| Literature DB >> 22211192 |
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 AACREntities:
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Year: 2011 PMID: 22211192 PMCID: PMC3247017 DOI: 10.1158/2159-8290.CD-11-0295
Source DB: PubMed Journal: Cancer Discov ISSN: 2159-8274 Impact factor: 39.397