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Tyrosine kinase inhibitor acquired resistance mechanism alternates between EGFR and ALK in a lung adenocarcinoma patient

机译:酪氨酸激酶抑制剂获得的抗性机制在肺腺癌患者的EGFR和ALK之间交替

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Drive gene mutation positive non-small cell lung cancer achieves reliable clinical responses to subsequent target therapy. However, most patients will inevitably develop disease progression with multiple treatment failure. Next generation sequencing can identify clear resistance mechanisms. We report a case of a late stage, non-smoking, male non-small cell lung cancer patient that developed dual mutations and our attempts to determine the novel resistance mechanism. After systematic chemotherapy, he was administered multiple target therapy according to different genotypes. Larger panel gene detection was adapted after the failure of different treatments to investigate the resistance mechanism. Re-biopsy and large panel NGS revealed an EGFR mutant lung adenocarcinoma with alternating changes in acquired resistance between EGFR and ALK. The total survival time was 73?months. The genotypes and treatments in this patient provide new insight of target therapy resistance mechanisms. Re-biopsy and large panel gene detection should be performed for each driver gene mutation to provide precision treatment strategies. ? 2019 The Authors. Thoracic Cancer published by China Lung Oncology Group and John Wiley & Sons Australia, Ltd.
机译:驱动基因突变阳性非小细胞肺癌达到可靠的临床反应对随后的靶疗法。然而,大多数患者将不可避免地发育疾病进展,具有多种治疗失败。下一代测序可以识别透明电阻机制。我们举报了一个晚期阶段,禁止吸烟,男性非小细胞肺癌患者,其开发了双重突变,并试图确定新抗性机制。在系统化疗后,他根据不同的基因型进行多种靶疗法。在不同处理失败后调整较大的面板基因检测以研究抗性机制。重新活组织检查和大型面板NGS揭示了EGFR突变体肺腺癌,具有EGFR和ALK之间获得性阻力的交替变化。总存活时间为73个月。该患者的基因型和治疗提供了对靶治疗抵抗机制的新洞察力。应对每个驾驶员基因突变进行再活检和大面板基因检测,以提供精密治疗策略。 ? 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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