Broad Institute of Harvard and the Massachusetts Institute of Technology, 7 Cambridge Center, Cambridge, MA 02142, USA.
Cell Res. 2013 Jan;23(1):13-4. doi: 10.1038/cr.2012.115. Epub 2012 Jul 31.
Two recent papers identify KRAS activation as a mechanism of acquired resistance to EGFR blockade in colorectal cancer. In doing so, they suggest that resistance to single-agent EGFR blockade will be unavoidable because these alterations exist as latent subclones within the tumor even prior to the initiation of therapy.
最近有两篇论文指出，KRAS 激活是结直肠癌对 EGFR 阻断获得性耐药的一种机制。这样一来，他们认为，由于这些改变在治疗开始之前就已经作为肿瘤内的潜伏亚克隆存在，因此对单药 EGFR 阻断的耐药将是不可避免的。
