Xu Jinyun, Gu Jiaowei, Zhao Yan, Meng Huihua, Du Li'an, Zhang Ruibo, Jiang Hao, Luo Jianming
Department of Pediatrics, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi, China.
Department of Pediatrics, Taihe Hospital, Hubei University of Medicine, Shiyan, Hubei, China.
Oncotarget. 2017 Sep 22;8(58):99041-99048. doi: 10.18632/oncotarget.21154. eCollection 2017 Nov 17.
A common deletion polymorphism of the gene Bcl-2 like protein 11 (BCL2L11, BIM) has been reported to cause tyrosine kinase inhibitors (TKIs) resistance in several malignant tumors. However, the conclusions were not consistent in chronic myeloid leukemia (CML) individuals. In order to obtain a reliable conclusion, we systematically searched PubMed, Embase, Web of Science, Chinese Biomedical Database, and China National Knowledge Infrastructure and performed the meta-analysis. Six published articles contain 760 East Asian patients were identified from these electronic databases. The methodological quality of one included trial was high, and the others were moderate. Meta-analysis showed that the rate of TKI resistance between the BIM deletion and wild-type group were no statistical significance (OR = 1.24, 95% CI 0.79-1.95). In conclusion, BIM deletion may not a predictor of TKI resistance in CML individuals in East Asia.
据报道,基因Bcl-2样蛋白11(BCL2L11,BIM)的一种常见缺失多态性会导致多种恶性肿瘤对酪氨酸激酶抑制剂(TKIs)产生耐药性。然而,在慢性粒细胞白血病(CML)患者中,结论并不一致。为了得出可靠的结论,我们系统检索了PubMed、Embase、Web of Science、中国生物医学数据库和中国知网,并进行了荟萃分析。从这些电子数据库中识别出6篇发表的文章,共纳入760名东亚患者。其中一项纳入试验的方法学质量较高,其他试验质量中等。荟萃分析表明,BIM缺失组和野生型组之间的TKI耐药率无统计学意义(OR = 1.24,95% CI 0.79 - 1.95)。总之,BIM缺失可能不是东亚CML患者TKI耐药的预测指标。