CRKL as a lung cancer oncogene and mediator of acquired resistance to EGFR inhibitors: Is it all that it is cracked up to be?

Abstract

Cheung and colleagues demonstrate that amplified CRKL can function as a driver oncogene in lung adenocarcinoma, activating both RAS and RAP1 to induce mitogen-activated protein kinase signaling. In addition, they show that CRKL amplification may be another mechanism for primary or acquired resistance to epidermal growth factor receptor kinase inhibitors. © 2011 American Association for Cancer Research.