期刊
FEBS LETTERS
卷 584, 期 12, 页码 2699-2706出版社
WILEY
DOI: 10.1016/j.febslet.2010.04.019
关键词
EGFR; Mutations; Kinase; Lung cancer; Glioblastoma; ErbB
资金
- Goldhirsh Foundation
- National Cancer Institute (NIH)
- Israel Science Foundation
- Israel Cancer Research Fund
- Prostate Cancer Research Foundation
- Dr. Miriam and Sheldon G. Adelson Medical Research Foundation
- German Research Foundation
The EGF-receptor is frequently mutated in a large variety of tumors. Here we review the most frequent mutations and conclude that they commonly enhance the intrinsic tyrosine kinase activity, or they represent loss-of-function of suppressive regulatory domains. Interestingly, the constitutive activity of mutant receptors translates to downstream pathways, which are subtly different from those stimulated by the wild-type receptor. Cancer drugs intercepting EGFR signaling have already entered clinical application. Both kinase inhibitors specific to EGFR, and monoclonal antibodies to the receptor are described, along with experimental approaches targeting the HSP90 chaperone. Deeper understanding of signaling pathways downstream to mutant receptors will likely improve the outcome of current EGFR-targeted therapies, as well as help develop new drugs and combinations. (C) 2010 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
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