Abstract
The RAF inhibitor vemurafenib (PLX4032) is effective against melanomas with activated BRAF (BRAF-V600E), but not against colorectal cancers (CRCs) harbouring the same mutation. Two papers now report, using RNA-interference screens and the analysis of signalling pathways in cell lines, that activation of epidermal growth factor receptor (EGFR) occurs following vemurafenib treatment in CRC cells, but not in melanoma cells, leading to vemurafenib resistance. Consequently, both studies found that combination treatment with vemurafenib and an EGFR inhibitor blocked CRC cell growth in vitro and CRC tumour growth in xenograft models. This could be a valid therapeutic strategy for patients with BRAF-mutant CRC.
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