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Mechanisms of tumor resistance to EGFR-targeted therapies Hopper-Borge EA; Nasto RE; Ratushny V; Weiner LM; Golemis EA; Astsaturov IExpert Opin Ther Targets 2009[Mar]; 13 (3): 339-62BACKGROUND: 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.|*Drug Resistance, Neoplasm[MESH]|ATP-Binding Cassette Transporters/metabolism[MESH]|Animals[MESH]|Antineoplastic Agents/*pharmacology[MESH]|Drug Delivery Systems[MESH]|ErbB Receptors/antagonists & inhibitors[MESH]|Gene Expression Regulation, Neoplastic[MESH]|Humans[MESH]|Neoplasms/*drug therapy[MESH]|Signal Transduction/drug effects[MESH] |
