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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 <jats:italic>BIM<\/jats:italic> deletion polymorphism was significantly associated with tyrosine kinase inhibitor (TKI) clinical efficacy in term of response rate (<jats:italic>P<\/jats:italic><jats:sub>h<\/jats:sub>\u2009=\u20090.349, HR\u2009=\u20090.438, 95%CI\u2009=\u20090.274\u20130.699) and disease control rate (<jats:italic>P<\/jats:italic><jats:sub>h<\/jats:sub>\u2009=\u20090.941, HR\u2009=\u20090.370, 95%CI\u2009=\u20090.202\u20130.678) in <jats:italic>EGFR<\/jats:italic>-mutated NSCLC population, not in CML and HCC subgroups. Additionally, <jats:italic>EGFR<\/jats:italic>-mutated NSCLC patient harbored <jats:italic>BIM<\/jats:italic> deletion polymorphism was associated with a shorter progression-free survival (PFS) than those with <jats:italic>BIM<\/jats:italic> wild polymorphism (<jats:italic>P<\/jats:italic><jats:sub>h<\/jats:sub>\u2009=\u20090.580, adjusted HR\u2009=\u20092.194, 95%CI\u2009=\u20091.710\u20132.814). However, no significant association was examined between <jats:italic>BIM<\/jats:italic> deletion polymorphism and overall survival (OS) and toxic adverse events in <jats:italic>EGFR<\/jats:italic>-mutated NSCLC population and it was not associated with PFS and OS in HCC subgroup. These findings revealed that <jats:italic>BIM<\/jats:italic> 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 <jats:italic>EGFR<\/jats:italic>-mutated NSCLC.<\/jats:p>","DOI":"10.1038\/srep11348","type":"journal-article","created":{"date-parts":[[2015,6,15]],"date-time":"2015-06-15T11:24:33Z","timestamp":1434367473000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":23,"title":["The effect of BIM deletion polymorphism on intrinsic resistance and clinical outcome of cancer patient with kinase inhibitor therapy"],"prefix":"10.1038","volume":"5","author":[{"given":"Hou-Qun","family":"Ying","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jie","family":"Chen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bang-Shun","family":"He","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yu-Qin","family":"Pan","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Feng","family":"Wang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qi-Wen","family":"Deng","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hui-Ling","family":"Sun","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xian","family":"Liu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shu-Kui","family":"Wang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2015,6,15]]},"reference":[{"key":"BFsrep11348_CR1","first-page":"411","volume":"4","author":"Y Lin","year":"2014","unstructured":"Lin, Y., Wang, X. & Jin, H. 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