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

Cancer Discov. 2011 Dec;1(7):560-1. doi: 10.1158/2159-8290.CD-11-0295.

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.

Publication types

  • Comment

MeSH terms

  • Adaptor Proteins, Signal Transducing / genetics*
  • Adenocarcinoma / genetics*
  • Adenocarcinoma / therapy*
  • Adenocarcinoma of Lung
  • ErbB Receptors / antagonists & inhibitors*
  • Humans
  • Lung Neoplasms / genetics*
  • Lung Neoplasms / therapy*
  • Nuclear Proteins / genetics*

Substances

  • Adaptor Proteins, Signal Transducing
  • CRKL protein
  • Nuclear Proteins
  • EGFR protein, human
  • ErbB Receptors