The BCL2L11 deletion polymorphism is not associated with imatinib resistance in chronic myeloid leukemia patients: meta-analysis

被引：0
|
作者：
Xu, Jinyun [1 ,2 ]
Gu, Jiaowei [2 ]
Zhao, Yan [2 ]
Meng, Huihua [1 ]
Du, Li'an [1 ]
Zhang, Ruibo [2 ]
Jiang, Hao [2 ]
Luo, Jianming [1 ]
机构：
[1] Guangxi Med Univ, Affiliated Hosp 1, Dept Pediat, Nanning, Guangxi, Peoples R China
[2] Hubei Univ Med, Taihe Hosp, Dept Pediat, Shiyan, Hubei, Peoples R China
来源：
ONCOTARGET | 2017年 / 8卷 / 58期
关键词：
BIM; chronic myeloid leukemia; tyrosine kinase inhibitor; genetic polymorphism; drug resistance; DIAGNOSED CHRONIC-PHASE; PATIENTS RECEIVING IMATINIB; FOLLOW-UP; CYTOGENETIC RESPONSES; INTRINSIC RESISTANCE; 1ST-LINE TREATMENT; TYROSINE KINASE; BIM; DASATINIB; NILOTINIB;
D O I：
10.18632/oncotarget.21154
中图分类号：
R73 [肿瘤学];
学科分类号：
100214 ;
摘要：
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.
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收藏
页码：99041 / 99048
页数：8
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