Mechanisms of tumor resistance to EGFR-targeted therapies.
Mechanisms of tumor resistance to EGFR-targeted therapies.
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DOI：
10.1517/14712590902735795
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发表时间：
2009-03
影响因子：
5.8
通讯作者：
Astsaturov I
中科院分区：
文献类型：
--
作者：
Hopper-Borge EA;Nasto RE;Ratushny V;Weiner LM;Golemis EA;Astsaturov I
基于 EGFR 在调节细胞生长中的作用，人们致力于开发针对 EGFR 的癌症疗法。小分子和抗体 EGFR 抑制剂因其对一部分癌症的功效而具有临床作用，通常作为联合疗法的组成部分。许多癌症要么最初对 EGFR 抑制剂产生耐药性，要么在治疗过程中产生耐药性，从而限制了这些试剂的功效。回顾 EGFR 靶向治疗的细胞耐药机制。这些机制中最经过验证的包括经典 ATP 结合盒 (ABC) 多药转运蛋白的激活； EGFR激活或突变；以及与 EGFR 相关的信号蛋白的过度表达或激活。我们讨论了克服这些阻力来源的当前努力和潜在策略。我们描述了新兴的基于系统生物学的 EGFR 靶向疗法替代耐药概念，并讨论了它们对使用 EGFR 靶向疗法和其他靶向疗法的影响。
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. To review cellular resistance mechanisms to EGFR-targeted therapies. 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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