探讨非小细胞肺癌(NSCLC)患者表皮生长因子受体(EGFR)突变率及与临床病理关系和酪氨酸酶抑制剂(TKI)靶向治疗效果。

选取2014年5月至2016年8月我院收治的NSCLC患者100例为研究对象，采用聚合酶链反应-直接测序法检测患者肿瘤组织EGFR基因18-21号外显子突变情况，分析EGFR突变与临床病理的关系及其突变特点，比较EGFR突变型与野生型采用TKI靶向治疗的疗效及1年生存率、2年生存率。

本次纳入的100例NSCLC患者中共44例发生EGFR突变，EGFR突变率为44.00%；NSCLC患者EGFR突变率特点：女性高于男性，吸烟患者高于不吸烟患者，腺癌高于非腺癌，差异对比均有统计学意义(P<0.05)；Logistic回归分析显示性别为女性、病理类型为腺癌是导致NSCLC患者发生EGFR突变的独立危险因素(P<0.05)；EGFR突变类型包括18号外显子点突变4.54%(2/44)、19号外显子缺失突变43.19%(19/44)、20号外显子插入突变及点突变11.36%(5/44)、21号外显子点突变40.91%(18/44)；EGFR突变型患者TKI治疗有效率68.18%明显高于EGFR野生型10.71%(P<0.05)；EGFR突变型与野生型患者1年、2年生存率对比差异无统计学意义(P>0.05)。

性别、病理类型是导致NSCLC患者发生EGFR基因突变的独立危险因素，对于EGFR突变型患者采用TKI靶向治疗可获得较好疗效，但2年生存率与EGFR野生型患者尚无明显差异。

To observe the mutation rate of epidermal growth factor receptor (EGFR) in the patients with non-small cell lung cancer (NSCLC) and its relationship with the clinical pathology and tyrosinase inhibitor (TKI)-targeted therapy effect.

A total of 100 NSCLC patients treated in our hospital from May 2014 to August 2016 were selected for this study. The mutations of EGFR gene 18-21 exons were detected by polymerase chain reaction (PCR)-direct sequencing. The mutation features and the relationship between EGFR mutations and the clinical pathology were analyzed. The efficacies of the mutant type and the wild type of EGFI treated with TKI-targeted therapy and their 1-year survival rate and 2-year survival rate were compared.

EGFR mutations occurred in 44 cases, with the EGFR mutation rate of 44% among the 100 NSCLC patients. The features of the EGFR mutation rate in NSCLC patients were that females had a higher risk than males, smokers had a higher risk than non-smokers, and the patients with adenocarcinoma had a higher risk than those without adenocarcinoma (P<0.05). Logistic regression analysis showed that the gender of female and the pathological type of adenocarcinoma were independent risk factors for EGFR mutation in the NSCLC patients (P<0.05). EGFR mutation types included point mutation of exon 18 in 2 cases (4.54%), deletion mutation of exon 19 in 19 cases (43.19%), insertion mutation and point mutation of exon 20 in 5 cases (11.36%), and point mutation of exon 21 in 18 cases (40.91%). The effective rate of TKI treatment in the EGFR mutant patients was significantly higher than that in the EGFR wild type patients (68.18% vs 10.71%, P<0.05). There was no significant difference in the EGFR mutant type and wild type about 1-year and 2-year survival rates (P>0.05).

Gender and pathological type are independent risk factors for EGFR mutations in the NSCLC patients. TKI-targeted therapy has better effect in the EGFR mutant patients, but there is no significant difference in the 2-year survival rate compared with EGFR wild type patients.