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Year : 2015  |  Volume : 11  |  Issue : 2  |  Page : 397-402

Association between BIM deletion polymorphism and clinical outcome of EGFR-mutated NSCLC patient with EGFR-TKI therapy: A meta-analysis

Department of Respiration, Nanjing First Hospital, Nanjing Medical University, Nanjing, Jiangsu, China

Correspondence Address:
Wei Gu
Department of Respiration, Nanjing First Hospital, Nanjing Medical University, 68 Changle Road, Nanjing
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Source of Support: The study was supported by the fund of health department of Jiangsu province (H201341), Conflict of Interest: None

DOI: 10.4103/2152-7806.157308

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Aim: BIM deletion polymorphism was deemed to be associated with downregulation of BIM, resulting in a decreased apoptosis induced by epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) in EGFR mutation-positive non-small cell lung cancer (NSCLC). However, accumulating evidences concerning the association between BIM deletion polymorphism and efficacy of EGFR-TKI and survival in EGFR-mutation-driven NSCLC patient reported contradictory results. Materials and Methods: A meta-analysis was conducted by combing six original eligible studies including 871 NSCLC patients. Results: Our study showed that BIM deletion polymorphism was significantly associated with poor response to EGFR-TKI therapy in mutant EGFRNSCLC patients (P h = 0.309, P z = 0.001, OR = 0.39, 95% confidence interval (CI) = 0.23-0.67). Disease control rate (DCR) in mutant EGFRNSCLC patient with treatment of EGFR-TKI was significantly decreased in patients with BIM deletion polymorphism comparing to patients harbored BIM wild variant (P h = 0.583, P Z = 0.007, OR = 0.46, 95%CI = 0.25-0.85). EGFR mutation-derived NSCLC patient carrying BIM deletion polymorphism had a shorter progression-free survival (PFS; P h < 0.001, P z < 0.001, hazard ratio (HR) = 1.37, 95%CI = 1.09-1.71) and overall survival (OS; P h = 0.90, P z = 0.003, HR = 1.25, 95%CI = 1.08-1.45), than those harbored BIM wild variant. Conclusion: These results suggested that BIM deletion polymorphism might be a cause that contributes to primary EGFR-TKI resistance, and it could be used as a genetic predictor for EGFR-TKI outcome and an independent prognostic factor of EGFR mutation-driven NSCLC patient.

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