Impact of Smoking Status on EGFR-TKI Efficacy for Advanced Non-Small-Cell Lung Cancer in EGFR Mutants: A Meta-analysis
Impact of Smoking Status on EGFR-TKI Efficacy for Advanced Non-Small-Cell Lung Cancer in EGFR Mutants: A Meta-analysis
复制标题
吸烟状况对 EGFR 突变体晚期非小细胞肺癌 EGFR-TKI 疗效的影响：一项荟萃分析。
DOI：
10.1016/j.cllc.2014.09.008
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发表时间：
2015-03-01
影响因子：
3.6
通讯作者：
Zhang, Li
中科院分区：
文献类型：
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作者：
Zhang, Yaxiong;Kang, Shiyang;Zhang, Li
我们评估了吸烟对表皮生长因子受体（EGFR）酪氨酸激酶抑制剂（TKI）治疗晚期非小细胞肺癌EGFR突变患者疗效的影响，纳入了9项研究，涉及1029例患者。EGFR-TKI治疗后，非吸烟者的无进展生存期比吸烟者更长。吸烟史应被认为是一个重要因素的研究EGFR靶向药物对EGFR mutants.Background：吸烟史和表皮生长因子受体（EGFR）突变的存在之间的强关联已被证明在非小细胞肺癌（NSCLC），这解释了良好的反应EGFR酪氨酸激酶抑制剂（EGFR-TKI）治疗非吸烟NSCLC患者。然而，很少有研究直接关注EGFR-TKI的疗效与NSCLC EGFR突变患者吸烟史之间的关系。方法：检索电子数据库中符合条件的文献。根据随机效应模型，提取并合成了按吸烟状态分层的客观缓解率、疾病控制率和无进展生存期（PFS）数据。进行了亚组和敏感性分析。结果：共纳入9项研究，共涉及1029例EGFR突变晚期NSCLC患者接受EGFR-TKI治疗后。总体而言，与曾经吸烟者相比，不吸烟与PFS显著延长相关（HR，0.73，0.60 - 0.88; P = .001）。然而，观察到客观缓解率（比值比，1.11; 95%置信区间，0.85至1.46; P = .433）和疾病控制率（比值比，1.04; 95%置信区间，0.82至1.33; P = .740）仅有轻微改善，无统计学意义。亚组分析显示，非吸烟者中PFS的获益主要体现在入组活动性EGFR突变患者的研究、涉及既往接受过治疗的患者的研究和回顾性研究的汇总结果中。此外，我们未能观察到非吸烟者在每个亚组的客观缓解率和疾病控制率方面的任何显著益处。结论：对于携带EGFR突变的晚期NSCLC患者，不吸烟与EGFR-TKI治疗后的PFS长于既往吸烟相关。吸烟史应被认为是研究EGFR靶向药物对EGFR突变患者的一个重要因素。(C)2015年，作者。爱思唯尔公司出版All rights reserved.
We assessed the impact of smoking on response to epidermal growth factor receptor (EGFR) etyrosine kinase inhibitors (TKIs) in advanced non-small-cell lung cancer EGFR-mutant patients incorporating 9 studies that involved 1029 patients. Nonsmokers had longer progression-free survival than ever smokers after EGFR-TKI treatment. Smoking history should be considered an essential factor in studies regarding EGFR-targeted agents toward EGFR mutants.Background: The strong association between smoking history and the presence of epidermal growth factor receptor (EGFR) mutations has been proven in non-small-cell lung cancer (NSCLC), which explains the favorable response to EGFR-tyrosine kinase inhibitor (EGFR-TKI) therapy in nonsmoking NSCLC patients. However, few studies directly focus on the relationship between EGFR-TKI's efficacy and smoking history in NSCLC EGFR-mutant patients. Methods: Electronic databases were searched for eligible literatures. Data on objective response rates, disease control rates, and progression-free survival (PFS) stratified by smoking status were extracted and synthesized on the basis of a random-effect model. Subgroup and sensitivity analyses were conducted. Results: A total of 9 studies that involved a total of 1029 EGFR-mutant advanced NSCLC patients after EGFR-TKI treatment were included. In overall, nonsmoking was associated with significant prolonged PFS (HR, 0.73, 0.60 to 0.88; P = .001) compared to ever smokers. However, only marginal improvements without statistical significance in objective response rates (odds ratio, 1.11; 95% confidence interval, 0.85 to 1.46; P = .433) and disease control rate (odds ratio, 1.04; 95% confidence interval, 0.82 to 1.33; P = .740) were observed. Subgroup analyses showed that the benefits of PFS in nonsmokers were predominantly presented in pooled results of studies enrolling patients with active EGFR mutations, studies involving previously treated patients, and retrospective studies. Additionally, we failed to observe any significant benefit from nonsmokers in every subgroup for objective response rates and disease control rate. Conclusion: For advanced NSCLC patients with EGFR mutations, nonsmoking is associated with longer PFS than ever smoking after EGFR-TKIs treatment. Smoking history should be considered an essential factor in studies regarding EGFR-targeted agents toward EGFR-mutant patients. (C) 2015 The Authors. Published by Elsevier Inc. All rights reserved.