GSTT1

Gene Summary

Gene:GSTT1; glutathione S-transferase theta 1
Location:22q11.23
Summary:The protein encoded by this gene, glutathione S-transferase (GST) theta 1 (GSTT1), is a member of a superfamily of proteins that catalyze the conjugation of reduced glutathione to a variety of electrophilic and hydrophobic compounds. Human GSTs can be divided into five main classes: alpha, mu, pi, theta, and zeta. The theta class includes GSTT1 and GSTT2. GSTT1 and GSTT2 share 55% amino acid sequence identity and both may play an important role in human carcinogenesis. The GSTT1 and GSTT2 genes have a similar structure, being composed of five exons with identical exon/intron boundaries. This GSTT1 gene is haplotype-specific and is absent from 38% of the population. Alternative splicing of this gene results in multiple transcript variants. Two related pseudogenes, which are also located on chromosome 22, have been identified. [provided by RefSeq, Jun 2014]
Databases:OMIM, HGNC, GeneCard, Gene
Protein:glutathione S-transferase theta-1
HPRD
Source:NCBIAccessed: 16 March, 2015

Ontology:

What does this gene/protein do?
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Cancer Overview

Research Indicators

Publications Per Year (1990-2015)
Graph generated 16 March 2015 using data from PubMed using criteria.

Literature Analysis

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Tag cloud generated 16 March, 2015 using data from PubMed, MeSH and CancerIndex

Latest Publications: GSTT1 (cancer-related)

Chirilă DN, Bălăcescu O, Popp R, et al.
GSTM1, GSTT1 and GSTP1 in patients with multiple breast cancers and breast cancer in association with another type of cancer.
Chirurgia (Bucur). 2014 Sep-Oct; 109(5):626-33 [PubMed] Related Publications
INTRODUCTION: breast cancer has the highest incidence in women.Glutathione S-transferases (GSTs) are a large group of enzymes involved in the metabolism of xenobiotics. The members of this gene superfamily are involved in the development of multiple cancers.
OBJECTIVES: the aim of the study was to see whether the GSTM1, GSTT1 and GSTP1 genetic polymorphisms are risk factors for patients diagnosed with multiple malignancies, of which at least one is located in the breast.
MATERIALS AND METHODS: in the period between 2005 and 2012,of the 520 patients diagnosed with breast cancer, 69 had multiple primitive malignant tumors, of which at least one was localized in the breast. The research on GSTM1, GSTT1 and GSTP1 genotypes consisted of 59 patients diagnosed with multiple breast cancers or with breast cancer in association with another type of cancer, compared with a group of healthy controls.
RESULTS: in the subgroup of patients with breast cancer in association with another type of cancer, the GSTM1 null genotype was present in 61.2% of patients, compared to 29% of controls; the subgroup of metachronous breast cancers, the presence of any of the GSTT1 or GSTM1 null genotypes was statistically significantly different from that of controls (65.2%vs. 28.5%); in the subgroup with synchronous cancers, the GSTM1 null genotype was found in 66.6% of patients compared to 9% for the controls, and the presence of any null genotype (GSTM1 and GSTT1) was also statistically significant in the case group.
CONCLUSIONS: the GSTM1 null genotype is a risk factor for synchronous breast cancers and for breast cancer associated with extramammary cancer; the presence of null genotypes(GSTM1 or GSTT1) is a risk factor for multiple breast cancer(bilateral or synchronous); the GSTT1 null genotype and the heterozygous variant allele (Ile105Val) and homozygous variant allele (Val105Val) of GSTP1 are not risk factors for the cases studied.

Så RA, Moreira Ados S, Cabello PH, et al.
Human glutathione S-transferase polymorphisms associated with prostate cancer in the Brazilian population.
Int Braz J Urol. 2014 Jul-Aug; 40(4):463-73 [PubMed] Related Publications
OBJECTIVE: To evaluate the influence of polymorphisms in GSTA1, GSTM1, GSTT1, and GSTP1 in the risk of developing Prostate Cancer (PCa) in a population of Rio de Janeiro and compare the distribution of allele and genotype frequencies of the polymorphisms analyzed in the present study population with other regions in the country and different ethnic groups.
MATERIALS AND METHODS: We analyzed a sample of the Brazilian population, comprising 196 patients with PCa treated by the urology services of the Brazilian National Cancer Institute (INCA) and Mario Kroeff Hospital (HMK), and 208 male blood donors from the Clementino Fraga Filho Hospital, Federal University of Rio de Janeiro (UFRJ). The polymorphisms were determined in DNA, extracted from peripheral blood leucocytes using the Polymerase Chain Reaction and Restriction Fragment Length Polymorphism (PCR-RFLP).
RESULTS: Our results showed that the distribution of polymorphisms can vary significantly according to the Brazilian region and ethnic groups. The distribution of allele and genotype frequencies of the polymorphism GSTA1 was statistically different between cases and controls. Genotypes (A / B + B / B) were associated with protection (OR = 0.61, 95% CI = 0.40-0.92) for PCa in comparison to genotype A / A.
CONCLUSION: The distribution of genotype frequencies of the polymorphism GSTA1 was statistically different between the case and control groups (p = 0.023), and the presence of genotypes A / B and B / B suggests a protective role against the risk of PCa compared to genotype A / A. This is the first study that reports the genotypic frequency of this polymorphism and its association with PCa in a Brazilian population sample.

