Receptor tyrosine kinases in cancer escape from BRAF inhibitors

• 来源期刊: 细胞研究（英文版）
• 年，卷（期）: 2012,（6）
• 页码范围: 945-947
• 页数: 3页
• 语种: 英文
• DOI: 10.1038/cr.2012.78

摘要

The BRAF inhibitors (BRAFi) induce anti-tumor responses in nearly 60％ of patients with advanced V600BRAF-mutant melanomas but only 5％ of patients with V600BRAFmutant 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.