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首页> 外文期刊>Cancer biology & therapy >Resistance to HER2-directed antibodies and tyrosine kinase inhibitors: mechanisms and clinical implications.
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Resistance to HER2-directed antibodies and tyrosine kinase inhibitors: mechanisms and clinical implications.

机译：对HER2定向抗体和酪氨酸激酶抑制剂的耐药性：机制和临床意义。

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摘要

The antibody trastuzumab and the tyrosine kinase inhibitor lapatinib are approved by the FDA for the treatment of HER2-overexpressing breast cancer. These anti-HER2 drugs are changing the natural history of HER2-overexpressing breast cancer. However, therapeutic resistance to trastuzumab or lapatinib, as either single-agents or in combination with chemotherapy in the metastatic setting, typically occurs within months of starting therapy. Several mechanisms of trastuzumab-resistance have been reported that include signaling from other HER receptors, signaling from receptor tyrosine kinases (RTKs) outside of the HER (ErbB) family, increased phosphatidylinositol 3-kinase signaling, and the presence of truncated forms of HER2. Mechanisms of resistance to lapatinib also point to increased phosphatidylinositol 3-kinase signaling as well as derepression/activation of compensatory survival pathways. In this review, we discuss how these models and mechanisms enhance our understanding of the clinical resistance to HER2-directed therapies.
机译：曲妥珠单抗和酪氨酸激酶抑制剂拉帕替尼已被FDA批准用于治疗HER2过表达的乳腺癌。这些抗HER2药物正在改变HER2过表达乳腺癌的自然史。但是，在转移性环境中，无论是单药治疗还是与化疗联合使用，对曲妥珠单抗或拉帕替尼的治疗抗性通常会在开始治疗后的几个月内发生。已报告了曲妥珠单抗耐药性的几种机制，包括来自其他HER受体的信号传导，HER（ErbB）家族之外的受体酪氨酸激酶（RTK）信号传导，磷脂酰肌醇3激酶信号传导增加以及HER2截短形式的存在。对拉帕替尼的抗药性机制还表明磷脂酰肌醇3-激酶信号转导增加以及代偿性生存途径的抑制/激活降低。在这篇综述中，我们讨论了这些模型和机制如何增强我们对HER2导向疗法的临床耐药性的了解。

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