Glutathione S-transferase P1 rs1695 A>G polymorphism and breast cancer risk: evidence from a meta-analysis.

Breast cancer (BC) is the most widespread cause of cancer-related deaths in women. Many published studies have assessed the association between the glutathione S-transferase P1 (GSTP1) rs1695 polymorphism and BC risk. However, the effect of the GSTP1 rs1695 polymorphism on BC risk has remained controversial. Therefore, this meta-analysis was conducted to obtain a comprehensive estimation of this association. A total of 20,615 cases and 20,481 controls from thirty-six case-control trials were extracted from an online literature survey. The meta-analysis indicated that the GSTP1 rs1695 A>G polymorphism did not contribute to the susceptibility of BC when the overall population was considered. However, intriguingly, this polymorphism was significantly associated with increased risk of BC in Asian women [GG vs AA: odds ratio (OR) = 1.4, 95% confidence interval (CI): 1.06-1.88, P = 0.02; AG vs AA: OR = 1.08, 95%CI = 1.00-1.16, P = 0.05; GG/AG vs AA: OR = 1.11, 95%CI = 1.04-1.19, P = 0.00]. Moreover, a subgroup analysis based on the source of control groups showed a marked increase in BC susceptibility in hospital-based control subjects (GG vs AA: OR = 1.28, 95%CI = 1.10-1.48, P= 0.00; GG vs AG/AA: OR = 1.22, 95%CI = 1.06-1.41, P = 0.00; GG/AG vs AA: OR = 1.10, 95%CI = 1.02-1.18, P = 0.00). In conclusion, our study indicated that the GSTP1 rs1695 A>G polymorphism was correlated with elevated BC risk in Asian women. Our results must be validated with further research.

Implicating the H63D polymorphism in the HFE gene in increased incidence of solid cancers: a meta-analysis.

A number of previous studies have demonstrated that the HFE H63D polymorphism is associated with increased risk of incidence multiple types of cancer, including colorectal cancer, breast cancer, liver cancer, pancreatic cancer, and gynecological malignant tumors. However, the clinical outcomes were inconsistent. Therefore, this meta-analysis was conducted to summarize the effect of the H63D variant on the incidence of solid tumor. PubMed and EMBASE databases were searched for articles associating the HFE H63D polymorphism with cancer risk. The relationships were evaluated by calculating the pooled odds ratios (ORs) with 95% confidence intervals (CIs). A total of 28 studies, including 7728 cancer cases and 11,895 controls, were identified. Statistically significant associations were identified between the HFE H63D polymorphism and solid cancer risk (CG vs CC, OR = 1.14, 95%CI = 1.07-1.23, P < 0.001; GG vs CC, OR = 1.28, 95%CI = 1.06-1.55, P = 0.010; CG/GG vs CC, OR = 1.16, 95%CI = 1.08-1.24, P < 0.001; GG vs CC/CG, OR = 1.24, 95%CI = 1.02-1.49, P = 0.027). In the subgroup analysis, we illustrated the effect of the H63D polymorphism on hepatocellular carcinoma and pancreatic cancer risk, particularly in the Asian and African subgroups; however, this was not observed in gynecological malignant tumors. In summary, this analysis provided strong evidence that the HFE H63D polymorphism may play a critical role in the increased aggressiveness of hepatocellular carcinoma and pancreatic cancer.

Clinical significance of SHMT1 rs1979277 polymorphism in Asian solid tumors: evidence from a meta-analysis.

Published data regarding the association between the cytosolic serine hydroxymethyltransferase (SHMT1) C1420T (Leu474Phe) polymorphism and solid tumor risk have shown inconclusive results. To derive a more precise estimation of the relationship, we performed a meta-analysis of 23 published studies that included 14,409 cancer cases and 16,996 controls. A comprehensive search was conducted to identify all eligible studies of the SHMT1 rs1979277 polymorphism and solid tumor risk. The pooled odds ratios (ORs) and the 95% confidence intervals (95%CIs) were calculated using a fixed- or random-effects model. Heterogeneity was represented by PH; publication bias and sensitivity analysis were also explored. Overall, no significant associations were found for any genetic models tested. However, upon stratification by cancer type, a significant decreased risk of breast cancer risk was identified in the homozygote comparison (OR = 0.79, 95%CI = 0.65-0.97 for TT versus CC). An analysis stratified by ethnicity and source of controls revealed an obvious decrease in risk among Asian groups in all genetic models, and among population-based controls only in the homozygote comparison and recessive model. Therefore, our meta-analysis suggested that the SHMT1 C1420T polymorphism was associated with decreased risk of breast cancer. Significant protective effects were found among Asian populations, but not in Caucasian groups. Due to some minor limitations, our findings should be confirmed by further studies.