Sun X, Guo M, Sun Q, et al.
The existence and role of microchimerism after microtransplantion.
Leuk Res. 2014; 38(11):1285-90 [PubMed] Related Publications
AIM: To study microchimerism's role and function after microtransplantation and identify novel genetic markers for microchimerism detection.
METHODS: Analyzing microchimerisms from patients microtransplanted to determine the presence of GSTT1, GSTM1, SRY and other genetic markers by real-time PCR.
RESULTS: Microchimerism could be detected for a short time after microtransplantation simultaneously with hematopoietic recovery. In conclusion, microchimerism might accelerate hematopoietic recovery and GSTT1 and GSTM1 genes could be used as genetic markers to differentiate donor cells.
DISCUSSION: Microchimerism could exist for a short time after microtransplantation and appears to function in hematopoietic recovery. According to published reports, cytokines secreted from microchimerisms could be detected in recipients and exhibit some function on the host. Therefore, cytokines secreted from donor cells are hypothesized to accelerate hematopoietic recovery. The evidence to prove a longer existence for microchimerism is insufficient and needs supports by additional experiments; however, we cannot deny its existence just because of the limited sensitivity of methods.

Davies A, Giannoudis A, Zhang JE, et al.
Dual glutathione-S-transferase-θ1 and -μ1 gene deletions determine imatinib failure in chronic myeloid leukemia.
Clin Pharmacol Ther. 2014; 96(6):694-703 [PubMed] Related Publications
Approximately 40% of patients with chronic myeloid leukemia (CML) receiving imatinib fail treatment. There is an increased risk of CML in subjects with (i) deletions of genes encoding glutathione-S-transferase (GST)-θ1 (GSTT1) and -μ1, (GSTM1) and (ii) the GST-π1 (GSTP1) single-nucleotide polymorphism (SNP) Ile105Val (GSTP1*B; rs1695); however, their effects on imatinib treatment outcome are not known. Here, we assess the role of these GSTs in relation to imatinib treatment outcome in 193 CML patients. Deletion of GSTT1 alone, or in combination with deletion of the GSTM1 gene, significantly increased the likelihood of imatinib failure (P = 0.021 and P < 0.001, respectively). The GSTP1*B SNP was not associated with time to imatinib failure. Losses of the GSTT1 and GSTM1 genes are therefore important determinants of imatinib failure in CML. Screening for GSTT1 and GSTM1 gene deletions during diagnosis may identify patients who may be better treated using an alternative therapy.

He HR, You HS, Sun JY, et al.
Glutathione S-transferase gene polymorphisms and susceptibility to acute myeloid leukemia: meta-analyses.
Jpn J Clin Oncol. 2014; 44(11):1070-81 [PubMed] Related Publications
OBJECTIVE: A large body of evidence has shown the possible relevance of polymorphisms of the genes that encode glutathione S-transferase μ, π and θ (GSTM1, GSTP1 and GST1, respectively) to the susceptibility of acute myeloid leukemia, but the exact association still remains uncertain. Therefore, we performed a meta-analysis to derive a more precise estimation of the relationship.
METHODS: A comprehensive literature search of PubMed and Web of Knowledge electronic databases was conducted to collect relevant studies until 20 February 2014. References of the retrieved articles were also screened. The extracted data were statistically analyzed, and pooled odds ratios with 95% confidence intervals were calculated to estimate the association strength using Review Manager version 5.2.
RESULTS: Twenty-nine studies were included in the meta-analysis. The pooled analyses revealed that the GSTM1-null genotype was associated with an increased risk of acute myeloid leukemia in East Asians (P = 0.01; odds ratio = 1.22; 95% confidence interval = 1.05-1.42), and GSTT1-null genotype in Caucasians (P < 0.0001; odds ratio = 1.48; 95% confidence interval = 1.29-1.69). There was also a predilection towards the female gender for both of these polymorphisms. For GSTP1 Ile105Val polymorphism, no significant association was found under any contrast model. In addition, the presence of the double-null genotypes increased the risk of acute myeloid leukemia in both Caucasians and East Asians.
CONCLUSIONS: This meta-analysis suggested that heritable GST status could influence the risk of developing acute myeloid leukemia.

Xiao Q, Deng D, Li H, et al.
GSTT1 and GSTM1 polymorphisms predict treatment outcome for acute myeloid leukemia: a systematic review and meta-analysis.
Ann Hematol. 2014; 93(8):1381-90 [PubMed] Related Publications
Glutathione S-transferases (GSTs) contribute to the metabolism of different xenobiotics and anticancer drugs and confer protection against oxidative stress thus may influence the treatment outcome of acute myeloid leukemia (AML). Studies regarding the association between GSTT1 and GSTM1 polymorphisms and treatment outcome in AML patients showed an inconsistent result. A systematic review and meta-analysis were performed to further explore this association. PubMed, Hartford User Group Exchange (HUGE), and China National Knowledge Infrastructure (CNKI) databases were searched for all related publications. Statistical analyses were analyzed by using RevMan 5.0 and Stata 9.0 softwares. A total of 1,837 patients in 11 studies were included. GSTT1 null genotype was found to be significantly associated with a reduced response after first course of induction chemotherapy (odds ratio (OR) = 0.894, 95 % confidence interval (CI) = 0.818-0.977, P = 0.013), progression-free survival (PFS; hazard ratio (HR) = 0.698, 95 % CI = 0.520-0.937, P = 0.017), and overall survival (OS; HR = 0.756, 95 % CI = 0.618-0.925, P = 0.007) in Asian population. GSTM1/GSTT1 double-null genotype was also identified to be significantly associated with response after the first course of induction chemotherapy (OR = 0.40, 95 % CI = 0.24-0.67, P = 0.0003). Our study suggested that GSTT1 null genotype and GSTT1/GSTM1 double-null genotype were associated with a worse treatment outcome for AML patients, especially in Asian population.

