A systematic review and meta-analyses of the relationship between glutathione S-transferase gene polymorphisms and renal cell carcinoma susceptibility

Abstract

BackgroundAssociation of GSTM1- and GSTT1-null genotypes, GSTP1 A/G gene polymorphism with renal cell carcinoma (RCC) susceptibility was detected, and the relationship between the GSTM1/GSTT1-null genotype and clinical TNM stages of RCC was assessed, using meta-analysis method.MethodsAssociation investigations according to eligibility criteria were searched and identified from the databases of Cochrane Library, PubMed, and Embase from establishment time of databases to July 1, 2017, and eligible reports were analyzed by meta-analysis. 95% confidence intervals (CI) were also detected, and odds ratios (OR) was used to express the results for dichotomous data.ResultsThis meta-analysis indicated that there was no an association between GSTM1-null genotype, GSTT1-null genotype, GSTP1 A/G gene polymorphism and RCC risk in the overall population of Caucasians or Asians. The dual GSTM1–GSTT1-null genotype was also not associated with RCC in the overall population of Caucasians. Interestingly, there was an association between the dual GSTM1-GSTT1-null genotype and the susceptibility of RCC in Asians. Relationship of the GSTM1-null genotype with clinical TNM stage of RCC was not observed in the overall population of Asians or Caucasians. In this meta-analysis, no association between the GSTT1-null genotype and clinical TNM stage of RCC was observed in Caucasians or Asians. Interestingly, GSTT1-null genotype was detected to be associated with the clinical TNM stages in patients with RCC in the overall population.ConclusionThe dual GSTM1-GSTT1-null genotype is detected to be associated with the onset of RCC in Asians, and there is an association between the GSTT1-null genotype and the clinical TNM stages in patients with RCC in the overall population.Electronic supplementary materialThe online version of this article (10.1186/s12881-018-0620-y) contains supplementary material, which is available to authorized users.

Concomitance of Polymorphisms in Glutathione Transferase Omega Genes Is Associated with Risk of Clear Cell Renal Cell Carcinoma

“…Furthermore, polymorphisms in GST genes could affect both individual response to carcinogen exposure and pharmacogenomic-based cancer treatment (Lo and Ali-Osman 2007). So far the association of common GST gene polymorphisms (GSTM1, GSTT1, GSTP1 and GSTA1), independently or in interaction with environmental factors, with increased risk of developing RCC has been shown (Coric et al 2016;Zhong et al 2018). Novel omega class GST consists of two isoenzymes, GSTO1-1 and GSTO2-2.…”

Ethacrynic Acid Enhances the Antitumor Effects of Afatinib in EGFR/T790M-Mutated NSCLC by Inhibiting WNT/Beta-Catenin Pathway Activation

“…However, no changes in GST were detected in this study. A meta-analysis in 2018 reported that glutathione S-transferase gene polymorphism (GST-PI) gene mRNA was high in NSCLC and was involved in the pathogenesis and prognosis of NSCLC [36,37]. In contrast, a study reported that the levels of GSH were low in EGFR-T790M NSCLC and increased GSH expression in acquired NSCLC cells resensitized by the EGFR TKIs [38].…”

Glutathione transferase genotypes may serve as determinants of risk and prognosis in renal cell carcinoma

“…By contrast, GSTM1‐active genotype was confirmed to be an independent predictor of poor RCC survival . What is more, it has been shown that the GSTM1‐null genotype was associated with a lower tumor grade, whereas the GSTT1‐null genotype was associated with more advanced TNM stages (Table ) …”

“…57 What is more, it has been shown that the GSTM1-null genotype was associated with a lower tumor grade, whereas the GSTT1-null genotype was associated with more advanced TNM stages (Table 2). 49,56,[73][74][75] GSTO1 also possesses numerous regulatory roles, such as modulation of ryanodine receptors (RyRs), posttranslational processing of interleukin-1β (IL1-β), and proposed antiapoptotic role. [77][78][79] Furthermore, it has been suggested that GSTO1-1 could also contribute to tumor chemoresistance by activation of survival signaling pathways (Akt and ERK1/2) and inhibition of apoptotic MAPK pathway (JNK1).…”