Literature DB >> 19236156

Mechanisms of tumor resistance to EGFR-targeted therapies.

Elizabeth A Hopper-Borge1, Rochelle E Nasto, Vladimir Ratushny, Louis M Weiner, Erica A Golemis, Igor Astsaturov.   

Abstract

BACKGROUND: Much effort has been devoted to development of cancer therapies targeting EGFR, based on its role in regulating cell growth. Small-molecule and antibody EGFR inhibitors have clinical roles based on their efficacy in a subset of cancers, generally as components of combination therapies. Many cancers are either initially resistant to EGFR inhibitors or become resistant during treatment, limiting the efficacy of these reagents. OBJECTIVE/
METHODS: To review cellular resistance mechanisms to EGFR-targeted therapies. RESULTS/
CONCLUSIONS: The best validated of these mechanisms include activation of classic ATP-binding casette (ABC) multidrug transporters; activation or mutation of EGFR; and overexpression or activation of signaling proteins operating in relation to EGFR. We discuss current efforts and potential strategies to override these sources of resistance. We describe emerging systems-biology-based concepts of alternative resistance to EGFR-targeted therapies, and discuss their implications for use of EGFR-targeted and other targeted therapies.

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Year:  2009        PMID: 19236156      PMCID: PMC2670612          DOI: 10.1517/14712590902735795

Source DB:  PubMed          Journal:  Expert Opin Ther Targets        ISSN: 1472-8222            Impact factor:   6.902


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