Reszka E, Jablonowski Z, Wieczorek E, et al.
Polymorphisms of NRF2 and NRF2 target genes in urinary bladder cancer patients.
J Cancer Res Clin Oncol. 2014; 140(10):1723-31 [PubMed] Free Access to Full Article Related Publications
PURPOSE: NRF2 transcription factor is involved in modulation of various antioxidant and metabolic genes and, therefore, may modulate anti-carcinogenic potential. Association between polymorphisms of NRF2 and five NRF2-regulated genes and urinary bladder cancer (BC) risk was analyzed.
METHODS: The study group included 244 BC patients, while the control group comprised 365 individuals with no evidence of malignancy. Genotyping of GSTM1 (deletion), GSTT1 (deletion), GSTA1 -69C/T (rs3957357), GSTP1 Ile105Val (rs1695), SOD2 Ala16Val (rs4880) and NRF2 -617C/A (rs6721961) in blood genomic DNA was performed by means of real-time PCR assays. The associations between gene polymorphism and BC risk were computed by logistic regression.
RESULTS: The frequency of GSTA1, GSTP1, SOD2 and NRF2 genotypes did not differ in both groups. A significantly higher BC risk was associated with GSTM1 null genotype after adjusting to age, sex and smoking habit (OR 1.85, 95 % CI 1.30-2.62; P = 0.001). GSTT1 null (OR 0.50, 95 % CI 0.31-0.81; P = 0.005) and GSTP1 Val105Val (OR 0.52, 95 % CI 0.27-0.98; P = 0.04) genotypes were associated with reduced BC risk separately or in combination (OR 0.24, 95 % CI 0.11-0.51; P < 0.0001) (P heterogeneity = 0.01). Combined GSTT1 null and SOD2 with at least one 16Val allele among never smokers encompass reduced BC risk (OR 0.14, 95 % CI 0.03-0.63; P = 0.01) (P heterogeneity = 0.04).
CONCLUSIONS: This study supports hypothesis that GSTM1 null genotype may be a moderate BC risk factor. The gene-gene and gene-environment interactions associated with combined GSTP1/GSTT1 and combined GSTT1/SOD2 genetic polymorphisms along with cigarette smoking habit may play a significant role in BC risk modulation.

Zhou TB, Drummen GP, Jiang ZP, Qin YH
GSTT1 polymorphism and the risk of developing prostate cancer.
Am J Epidemiol. 2014; 180(1):1-10 [PubMed] Related Publications
A possible association between glutathione S-transferase theta 1 gene (GSTT1) polymorphism and the risk of developing prostate cancer is currently hotly debated, but evidence from various epidemiologic studies remains unclear. This investigation was performed to assess whether an association between GSTT1 polymorphism and prostate cancer risk exists by using meta-analysis to combine comparable studies, thereby increasing sample size and statistical significance, as well as to identify patterns in various studies. The association reports were identified from the PubMed database and the Cochrane Library on March 1, 2013, and data from eligible studies (from 1999-2012) were synthesized. Thirty-eight reports were included in this meta-analysis on the association of the null genotype of GSTT1 with prostate cancer risk. No solid association between the GSTT1 null genotype and prostate cancer risk could be established for the overall population (odds ratio = 1.11, 95% confidence interval: 0.97, 1.27; P = 0.13). However, the GSTT1 null genotype was distinctly associated with prostate cancer risk in Caucasians (odds ratio = 1.24, 95% confidence interval: 1.03, 1.48, P = 0.02). In conclusion, the GSTT1 null genotype is associated with prostate cancer risk in Caucasians, but not in the overall population.

Sui C, Ma J, He X, et al.
Interactive effect of glutathione S-transferase M1 and T1 polymorphisms on hepatocellular carcinoma.
Tumour Biol. 2014; 35(8):8235-41 [PubMed] Related Publications
Glutathione S-transferase M1 (GSTM1) and T1 (GSTT1) have been involved in the risk of hepatocellular carcinoma (HCC). However, the interactive effect of GSTM1 and GSTT1 has not been reported previously. The aim of this work was to investigate the interaction and synergism of their variants. We identified nine publications including 1,085 cases and 2,396 controls containing both GSTM1 and GSTT1, and the bi-factor variance analysis of equal repeated test, binary class logistic regression analysis, meta-analysis and probability method were used in this analysis. Data showed there was no interaction between GSTM1 and GSTT1 null genotype variation in HCC development. In addition, individuals with at least one null genotype of GSTM1 and GSTT1 had higher susceptibility to HCC (OR = 2.99, 95 % CI 2.21-4.02). In the control group, the probability of individuals with at least one null genotype of GSTM1 and GSTT1 was 0.6624, while in the case group, the probability to develop HCC with at least one null genotype of GSTM1 and GSTT1 increased to 0.1760, which was considered as the changing characteristics of HCC occurrence in Chinese population. Our result suggests that there would be no direct interaction of GSTM1 and GSTT1 genotype in HCC risk. We speculate that GSTM1 and GSTT1 genotype variations have their own independent function in HCC development and may mutate independently to cause HCC. The synergism variants of the two genes in HCC development have bigger risk in Chinese population.

