Volume 22, No 6, Jun 2012

ISSN: 1001-0602 
EISSN: 1748-7838 2018 
impact factor 17.848* 
(Clarivate Analytics, 2019)

Volume 22 Issue 6, June 2012: 945-947

RESEARCH HIGHLIGHTS

Receptor tyrosine kinases in cancer escape from BRAF inhibitors

Roger S Lo^1,2

¹Division of Dermatology, Department of Medicine

²Department of Molecular and Medical Pharmacology, Jonsson Comprehensive Cancer Center, David Geffen School of Medicine, University of California, Los Angeles, 52-121 CHS, 10833 Le Conte Ave, Los Angeles, CA 90095-1750, USA Correspondence: Roger S. Lo,(rlo@mednet.ucla.edu)

The BRAF inhibitors (BRAFi) induce anti-tumor responses in nearly 60% of patients with advanced V600BRAF-mutant melanomas but only 5% of patients with V600BRAF-mutant colorectal carcinomas. Earlier studies of how a subset of melanoma that initially responds to BRAFi but later acquires drug resistance pointed to the importance of receptor tyrosine kinases (RTKs) in drug escape. In a pair of recent reports, this RTK-mediated mechanism of acquired BRAFi resistance in melanoma is re-surfacing in the context of innate or primary BRAFi resistance in V600BRAF-mutant colorectal carcinomas, suggesting potential upfront therapeutic strategies to prevent BRAFi resistance.

Cell Research (2012) 22:945-947. doi:10.1038/cr.2012.78; published online 8 May 2012

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