| Literature DB >> 24523613 |
K Connolly1, D Brungs1, E Szeto1, R J Epstein1.
Abstract
Mismatch-repair-deficient colorectal cancers often contain kinase-activating V600E BRAF mutations, but no clinical utility has yet been demonstrated in this setting for monotherapy using oral braf kinase inhibitors such as vemurafenib or dabrafenib. Recent studies have indicated that tumour resistance to braf inhibition is mediated by upregulated epidermal growth factor receptor (egfr) signalling, disruption of which is a routine treatment strategy in KRAS wild-type colorectal cancer. In this report, we describe the clinical course of a heavily pretreated patient who elected to receive off-label dual-targeted braf- and egfr-inhibitory therapy with good tolerance and apparent clinical benefit.Entities:
Keywords: Colorectal neoplasms; combination drug therapy; genomic profiling; personalized oncology; precision medicine
Year: 2014 PMID: 24523613 PMCID: PMC3921040 DOI: 10.3747/co.21.1661
Source DB: PubMed Journal: Curr Oncol ISSN: 1198-0052 Impact factor: 3.677