines/ in vivo models and their opposing functions as inhibitors or activators of the MAPK pathway, depending on the cellular context; (b) drug development from non-selective RAF inhibitors to selective BRAF inhibitors, such as PLX4032 and GSK2118436, with emphasis in the clinical efficacy and toxicity of these agents; and (c) possible mechanisms of resistance to BRAF inhibitors and strategies to overcome its development in BRAF mutant tumors. © 2011 Bentham Science Publishers Ltd.
    Original languageEnglish
    Pages (from-to)285-295
    JournalAnti-Cancer Agents in Medicinal Chemistry
    Issue number3
    Publication statusPublished - 1 Jan 2011


    • BRAF inhibitor
    • BRAF V600
    • Melanoma
    • RAF inhibitor
    • Resistance
    • Targeted therapy


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