Kap EJ, Richter S, Rudolph A, et al.
Genetic variants in the glutathione S-transferase genes and survival in colorectal cancer patients after chemotherapy and differences according to treatment with oxaliplatin.
Pharmacogenet Genomics. 2014; 24(7):340-7 [PubMed] Related Publications
INTRODUCTION: The glutathione S-transferase (GST) enzymes are involved in the detoxification of a range of carcinogenic compounds as well as chemotherapeutic agents. Therefore, genetic variants in the GST genes could influence survival in patients with colorectal cancer (CRC). Results from previous studies have been inconsistent and therefore we investigated the association between the GSTP1 ile105val polymorphism and the copy number variants of the GSTM1 and GSTT1 genes and survival in CRC patients treated with adjuvant/palliative chemotherapy.
PATIENTS AND METHODS: We included 755 CRC patients with stage II-IV disease from two population-based studies carried out in Germany. Genotyping of the GSTP1 polymorphism was carried out using fluorescence-based melting curve analysis and copy number variants were determined using a multiplex PCR. Survival analysis was carried out using the Cox regression model, adjusting for age, sex, UICC stage, cancer site, and radiation therapy.
RESULTS: Compared with noncarriers, CRC patients who were homozygote carriers of GSTM1 had significantly poorer survival after treatment with oxaliplatin [hazard ratio (HR) 2.25, 95% confidence interval (CI) 0.93-5.44] than those not treated with oxaliplatin (HR 0.64, 95% CI 0.30-1.34; P for heterogeneity=0.031). The association was significant in metastatic CRC patients treated with oxaliplatin (HR 3.59, 95% CI 1.29-10.03). Neither the GSTP1 105val allele nor the GSTT1 deletion was significantly associated with CRC survival.
CONCLUSION: Our data suggest that GSTM1 may be a predictive marker for oxaliplatin therapy; however, independent large studies are warranted to confirm these results.

Stosic I, Grujicic D, Arsenijevic S, et al.
Glutathione S-transferase T1 and M1 polymorphisms and risk of uterine cervical lesions in women from central Serbia.
Asian Pac J Cancer Prev. 2014; 15(7):3201-5 [PubMed] Related Publications
The aim of this study was to investigate the frequencies of GSTT1 and GSTM1 deletion polymorphisms in newly-diagnosed patients with uterine cervical lesions from central Serbia. Polymorphisms of GST genes were genotyped in 97 patients with cervical lesions and 50 healthy women using a multiplex polymerase chain reaction (PCR). The GSTM1 null genotype was significantly more prominent among the patients than in controls (74.2% vs 56.0%), the risk associated with lesions being almost 2.3-fold increased (OR=2.26, 95%CI=1.10-4.65, p=0.03) and 3.17-fold higher in patients above >45 years old (95%CI=1.02-9.79, p=0.04). The analysis of the two genotypes demonstrated that GSTM1 null genotype significantly increased risk only for low grade squamous intraepithelial lesion-LSIL (OR=2.81, 95%CI=1.03-7.68, p=0.04). GSTT1 null genotype or different genotype combinations were not found to be risk factors, irrespective to lesion stages, age or smoking. We found that the risk of cervical lesions might be significantly related to the GSTM1 null genotype, especially in women aged above 45 years. Furthermore, the GSTM1 polymorphism might have greater role in development of early stage lesions.

Pan C, Zhu G, Yan Z, et al.
Glutathione S-transferase T1 and M1 polymorphisms are associated with lung cancer risk in a gender-specific manner.
Oncol Res Treat. 2014; 37(4):164-9 [PubMed] Related Publications
BACKGROUND: Glutathione S-transferase (GST) T1 and M1 are detoxification enzymes which neutralize various carcinogenic compounds. Polymorphisms of the GSTT1 and GSTM1 genes which encode the enzymes could be associated with cancer risk.
PATIENTS AND METHODS: We investigated the association of GSTT1 and GSTM1 null polymorphisms with lung cancer risk in a tightly matched, considerably large sample in China. Genotyping was performed utilizing polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) analysis and DNA sequencing, and associations were measured by using logistic regression analysis.
RESULTS: We found that the null genotypes of both polymorphisms resulted in an increased lung cancer risk, with an odds ratio (OR) of 1.57 (95% confidence interval (CI) 1.23-2.00) for GSTT1 and OR 1.87 (95% CI 1.46-2.39) for GSTM1 (p < 0.01). Significant associations remained after stratification by histopathology (p < 0.01) and smoking status (p < 0.05). When gender-stratified association was performed, we found that the GSTT1 null genotype resulted in an increased risk among males (adjusted OR 2.95, 95% CI 2.07-4.20; p < 0.01) but not females (p > 0.05), while the GSTM1 null genotype resulted in an increased risk among females (adjusted OR 2.18, 95% CI 1.54-3.10; p < 0.01) but not males (p < 0.05).
CONCLUSION: Polymorphisms in GSTT1 and GSTM1 are associated with the risk of lung cancer in a gender-specific manner.

