Open AccessCRKL as a Lung Cancer Oncogene and Mediator of Acquired Resistance to EGFR Inhibitors: Is It All That It Is Cracked Up to Be?
Author(s) -
Marc Ladanyi
Publication year - 2011
Publication title -
cancer discovery
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.795
H-Index - 163
eISSN - 2159-8290
pISSN - 2159-8274
DOI - 10.1158/2159-8290.cd-11-0295
Subject(s) - cancer research , oncogene , mediator , epidermal growth factor receptor , kinase , lung cancer , function (biology) , cancer , chemistry , biology , medicine , microbiology and biotechnology , oncology , genetics , cell cycle
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.
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