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 AACR
MeSH terms
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Adaptor Proteins, Signal Transducing / genetics*
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Adenocarcinoma / genetics*
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Adenocarcinoma / therapy*
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Adenocarcinoma of Lung
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ErbB Receptors / antagonists & inhibitors*
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Humans
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Lung Neoplasms / genetics*
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Lung Neoplasms / therapy*
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Nuclear Proteins / genetics*
Substances
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Adaptor Proteins, Signal Transducing
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CRKL protein
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Nuclear Proteins
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EGFR protein, human
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ErbB Receptors