Journal
BIOCHEMICAL SOCIETY TRANSACTIONS
Volume 42, Issue -, Pages 776-783Publisher
PORTLAND PRESS LTD
DOI: 10.1042/BST20140129
Keywords
acquired resistance; BRAF; extracellular-signal-regulated kinase 1/2 (ERK1/2); intrinsic resistance; mitogen-activated protein kinase (MAPK)/extracellular-signal-regulated kinase (ERK) kinase 1/2 (MEK1/2); RAS
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Funding
- Biotechnology and Biological Sciences Research Council
- Biotechnology and Biological Sciences Research Council Institute Strategic Programme Grant
- AstraZeneca
- Babraham Institute
- BBSRC [BBS/E/B/000C0419] Funding Source: UKRI
- Biotechnology and Biological Sciences Research Council [BBS/E/B/0000C199, BBS/E/B/000C0419] Funding Source: researchfish
- Cancer Research UK [14867] Funding Source: researchfish
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Recent clinical data with BRAF and MEK1/2 [MAPK (mitogen-activated protein kinase)/ERK (extracellular-signal-regulated kinase) kinase 1/2] inhibitors have demonstrated the remarkable potential of targeting the RAF-MEK1/2-ERK1/2 signalling cascade for the treatment of certain cancers. Despite these advances, however, only a subset of patients respond to these agents in the first instance, and, of those that do, acquired resistance invariably develops after several months. Studies in vitro have identified various mechanisms that can underpin intrinsic and acquired resistance to MEK1/2 inhibitors, and these frequently recapitulate those observed clinically. In the present article, we review these mechanisms and also discuss recent advances in our understanding of how MEK1/2 inhibitor activity is influenced by pathway feedback.
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