Work

CRKL as a Lung Cancer Oncogene and Mediator of Acquired Resistance to EGFR Inhibitors: Is It All That It Is Cracked Up to Be?

Year: 2011

Type: article

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. Cancer Discovery; 1(7); 560–1. ©2011 AACR. Commentary on Cheung et al., p. 608.

Source: Cancer Discovery

DOI: 10.1158/2159-8290.cd-11-0295

Author: Marc Ladanyi

Institution: Memorial Sloan Kettering Cancer Center

Language: English

Topic: Lung Cancer Treatments and Mutations

Subfield: Pulmonary and Respiratory Medicine

Field: Medicine

Domain: Health Sciences

SDG: Good health and well-being

Open Access status: green

Funder: National Cancer Institute