冗余激酶激活与表皮生长因子受体酪氨酸激酶抑制剂耐药性
Redundant kinase activation and resistance of EGFR-tyrosine kinase inhibitors.
作者信息
Luo Min, Fu Li-Wu
机构信息
Sun Yat-Sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine Guangzhou, 510060, China.
出版信息
Am J Cancer Res. 2014 Nov 19;4(6):608-28. eCollection 2014.
Abstract
Epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) have shown dramatic effects against that tumors harboring EGFR activating mutations in the EGFR intracytoplasmic tyrosine kinase domain and resulted in cell apoptosis. Unfortunately, a number of patients ultimately developed resistance by multiple mechanisms. Thus, elucidation of the mechanism of resistance to EGFR-TKIs can provide strategies for blocking or reversing the situation. Recent studies suggested that redundant kinase activation plays pivotal roles in escaping from the effects of EGFR-TKIs. Herein, we aimed to characterize several molecular events involved in the resistance to EGFR-TKIs mediated by redundant kinase activation.
摘要
表皮生长因子受体（EGFR）酪氨酸激酶抑制剂（TKIs）已显示出对那些在EGFR胞质内酪氨酸激酶结构域中存在EGFR激活突变的肿瘤具有显著疗效，并导致细胞凋亡。不幸的是，许多患者最终通过多种机制产生了耐药性。因此，阐明对EGFR-TKIs的耐药机制可为阻断或扭转这种情况提供策略。最近的研究表明，冗余激酶激活在逃避EGFR-TKIs的作用中起关键作用。在此，我们旨在描述由冗余激酶激活介导的对EGFR-TKIs耐药所涉及的几个分子事件。
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