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存在驱动基因突变肺鳞癌患者的临床病理特征及预后分析
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存在驱动基因突变肺鳞癌患者的临床病理特征及预后分析
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Journal Article
存在驱动基因突变肺鳞癌患者的临床病理特征及预后分析
2016
Overview
背景与目的表皮生长因子受体（epidermal growth factor receptor,EGFR）、间变淋巴瘤激酶（anaplastic lymphoma kinase,ALK）以及KRAS基因是非小细胞肺癌（non-small cell lung cancer,NSCLC）常见的驱动基因。多项临床研究已证实,EGFR敏感突变及棘皮动物微管相关类蛋白4-间变淋巴瘤激酶（echinoderm microtubule-associated protein like 4-anaplastic lymphoma kinase,EML4-ALK）基因重排的晚期肺腺癌患者,一线治疗选择靶向药物优于化疗,其在总缓解率（overall response rate,ORR）、无进展生存期（progression-free survival,PFS）及生活质量方面均有明显优势。然而,在肺鳞癌患者中,目前尚无明确的基因检测位点及靶向药物来指导临床治疗。本研究旨在分析肺鳞癌患者EGFR、ALK以及KRAS基因的突变状态,以及相关的临床病理特征,从而为今后的治疗提供相应指导。方法回顾性分析已行相关驱动基因检测的肺鳞癌患者90例,利用突变扩增阻滞系统（amplification refractory mutation system,ARMS）的方法进行EGFR及KRAS基因检测,荧光原位杂交（fluorescence in situ hybridization,FISH）技术进行ALK基因融合检测。结果 90例患者均进行了EGFR及KRAS基因检测,8例患者为EGFR基因突变（8.8%）;2例患者为KRAS基因突变（2.2%）;18例患者通过FISH方法进行了ALK基因融合检测,1例患者存在EML4-ALK基因融合（5.6%）。女性患者的EGFR基因突变率高于男性（P=0.022）。EGFR突变及野生型患者在病理分期（P=0.042）及分化程度（P=0.003）上均有差异。以胸膜为首发转移部位的EGFR突变患者比率高于EGFR野生型患者（P=0.013）。靶向治疗与化疗对EGFR突变患者的PFS无影响（P=0.607）。结论 ALK基因融合患者应用靶向治疗后可获得理想疗效。
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