SynthesisTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2014
Polymorphisms of glutathione S-transferase M1 (GSTM1) and T1 (GSTT1) in ovarian cancer risk.
Synthesis in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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2 citing papers in PubMed, 1 synthesis or guideline pooled it, 4 citations in OpenAlex.
- Individual effects ofFrontiers in genetics · 2022Pooled it
- Cancer Risk and Eicosanoid Production: Interaction between the Protective Effect of Long Chain Omega-3 Polyunsaturated Fatty Acid Intake and Genotype.Journal of clinical medicine · 2016Review
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2 authors at 1 institution in 1 country.
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Abstract
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.
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