The relationship between BIM deletion polymorphism and clinical significance of epidermal growth factor receptor-mutated non-small cell lung cancer patients with epidermal growth factor receptor-tyrosine kinase inhibitor therapy: a meta-analysis

被引:13
|
作者
Zou, Qian [1 ]
Zhan, Ping [1 ]
Lv, Tangfeng [1 ]
Song, Yong [1 ]
机构
[1] Nanjing Univ, Jinling Hosp, Sch Med, Dept Resp Med, 305 East Zhongshan Rd, Nanjing 210002, Jiangsu, Peoples R China
基金
中国国家自然科学基金;
关键词
BIM; polymorphism; epidermal growth factor receptor (EGFR); tyrosine kinase inhibitors (TKIs); non-small cell lung cancer (NSCLC);
D O I
10.3978/j.issn.2218-6751.2015.12.09
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Background: BIM deletion polymorphism is a germline that might lead to little or no BH3 expression, which affects epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) related apoptosis. Recent studies show that BIM deletion polymorphism might be a critical factor leading to the resistance of EGFR-TKIs in EGFR mutation-positive non-small cell lung cancer (NSCLC) patients. Methods: Thus, a meta-analysis was conducted by combing seven original eligible studies including 778 NSCLC patients to investigate a steady and reliable conclusion. Results: Our study indicated that BIM deletion polymorphism was significantly associated with the poor objective response rate (ORR) of EGFR-TKIs in EGFR-mutated NSCLC patients [odds ratios (OR) =0.55, 95% confidence interval (CI), 0.33-0.92]. And disease control rate (DCR) in EGFR-mutate NSCLC patients treated with EGFR-TKIs was significantly decreased in patients with BIM deletion polymorphism (OR =0.55, 95% CI, 0.27-1.12). Moreover, the progression-free survival (PFS) of patients with BIM deletion polymorphism is shorter. Conclusions: These findings suggested that BIM deletion polymorphism might be a genetic cause of intrinsic resistance to TKI therapy and it could be emerged as an independent predictor to identify patients who would benefit from TKI targeted therapy in EGFR-mutated NSCLC.
引用
收藏
页码:792 / 796
页数:5
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