期刊
GENE
卷 510, 期 1, 页码 14-21出版社
ELSEVIER
DOI: 10.1016/j.gene.2012.08.042
关键词
CYP1A1 MspI; Acute lymphoblastic leukemia; Malignancy; Susceptibility; Meta-analysis; Polymorphism
Previous studies indicated that cytochrome P450 1A1 (CYP1A1) MspI polymorphism might be a possible risk factor for several malignancies. Increasing investigations have been conducted on the association of CYP1A1 MspI polymorphisms with acute lymphoblastic leukemia (ALL). However, the results were controversial. The goal of the present study was to address this controversy by pooling and analyzing the published data. Therefore, quantitative meta-analyses evaluating the association of CYP1A1 MspI variation with ALL were performed and subgroup analyses on ethnicity, age groups and source of controls were further carried out. After a rigorous search in the Medline, EMBASE, OVID, ScienceDirect, and CNKI databases, all eligible studies for the period up to May 2012 were identified and screened according to the inclusion and exclusion criteria. Consequently, a total of fourteen case-control studies including 2013 cases and 2903 controls were selected for analysis. The overall data indicated a significant association of CYP1A1 MspI polymorphism with ALL risk (CC+TC vs TT: OR=1.33; 95%CI=1.05-1.69). In a subgroup analysis according to ethnicity, no associations were shown among Asians, Caucasians and Mixed ethnicity subgroups. In the subgroup analysis regarding age groups, increased risk was observed in the childhood ALL subgroup (C vs T: OR=1.23; 95%CI=1.04-1.45; CC+TC vs TT: OR=1.31; 95%CI=1.08-1.59). In the subgroup analysis stratified by source of controls, significant associations were observed in the population-based subgroup (CC+TC vs TT: OR=1.33; 95%CI=1.03-1.71). In conclusion, the results of the present study suggest that CYP1A1 MspI polymorphism might be a risk factor for ALL, particularly childhood ALL Future well-designed high quality investigations with large sample sizes are required to elucidate the gene polymorphism-ALL relationship and gene-environment interactions. (C) 2012 Elsevier B.V. All rights reserved.
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