GSTT1 Null Genotype Significantly Increases the Susceptibility to Urinary System Cancer: Evidences from 63,876 Subjects
gene plays an important role in detoxification and clearance of reactive oxygen species(ROS). A null variant in this gene has been demonstrated to confer cancer susceptibility. Although many studies have demonstrated the association between null polymorphism and urinary system cancer susceptibility,...
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Published in | Journal of Cancer Vol. 7; no. 12; pp. 1680 - 1693 |
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Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
Published |
Australia
Ivyspring International Publisher
01.01.2016
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Subjects | |
Online Access | Get full text |
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Summary: | gene plays an important role in detoxification and clearance of reactive oxygen species(ROS). A null variant in this gene has been demonstrated to confer cancer susceptibility. Although many studies have demonstrated the association between
null polymorphism and urinary system cancer susceptibility, several publications reported opposite conclusions. For better understanding the effects of this polymorphism on the risk of urinary system cancer, a updated meta-analysis was performed with a total of 26,666 cases and 37,210 controls extracted from 117 studies, by following the latest meta-analysis guidelines (PRISMA). The results suggested that the
null genotype was significantly associated with an increased risk of urinary system cancer (OR=1.13, 95%CI=1.05-1.22). Furthermore, stratified analyses by the type of cancer, ethnicity, source of control and quality score presented a significantly increased risk associated with
null genotype in bladder and prostate cancer subgroup, Caucasians and Indians subgroup, population-based(PB) subgroup, medium quality and low quality subgroup. Overall, our meta-analysis suggested that
null genotype is a potential cancer susceptibility variant. Well-designed and large-cohort studies are needed to confirm the association between
null genotype and urinary system cancer risk. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 These authors contributed equally to this work. Competing Interests: The authors have declared that no competing interest exists. |
ISSN: | 1837-9664 1837-9664 |
DOI: | 10.7150/jca.15494 |