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目的:探讨表皮生长因子受体（EGFR）突变晚期非小细胞肺癌（NSCLC）EGFR-酪氨酸激酶抑制剂（EGFR-TKI）治疗效果的影响因素。方法:收集2015年1月至2019年10月南京医科大学附属无锡第二医院接受EGFR-TKI治疗的104例EGFR突变晚期NSCLC患者的临床资料。分析EGFR突变类型与患者的临床病理特征、血液学检查结果以及治疗方式的相关性，采用Cox比例风险回归模型分析EGFR突变类型、临床病理特征、血液学相关指标及治疗方式与患者EGFR-TKI治疗的无进展生存（PFS）时间的相关性，采用Kaplan-Meier法分析独立影响因素分层患者PFS。结果:患者疾病控制率（DCR）为92.3%（96／104）。Cox单因素分析显示，EGFR突变晚期NSCLC患者应用EGFR-TKI时癌胚抗原（CEA）、糖类抗原125（CA125）、D-二聚体水平、既往手术治疗史、联合治疗及治疗药物与PFS时间有关（均n P<0.05）；Cox多因素分析显示，EGFR突变类型（n HR＝2.371，95% n CI 1.298～4.332，n P＝0.005）、联合治疗（n HR＝0.489，95% n CI 0.245~0.978，n P＝0.043）、治疗药物的选择（n HR＝0.261，95% n CI 0.113～0.606，n P＝0.002）是EGFR-TKI治疗患者PFS的独立影响因素。EGFR第19号外显子突变晚期NSCLC患者的PFS优于EGFR第21号外显子突变患者（中位PFS时间：14.0个月比9.5个月，n P<0.05），联合放疗或化疗者PFS优于单药EGFR-TKI治疗者（中位PFS时间：15.0个月比9.0个月，n P<0.05），厄洛替尼治疗者PFS优于吉非替尼治疗者（n P<0.05）。EGFR第19号外显子突变患者一线治疗中选择EGFR-TKI者较二线及以上使用者获得更好的PFS（中位PFS时间：14.0个月比9.5个月，n P<0.05）；EGFR-TKI治疗时，CA125<85 U／ml的EGFR第19号外显子突变患者较CA125≥85 U／ml者获得更好的PFS（中位PFS时间：14.0个月比6.5个月，n P<0.05）。n 结论:EGFR-TKI治疗晚期EGFR突变NSCLC的疗效肯定，CA125低水平的EGFR第19号外显子突变的NSCLC患者一线选择EGFR-TKI治疗可获得更好的PFS。“,”Objective:To investigate the influencing factors of the therapeutic effect of epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) in patients with epidermal growth factor receptor (EGFR) mutant advanced non-small cell lung cancer (NSCLC).Methods:The clinical data of 104 EGFR mutant advanced NSCLC patients who received EGFR-TKI treatment in Wuxi No.2 Hospital Affiliated to Nanjing Medical University from January 2015 to October 2019 were collected. The correlation of different types of EGFR mutation with the clinicopathological characteristics, the hematological examination results and the treatment mode of patients was analyzed. Cox proportional hazard model was used to analyze the association of the progression-free survival (PFS) time of patients receiving EGFR-TKI treatment with the different types of EGFR mutation, the clinicopathological characteristics, hematological related indexes and treatment mode. Kaplan-Meier method was used to analyze the independent influencing factors for the PFS of the stratified patients.Results:The overall disease control rate (DCR) of patients receiving EGFR-TKI treatment was 92.3% (96/104). Cox univariate analysis showed that the levels of carcinoembryonic antigen (CEA), carbohydrate antigen 125 (CA125), D-dimer, and previous surgical treatment history of patients receiving EGFR-TKI treatment were associated with PFS of patients (all n P < 0.05). Cox multi-factor analysis showed that EGFR mutation type ( n HR =2.371, 95% n CI 1.298-4.332, n P = 0.005), combination therapy (n HR = 0.489, 95% n CI 0.245-0.978, n P = 0.043) and choice of therapeutic drugs (n HR = 0.261, 95% n CI 0.113-0.606, n P = 0.002) were independent influencing factors for the PFS of patients receiving EGFR-TKI treatment. The PFS of EGFR 19 exon-mutant patients with advanced NSCLC was longer than that of those with EGFR 21 exon-mutant (median PFS time: 14.0 months vs.9.5 months, n P<0.05); the PFS of combination of radiotherapy or chemotherapy was longer than that of EGFR-TKI single therapy (median PFS time: 15.0 months vs. 9.0 months,n P<0.05), the PFS of patients receiving erlotinib was better than that of those receiving gefitinib (n P<0.05). According to EGFR mutation types, it was found that EGFR 19 exon-mutant patients receiving EGFR-TKI in first-line treatment could obtain better PFS than those who receiving EGFR-TKI in second-line and above treatment (median PFS time: 14.0 months vs. 9.5 months,n P<0.05). When receiving EGFR-TKI, EGFR 19 exon-mutant patients with CA125 <85 U/ml could obtain longer PFS time than those with CA125 ≥85 U/ml (median PFS time: 14.0 months vs. 6.5 months,n P<0.05).n Conclusions:The therapeutic effect of EGFR-TKI in EGFR-mutant patients with advanced NSCLC is positive. EGFR 19 exon-mutant NSCLC patients with low-level CA125 receiving EGFR-TKI in first-line treatment can obtain better PFS.