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首页> 外文期刊>Thoracic cancer. >Chemotherapy combined with Endostar as salvage treatment for EGFR-tyrosine kinase inhibitor primary resistance in an advanced non-small cell lung cancer patient with EGFR L858R mutation and ROS1 fusion: A case report
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Chemotherapy combined with Endostar as salvage treatment for EGFR-tyrosine kinase inhibitor primary resistance in an advanced non-small cell lung cancer patient with EGFR L858R mutation and ROS1 fusion: A case report

机译：化疗联合Endostar作为EGFR-Tyrosine激酶抑制剂初级抗性的矿物质治疗，高级非小细胞肺癌患者EGFR L858R突变和ROS1融合：案例报告

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EGFR-activating mutations have been recognized as the most important predictor of response to EGFR-tyrosine kinase inhibitors (TKIs); however, 20-30% of patients harboring EGFR-activating mutations show poor responses. The mechanisms of such EGFR-TKI primary resistance are still poorly understood. In our case, a non-small cell lung cancer patient developed intrinsic EGFR-TKI resistance and was then confirmed to simultaneously harbor an L858R mutation and ROS1 rearrangement. Salvage chemotherapy plus Endostar showed enduring therapeutic effects, achieving a disease-free survival period of 24?months and overall survival of 30?months. This suggests that co-activation of different oncogenic signal pathways might be a potential mechanism of EGFR-TKI primary resistance. Chemotherapy combined with anti-angiogenesis should be considered an important salvage strategy. Further studies are warranted to verify these findings and explore the underlying mechanisms involved. ? 2019 The Authors. Thoracic Cancer published by China Lung Oncology Group and John Wiley & Sons Australia, Ltd.
机译：EGFR激活突变已被认为是对EGFR-酪氨酸激酶抑制剂（TKI）的反应最重要的预测因子;然而，20-30％的患者患EGFR激活突变的患者表现出差的反应。这种EGFR-TKI初级抗性的机制仍然很差。在我们的情况下，非小细胞肺癌患者开发了内在的EGFR-TKI抗性，然后证实同时涉及L858R突变和ROS1重排。抢救化疗加上endoStar表现出持久的治疗效果，实现了24个月的无病生存期和30个月的整体生存。这表明不同致癌信号途径的共激活可能是EGFR-TKI初级电阻的潜在机制。化疗结合抗血管生成应被视为一个重要的救助策略。有权进一步研究以核实这些调查结果并探索所涉及的潜在机制。 ？ 2019年的作者。中国肺部肿瘤集团和约翰瓦里和儿子澳大利亚发表的胸癌

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