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目的肺癌是目前发病率第1位的肿瘤,是癌症相关死亡最重要的原因。表皮生长因子受体-酪氨酸激酶抑制剂(epidermal growth factor receptor tyrosine kinase inhibitor,EGFR-TKI)可延长患者的生存期。本研究探讨非小细胞肺癌(non-small cell lung cancer,NSCLC)患者的EGFR突变状态与临床病理特征的关系,以及TKI治疗不同基因突变NSCLC患者的预后分析。方法回顾性分析2013-09-03-2014-09-13在郑州大学第一附属医院进行EGFR检测的758例NSCLC住院患者临床资料,分析临床病理特征与突变状态的关系,并比较常见突变TKI治疗的疗效。结果758例NSCLC患者中,EGFR突变377例(49.7%),其中男性突变率为37.9%(150/396),女性为62.7%(227/362),χ2=46.634,P<0.001。<60岁突变率为52.7%(186/353),≥60岁为47.2%(191/405),χ2=2.308,P=0.074。吸烟患者突变率为55.1%(298/541),不吸烟患者为36.4%(79/217),χ2=21.612,P<0.001。腺癌突变率为54.4%(360/662),非腺癌为17.7%(17/96),χ2=45.103,P<0.001。在非腺癌中,鳞癌突变率为15.3%(9/59),腺鳞癌为54.5%(6/11),黏液表皮样癌为10.0%(1/10),其他为6.3%(1/16)。多因素Logistic回归分析显示,女性、腺癌为EGFR突变的独立危险因素,P<0.001;而吸烟史为非独立相关因素,P=0.681。常见突变为19缺失突变(25.9%,196/758)和21点突变(20.6%,156/758)。TKI治疗19突变的中位无进展生存期(progression-free survival,PFS)为7.0个月,95%CI为6.344~7.656;21突变的中位PFS为7.7个月,95%CI为5.986~9.414;19突变的中位PFS略短于21突变,但二者之间的差异无统计学意义,χ2=1.194,P=0.274。结论 EGFR突变在女性、无吸烟史及腺癌患者中较高,且女性及腺癌为独立危险因素;但也应重视对鳞癌及有吸烟史患者的EGFR突变检测。TKI治疗19和21突变NSCLC患者的PFS差异无统计学意义。
Purpose Lung cancer is currently the No. 1 tumor and is the most important cause of cancer-related deaths. Epidermal growth factor receptor tyrosine kinase inhibitor (epidermal growth factor receptor tyrosine kinase inhibitor, EGFR-TKI) can extend the survival of patients. This study was to investigate the relationship between EGFR mutation status and clinicopathological features in patients with non-small cell lung cancer (NSCLC) and the prognosis of TKI patients with NSCLC. Methods The clinical data of 758 patients with NSCLC admitted to the First Affiliated Hospital of Zhengzhou University from September 9, 2013 to March 30, 2013 were retrospectively analyzed. The relationship between the clinicopathological features and the status of the mutation was analyzed. Efficacy. Results Among 758 patients with NSCLC, 377 (49.7%) were EGFR mutations, of which 37.9% (150/396) were male, 62.7% (227/362) were women, and χ2 = 46.634 (P <0.001). <60 years old had a mutation rate of 52.7% (186/353), ≥60 years old had 47.2% (191/405), χ2 = 2.308, P = 0.074. The mutation rate was 55.1% (298/541) in smokers, 36.4% (79/217) in non-smokers, and 21.612 in smokers, P <0.001. The mutation rate of adenocarcinoma was 54.4% (360/662), non-adenocarcinoma was 17.7% (17/96), χ2 = 45.103, P <0.001. In non-adenocarcinoma, the rate of squamous cell carcinoma was 15.3% (9/59), adenosquamous carcinoma was 54.5% (6/11), mucoepidermoid carcinoma was 10.0% (1/10), others were 6.3% (1 / 16). Multivariate Logistic regression analysis showed that female and adenocarcinoma were independent risk factors of EGFR mutation, P <0.001; while the history of smoking was a non-independent related factor, P = 0.681. Common mutations were 19 deletion mutations (25.9%, 196/758) and 21 point mutations (20.6%, 156/758). The median progression-free survival (PFS) for TKI-19 mutation was 7.0 months and the 95% CI was 6.344-7.656. The median PFS for 21 mutations was 7.7 months and the 95% CI was 5.986-9.414 ; 19 median mutation PFS slightly shorter than 21 mutations, but the difference between the two was not statistically significant, χ2 = 1.194, P = 0.274. Conclusions EGFR mutation is higher in women with no history of smoking and in patients with adenocarcinoma, and female and adenocarcinoma are independent risk factors. However, EGFR mutation detection in patients with squamous cell carcinoma and smoking history should also be emphasized. There was no significant difference in PFS between 19 and 21 TKI patients with NSCLC.