Polymorphisms of glutathione S-transferase M1 (GSTM1) and T1 (GSTT1) in ovarian cancer risk
Glutathione S -transferases (GSTs) are ubiquitous, multifunctional phase II metabolic enzymes responsible for the detoxification of estrogen involved in the development of ovarian cancer. Data from epidemiological studies show conflicting results that remain to be further clarified. We estimated in...
        Saved in:
      
    
          | Published in | Tumor biology Vol. 35; no. 6; pp. 5267 - 5272 | 
|---|---|
| Main Authors | , | 
| Format | Journal Article | 
| Language | English | 
| Published | 
        Dordrecht
          Springer Netherlands
    
        01.06.2014
     Springer Nature B.V  | 
| Subjects | |
| Online Access | Get full text | 
| ISSN | 1010-4283 1423-0380 1423-0380  | 
| DOI | 10.1007/s13277-014-1685-7 | 
Cover
| Summary: | Glutathione
S
-transferases (GSTs) are ubiquitous, multifunctional phase II metabolic enzymes responsible for the detoxification of estrogen involved in the development of ovarian cancer. Data from epidemiological studies show conflicting results that remain to be further clarified. We estimated in this study the genetic effects of
GSTM1
and
GSTT1
polymorphisms on ovarian cancer risk. Eligible studies of the two polymorphisms and ovarian cancer risk were identified from China National Knowledge Infrastructure (CNKI), PubMed, Embase, and Web of Science. We summarized all data and performed a meta-analysis. Odds ratio (OR) and 95 % CI was calculated by using the fixed effects model to estimate the associations. Eight eligible studies were finally identified providing 2,397 cases and 2,910 controls for
GSTM1
polymorphism and 2,049 cases and 2,668 controls for
GSTT1
polymorphism. The overall data showed that carries of the
GSTM1
null genotype did not have significantly increased ovarian cancer risk compared with those who carried the
GSTM1
present genotype (null vs. present—OR, 1.01; 95 % CI, 0.91–1.11; heterogeneity,
P
 = 0.672). Similarly, for
GSTT1
polymorphism, we observed no association under the investigated model in the overall analysis (null vs. present—OR, 1.02; 95 % CI, 0.89–1.17; heterogeneity,
P
 = 0.372), and in the subgroup of Caucasian subjects (null vs. present—OR, 0.99; 95 % CI, 0.86–1.14; heterogeneity,
P
 = 0.959). The meta-analysis does not provide a strong evidence for causal associations between
GSTM1
and
GSTT1
polymorphisms and risk of ovarian cancer in Caucasians. | 
|---|---|
| Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 14 ObjectType-Article-1 ObjectType-Feature-2 content type line 23  | 
| ISSN: | 1010-4283 1423-0380 1423-0380  | 
| DOI: | 10.1007/s13277-014-1685-7 |