Please use this identifier to cite or link to this item: https://doi.org/10.1172/JCI74609
Title: Dangerous liaisons: Flirtations between oncogenic BRAF and GRP78 in drug-resistant melanomas
Authors: Shenolikar, S. 
Issue Date: 3-Mar-2014
Abstract: BRAF mutations in aggressive melanomas result in kinase activation. BRAF inhibitors reduce BRAFV600E tumors, but rapid resistance follows. In this issue of the JCI, Ma and colleagues report that vemurafenib activates ER stress and autophagy in BRAFV600E melanoma cells, through sequestration of the ER chaperone GRP78 by the mutant BRAF and subsequent PERK activation. In preclinical studies, treating vemurafenib-resistant melanoma with a combination of vemurafenib and an autophagy inhibitor reduced tumor load. Further work is needed to establish clinical relevance of this resistance mechanism and demonstrate efficacy of autophagy and kinase inhibitor combinations in melanoma treatment.
Source Title: Journal of Clinical Investigation
URI: http://scholarbank.nus.edu.sg/handle/10635/126581
ISSN: 00219738
DOI: 10.1172/JCI74609
Appears in Collections:Staff Publications

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