Ghosh SK, Singh AS, Mondal R, et al.
Dysfunction of mitochondria due to environmental carcinogens in nasopharyngeal carcinoma in the ethnic group of Northeast Indian population.
Tumour Biol. 2014; 35(7):6715-24 [PubMed] Related Publications
Nasopharyngeal carcinoma (NPC) is a rare cancer worldwide, but in India, NPC is uncommon in its subcontinent except in the north-eastern part of the country. NPC is thought to be caused by the combined effects of environmental carcinogens, genetic susceptibility and Epstein-Barr virus (EBV). This is the first study that aimed to examine the selected risk factors, mostly dietary, viral environmental, metabolic gene polymorphisms, mitochondrial DNA (mtDNA) copy number variation and their risk, in subjects who are highly prone to NPC in the ethnic groups of Northeast India, which has included cases, first-degree relatives and controls. The cases and controls were selected from three ethnic groups (Manipuri, Naga and Mizo) of Northeast India with high prevalence of NPC. This case-control family study includes 64 NPC patients, 88 first-degree relatives and 100 controls having no history of cancer. PCR-based detection was done for EBV-latent membrane protein 1 (LMP1) gene and glutathione S-transferase Mu 1 (GSTM1)-glutathione S-transferase theta 1 (GSTT1) polymorphism. A comparative ΔCt method was used for the determination of mtDNA content. An increased risk of 2.00-6.06-folds to NPC was observed with those who intake smoked meat and fish, salted fish and fermented fish; betel nut chewers; tobacco smokers; alcohol drinkers; and those who have kitchen inside the living room, glutathione S-transferase null genotype and EBV infection. The risk of NPC increased in cases with decreased mtDNA copy number (P trend = 0.007). A significant difference between GST null genotypes and EBV infection with mtDNA content was found in the cases (P < 0.0001). The understandings of environment-genetic risk factors and their role in the etiology of NPC are helpful as preventive measures and screening.

Al-Achkar W, Azeiz G, Moassass F, Wafa A
Influence of CYP1A1, GST polymorphisms and susceptibility risk of chronic myeloid leukemia in Syrian population.
Med Oncol. 2014; 31(5):889 [PubMed] Related Publications
In the present study, we investigated the associations of polymorphisms in cytochrome P450 gene (CYP1A1), glutathione S-transferase genes (GSTM1 and GSTT1) with chronic myelogenous leukemia (CML). A total of 126 patients with CML and 172 healthy volunteers were genotyped, and the DNA was isolated from their blood samples. The polymorphisms were assessed by polymerase chain reaction (PCR) restriction fragment length polymorphism-based methods and multiplex PCR. Logistic regression analyses showed significant risk of CML associated with CYP1A1 Val allele [odds ratio (OR) 3.3, 95% confidence intervals (CI) 1.96-5.53], (p < 0.0001) while CYP1A1 Val/Val homozygotes were observed only in the CML patients. There was statistically significant difference in the frequency of GSTM1 and GSTT1 null genotypes. The GSTT1-null genotype was slightly higher in 27% of CML cases and 16.7% of controls (OR 1.98, 95% CI 1.12-3.5) (p < 0.020). The GSTM1 null was higher in 42.8% of CML cases and 22.7% of controls (OR 2.55, 95% CI 1.54-4.22) (p < 0.00024). The individuals carrying CYP1A1 Ile/Val (AG) and GSTM1 null genotype have 9.9 times higher risk to be CML than those carrying CYP1A1 Ile/Ile (AA) and GSTM1 present genotype (OR 9.9, 95% CI 2.7-36.3) (p < 0.0001). This suggests that the association of the GSTM1 null genotype, either alone or in combination with GSTT1 null, with CYP1AI heterozygous leads to the CML risk.

He HR, Zhang XX, Sun JY, et al.
Glutathione S-transferase gene polymorphisms and susceptibility to chronic myeloid leukemia.
Tumour Biol. 2014; 35(6):6119-25 [PubMed] Related Publications
Glutathione S-transferase (GST), a phase II metabolizing enzyme, plays an important role in the cellar defense system, and its activity may modulate leukemia risk. A large body of evidence has shown the possible relevance of functional polymorphisms of the genes that encode GSTs μ, π, and θ (GSTM1, GSTP1, and GST1, respectively) to the genetic susceptibility of chronic myeloid leukemia (CML). Because of the lack of available conclusive data, we performed a meta-analysis of all relevant available studies to derive a more precise estimation of the relationship. A comprehensive literature search of PubMed and Web of Knowledge electronic databases was conducted to collect relevant studies until December 20, 2013, and the extracted data were statistically analyzed using Review Manager version 5.2. Finally, 16 eligible studies were identified in the literature. The GSTT1 null genotype was associated with an increased risk of CML, as were the double null GSTT1 and GSTM1 genotypes. These findings suggest that heritable GST status influences the risk of developing CML and that more attention should be paid to carriers of these susceptibility genes.

