摘要：A common deletion polymorphism within B-cell chronic lymphocytic leukemia-lymphoma like 11 gene ( BIM ) was deemed to be a genetic cause leading to compromised kinase inhibitor therapeutic efficacy in cancer individuals. However, the results reported were not consistent. Thus, a comprehensive meta-analysis containing 12 eligible studies including 1,532 Asian patients was conducted to investigate a steady and reliable conclusion. The results showed that BIM deletion polymorphism was significantly associated with tyrosine kinase inhibitor (TKI) clinical efficacy in term of response rate ( P h = 0.349, HR = 0.438, 95%CI = 0.274–0.699) and disease control rate ( P h = 0.941, HR = 0.370, 95%CI = 0.202–0.678) in EGFR -mutated NSCLC population, not in CML and HCC subgroups. Additionally, EGFR -mutated NSCLC patient harbored BIM deletion polymorphism was associated with a shorter progression-free survival (PFS) than those with BIM wild polymorphism ( P h = 0.580, adjusted HR = 2.194, 95%CI = 1.710–2.814). However, no significant association was examined between BIM deletion polymorphism and overall survival (OS) and toxic adverse events in EGFR -mutated NSCLC population and it was not associated with PFS and OS in HCC subgroup. These findings revealed 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.
