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作 者:赵俊军[1] 李平[1] ZHAO Jun-ping;LI Ping(Pathology Department,Dalian Municipal Central Hospital,Dalian 116033,China)
机构地区:[1]大连市中心医院病理科,116033
出 处:《中国实用医药》2020年第25期204-206,共3页China Practical Medicine
摘 要:目的探究胸水中表皮生长因子受体(EGFR)基因突变检测在酪氨酸激酶抑制剂治疗肺腺癌中的应用效果。方法 176例突变肺腺癌患者,采用表皮生长因子受体酪氨酸激酶抑制剂(EGFR-TKI)治疗12个月后均复发胸水,对胸水样本进行收集,制作胸水细胞块,提取各样本脱氧核糖核酸(DNA),使用人类ADx-EGFR基因突变检测试剂盒检测胸水中EGFR T790M耐药突变情况,并对其影响因素进行分析。结果 176例EGFR-TKI治疗耐药患者的胸水样本中, T790M基因突变128例,占比为72.7%,无T790M基因突变48例,占比为27.3%。男性发生T790M基因突变60例(74.07%),女性发生T790M基因突变68例(72.29%);<65岁患者发生T790M基因突变36例(69.23%),≥65岁患者发生T790M基因突变92例(74.19%);吸烟患者发生T790M基因突变47例(73.44%),非吸烟患者发生T790M基因突变81例(72.32%);腺癌患者发生T790M基因突变121例(73.33%),非腺癌患者发生T790M基因突变7例(63.64%);不同性别、年龄、吸烟情况、腺癌患者发生T790M基因突变的占比与非T790M突变患者比较,差异无统计学意义(P>0.05)。结论检测胸水样本中EGFR基因状态对于预测EGFR-TKI耐药性具有很好的应用价值,可为肺腺癌患者的耐药临床监测提供参考。Objective To investigate the effect of epidermal growth factor receptor(EGFR) gene mutation detection on lung adenocarcinoma treated with tyrosine kinase inhibitor. Methods There were 176 patients with mutated lung adenocarcinoma treated with epidermal growth factor receptor tyrosine kinase inhibitor(EGFR-TKI) in our hospital. After 12 months of treatment, all the patients had recurrent pleural effusion. The samples of pleural effusion were collected, and the cell blocks were made. The deoxyribonucleic acid(DNA) of each sample was extracted. The EGFR T790M resistance mutation in pleural effusion was detected by human ADx-EGFR gene mutation detection kit, and the influencing factors were analyzed. Results In 176 patients with drug resistance treated by EGFR-TKI, 128 cases had T790M gene mutation, accounting for 72.7%, and 48 cases had no T790 M gene mutation, accounting for 27.3%. 60 cases(74.07%) of males with T790M gene mutation, 68 cases(72.29%) of females with T790M gene mutation;there were 36 cases(69.23%) of T790M gene mutation in patients <65 years old, 92 cases(74.19%) in patients ≥65 years old;47 cases(73.44%) in smoking patients, 81 cases(72.32%) in nonsmoking patients;121 cases(73.33%) in adenocarcinoma patients and 7 cases(63.64%) in non-adenocarcinoma patients. There was no statistically significant difference in the proportion of T790 M gene mutation between patients with different gender, age, smoking and adenocarcinoma compared with those without T790M mutation(P>0.05). Conclusion The detection of EGFR gene status in pleural fluid samples has a good application value in predicting the resistance of EGFR-TKI, and can provide a reference for clinical monitoring of drug resistance in patients with lung adenocarcinoma.
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