Yang F, Xiong J, Jia XE, et al.
GSTT1 deletion is related to polycyclic aromatic hydrocarbons-induced DNA damage and lymphoma progression.
PLoS One. 2014; 9(2):e89302 [PubMed] Free Access to Full Article Related Publications
The interrelationship between genetic susceptibility and carcinogenic exposure is important in cancer development. Polymorphisms in detoxification enzymes of the glutathione-S-transferases (GST) family are associated with an increased incidence of lymphoma. Here we investigated the molecular connection of the genetic polymorphism of GSTT1 to the response of lymphocytes to polycyclic aromatic hydrocarbons (PAH). In neoplastic situation, GSTT1 deletions were more frequently observed in lymphoma patients (54.9%) than in normal controls (42.0%, P = 0.009), resulting in an increased risk for lymphoma in individuals with GSTT1-null genotype (Odds ratio = 1.698, 95% confidence interval = 1.145-2.518). GSTT1 gene and protein expression were accordingly decreased in GSTT1-deleting patients, consistent with activated profile of cell cycle regulation genes. Mimicking environmental exposure using long-term repeat culture with low-dose PAH metabolite Hydroquinone, malignant B- and T-lymphocytes presented increased DNA damage, pCHK1/MYC expression and cell proliferation, which were counteracted by ectopic expression of GSTT1. Moreover, GSTT1 expression retarded xenograft tumor formation of Hydroquinone-treated lymphoma cells in nude mice. In non-neoplastic situation, when zebrafish was exposed to PAH Benzo(a)pyrene, molecular silencing of gstt1 enhanced the proliferation of normal lymphocytes and upregulated myca expression. Collectively, these findings suggested that GSTT1 deletion is related to genetic predisposition to lymphoma, particularly interacting with environmental pollutants containing PAH.

Oliveira AL, Oliveira Rodrigues FF, Dos Santos RE, et al.
 GSTT1, GSTM1, and GSTP1 polymorphisms as a prognostic factor in women with breast cancer.
Genet Mol Res. 2014; 13(2):2521-30 [PubMed] Related Publications
The glutathione S-transferase (GST) family comprises phase-II cellular detoxification enzymes that catalyze the conjugation of chemotherapy drugs to glutathione and act on the apoptotic pathway. The aim of this study was to determine whether polymorphisms of the GSTT1, GSTM1, and GSTP1 genes are associated with different rates of overall survival (OS) and disease-free survival (DFS) after neoadjuvant chemotherapy in the management of locally advanced breast cancer, using either simple or combined analyses, and in relation to the post-therapy axillary lymph node status. Forty women with invasive ductal carcinoma of the breast submitted to neoadjuvant chemotherapy with 5-fluorouracil, epirubicin, and cyclophosphamide were genotyped for GSTT1, GSTM1, and GSTP1. Comparisons were performed for the three genes, either isolated or in pairs, in polymorphic or wild-type combinations. Finally, the OS and DFS of patients were analyzed with respect to axillary lymph node status and with respect to wild-type or polymorphic presentations of each gene. No statistically significant difference in OS and DFS was evident between women with wild-type or polymorphic forms of the genes, either isolated or in pairs, after neoadjuvant chemotherapy. By contrast, after treatment, lymph node-negative women had better OS and DFS only in the presence of polymorphisms of GSTP1, and improved DFS only in the presence of the polymorphic types of GSTT1 and GSTM1 compared to women with positive lymph nodes. The presence of polymorphic forms of GSTP1, GSTM1, and GSTT1 was crucial to conferring better OS and DFS among women with negative axillary lymph nodes.

Silva TM, Marques CR, Marques Filho MF, et al.
Association of the GSTT1 polymorphism in upper aerodigestive tract cancer with tobacco smoking.
Genet Mol Res. 2014; 13(1):528-37 [PubMed] Related Publications
Polymorphisms in genes encoding xenobiotic-metabolizing enzymes might explain differences in the susceptibility to upper aerodigestive tract (UADT) cancers in individuals exposed to tobacco or other carcinogens. The present study aimed to evaluate the association of polymorphisms in the glutathione S-transferase (GST) candidate genes GSTM1, GSTT1, and GSTP1 with the risk of UADT cancers. GST gene polymorphisms were determined in 116 individuals with UADT cancer and 224 healthy controls using polymerase chain reaction-based methods. The GSTT1-null polymorphism was found to be a protective factor for UADT cancer [(odds ratio (OR) = 0.5, 95% confidence interval (CI) = 0.27-0.93)], although this association was not confirmed when adjusted for gender, age, smoking, alcoholism, and self-reported skin color in the multivariate logistic regression model (OR = 0.61, 95%CI = 0.29-1.28). The combined effect of GSTT1-positive genotypes with either the GSTP1 wild-type genotype (Ile/Ile) or the GSTP1 variant genotypes (Ile/Val or Val/Val) increased the risk for UADT cancer (OR = 4.34, 95%CI = 1.06-17.78 and OR = 4.55, 95%CI = 1.12-18.42, respectively). A significant interaction was observed among moderate smokers carrying the GSTT1-positive genotype. In this population, the significant gene-gene and gene-environment interactions of GST polymorphisms may confer a substantial risk to UADT cancers.

Yamada I, Matsuyama M, Ozaka M, et al.
Lack of associations between genetic polymorphisms in GSTM1, GSTT1 and GSTP1 and pancreatic cancer risk: a multi-institutional case-control study in Japan.
Asian Pac J Cancer Prev. 2014; 15(1):391-5 [PubMed] Related Publications
BACKGROUND: We aimed to evaluate the role of genetic polymorphisms in tobacco carcinogen-metabolizing genes and their interactions with smoking in a hospital-based case-control study of Japanese subjects.
MATERIALS AND METHODS: We examine the associations of pancreatic cancer risk with genetic polymorphisms in GSTM1, GSTT1 and GSTP1, phase II enzymes that catalyze the conjugation of toxic and carcinogenic electrophilic molecules. The study population consisted of 360 patients and 400 control subjects, who were recruited from several medical facilities in Japan. Unconditional logistic regression methods were used to estimate odds ratios (ORs) and 95% confidence intervals (CIs) for the associations between genotypes and pancreatic cancer risk.
RESULTS: Among the control subjects, the prevalence of the GSTM1-null genotype and the GSTT1-null genotype was approximately 56% and 48%, respectively. Cases and controls were comparable in terms of GSTM1 and GSTT1 genotype distributions. Neither of the deleted polymorphisms in GSTM1 and GSTT1 was associated with the risk of pancreatic cancer, with an age- and sex-adjusted OR of 0.99 (95%CI: 0.74-1.32) for the GSTM1-null genotype, and 0.98 (95%CI: 0.73-1.31) for the GSTT1-null genotype. The OR was 0.97 (95%CI: 0.64-1.47) for individuals with the GSTM1 and GSTT1-null genotypes compared with those with the GSTM1 and GSTT1- present genotypes. No synergistic effects of smoking or GST genotypes were observed.
CONCLUSIONS: Our results indicate no overall association between the GSTM1 and GSTT1 deletion polymorphisms and pancreatic cancer risk in the Japanese subjects in our study.

Panic N, Mastrostefano E, Leoncini E, et al.
Susceptibility to Helicobacter pylori infection: results of an epidemiological investigation among gastric cancer patients.
Mol Biol Rep. 2014; 41(6):3637-50 [PubMed] Related Publications
The aim of this study was to identify the clinical, demographic, lifestyle factors and selected genetic polymorphisms that affect the susceptibility towards Helicobacter pylori (H. pylori) infection in gastric cancer patients. Histological confirmed gastric adenocarcinoma cases that underwent curative gastrectomy between 2002 and 2012 were included. Gastric biopsy samples were obtained to determine the H. pylori status, and further cagA status and vacA m and s genotypes by polymerase chain reaction. Patients were interviewed with structured questionnaires, and blood samples were collected for EPHX1, GSTM1, GSTT1, IL1B, IL1-RN, MTHFR and p53 genotyping. Proportions were compared in univariate analysis, while the relation between putative risk factors and H. pylori status and genotype were measured using logistic regression analysis. One hundred forty-nine gastric cancer patients were included, of which 78.5% were H. pylori positive. Among positive patients 50% were cagA+, 72.5% vacA m1 and 80.7% vacA s1. The presence of cagA was less frequent among vacA m1 (p = 0.031) and vacA s1 (p = 0.052) subtypes. The presence of father history for any cancer was a significant risk factor for H. pylori infection [adjusted odds ratio (OR) = 8.18, 95% confidence interval (CI) 1.04-64.55]. EPHX1 exon 3 T > C (OR = 0.35, CI 95% 0.13-0.94), IL1B-511 T > C (OR = 0.38, CI 95% 0.15-0.97) and IL1-RN VNTR (OR = 0.19, CI 95% 0.06-0.58) polymorphisms were protective towards H. pylori infection in the univariate analysis. Wine consumption was associated with higher risk of carrying the H. pylori vacA m1 virulent subtype (p = 0.034). Lastly, cardiovascular diseases were less common among cagA positive subjects (p = 0.023). Father history of any cancer is a risk factor for H. pylori infection. Polymorphisms in IL1B-511, IL1-RN and EPHX1 exon 3 genes might be protective towards H. pylori infection.

Kant Shukla R, Kant S, Mittal B, Bhattacharya S
Comparative study of GST polymorphism in relation to age in COPD and lung cancer.
Tuberk Toraks. 2013; 61(4):275-82 [PubMed] Related Publications
INTRODUCTION: Glutathione-S-transferase is involved in detoxification of xenobiotic compounds. GSTs gene polymorphisms have been considered as a potential modifier for the respiratory disease. COPD is a chronic inflammatory disease of the lungs, which progresses very slowly and the majority of patients are therefore elderly, and few study suggested that age is major risk factor for cancer. Whether age in metabolism of phases 2 enzyme gene polymorphisms GSTT1 and GSTM1 in Northern Indian COPD and lung cancer patients.
MATERIALS AND METHODS: We have enrolled lung cancers, COPD patients and for the comparison we enrolled controls. Peripheral blood of COPD and lung cancer patients was taken after spirometry evaluation and histopathology. All genotyping were done by PCR-RFLP method. Independent sample t-test was performed to compare the mean values of continuous data. Statistical significance of differences in genotype frequencies between patients and controls was estimated by the chi-square two test.
RESULTS: GSTM1 null polymorphism was found to be significantly higher in COPD patients as compared with healthy controls (OR= 2.08; 95%; CI= 1.40-3.09; p= 0.0001), but there were no significant differences polymorphisms of GSTT1 null patients and healthy controls. In lung cancer GSTT1 null was found significantly associated (OR= 1.87; 95%; CI= 1.25-2.80; p= 0.002) however GSTM1 null was not associated with lung cancer patients. In subgroup analysis, we found GSTM1 Null significantly associated between age 46-65 years in COPD patients and healthy controls (62.2%/37.8%, OR= 3.20; 95%; CI= 1.97-5.18; p= 0.001), In lung cancer and controls (55.6%/44.4% OR= 1.07; 95% CI= 0.68-1.69; p= 0.774).
CONCLUSION: The effects of the GSTM1 null genotype seemed strong association with COPD and GSTT1 null genotype with lung cancer patients. GSTM1 null genotype is associated with an increased risk of COPD, especially in middle age.

Gataa I, Emile G, Loriot MA, et al.
Association between high antitumor activity of oxaliplatin and cyclophosphamide and constitutional GSTM1 homozygous deletion in an advanced ovarian cancer patient.
Chemotherapy. 2013; 59(4):290-3 [PubMed] Related Publications
BACKGROUND: Although the efficiency of oxaliplatin in patients with advanced ovarian cancer has been demonstrated, it is not commonly used. In cells, oxaliplatin is metabolized by the enzymes belonging to the glutathione-S-transferase (GST) family.
CASE: A 55-year-old woman with advanced ovarian cancer received 6 cycles of paclitaxel and carboplatin after debulking surgery. Six months later, she experienced a clinical recurrence. A second-line chemotherapy combining 500 mg/m² cyclophosphamide with 100 mg/m² oxaliplatin was initiated and maintained for 10 cycles. The patient thus experienced a second complete remission that lasted for 6 years. We found that she had deficient GSTM1 enzyme activity with homozygous deletion and normal GSTP1 and GSTT1 activities.
CONCLUSION: The association of a homozygous deletion of GSTM1 with hypersensitivity to oxaliplatin and cyclophosphamide combination chemotherapy has not been described to date in ovarian cancer. Further study of its potential interest to personalized second-line therapy in these patients is called for.

Liu HZ, Peng J, Zheng F, et al.
Lack of assocation of glutathione S-transferase T1 gene null and susceptibility to lung cancer in china: a meta-analysis.
Asian Pac J Cancer Prev. 2013; 14(12):7215-9 [PubMed] Related Publications
BACKGROUND: Variation in metabolic genes is regarded as an important factor in processes leading to cancer. However, the effect of GSTT1 null genotype is divergent in the form of lung cancer.
METHODS: Studies were conducted at different research databases from 1990 to 2013 and the total odds ratio (OR) and 95% confidence interval (CI) were calculated for lung cancer. Review Manager 5.2 and STATE 12 are employed.
RESULTS: Total OR value is calculated from 17 articles with 2,118 cases and 2,915 controls. We discovered no significant increase in lung cancer risk among subjects carrying GSTT1 null genotype [OR = 1.15; 95% CI 0.97-1.36] in this meta- analysis.
CONCLUSION: The GSTT1 deletion polymorphism does not have a significant effect on the susceptibility to lung cancer overall in China.

de Araújo RM, de Melo CF, Neto FM, et al.
Association study of SNPs of genes IFNGR1 (rs137854905), GSTT1 (rs71748309), and GSTP1 (rs1695) in gastric cancer development in samples of patient in the northern and northeastern Brazil.
Tumour Biol. 2014; 35(5):4983-6 [PubMed] Related Publications
Cancer is a multifactorial disease with a high mortality rate in Brazil and worldwide. Gastric cancer (GC) is considered the fourth type of malignancy more frequent in the population worldwide and the second leading cause of death. This work aimed to evaluate single nucleotide polymorphisms (SNPs) of IFNGR1, GSTT1, and GSTP1 genes samples in gastric cancer. We analyzed 60 samples of gastric cancer, 26 diffuse and 34 intestinal types, totaling 120 alleles for each SNP. The results were obtained by PCR and allele-specific PCR. Statistical analyzes performed using BioEstat 5.0 software, applying the Fisher's exact test and chi-square. Only the SNP gene GSTP1 (rs1695) were significantly associated with gastric cancer in the samples analyzed (χ(2) = 8.73, P < 0.05). Our results suggest that the GSTP1 gene SNP (rs1695) can be considered a risk factor associated with gastric carcinogenesis.

Masood N, Yasmin A, Kayani MA
Genetic variations and head and neck cancer risks.
Mol Biol Rep. 2014; 41(4):2667-70 [PubMed] Related Publications
Variations in CYP1A1, GSTM1, GSTT1 and GSTP1 in head and neck cancer have been frequently found in literature. But these studies give an overview of these genetic variations in different populations. The current mini review focus on the analysis of these genetic variations at DNA, mRNA and protein levels in the same study group. Eight publications were reviewed on the same study samples yielding results at DNA, mRNA and protein levels. At DNA level, CYP1A1 showed significantly higher mutations in head and neck cancer patients compared to controls at g.2842A>C and g.2842_2843insT. GSTM1 and GSTT1 showed deletion polymorphisms and heterozygous deletion confers protection against cancer. Mutations were also found in GSTP1 at g.2848A>T, g.2849G>A, g.1074delC and g.1466delC. mRNA and protein expressional analysis revealed underexpression of CYP1A1, loss or underexpression of GSTM1 and GSTT1 and overexpression of GSTP1. In addition an unusual intronic variant of GSTP1 mRNA was also found, retaining the intronic portion between exons. The current review gives a complete study overview regarding CYP1A1, GSTM1, GSTT1 and GSTP1 variations at DNA, mRNA and protein levels in head and neck cancer. The review is helpful in designing a new experiment or gene therapy for head and neck cancer patients.

Shen YH, Chen S, Peng YF, et al.
Quantitative assessment of the effect of glutathione S-transferase genes GSTM1 and GSTT1 on hepatocellular carcinoma risk.
Tumour Biol. 2014; 35(5):4007-15 [PubMed] