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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.

The effect of BIM deletion polymorphism on intrinsic resistance and clinical outcome of cancer patient with kinase inhibitor therapy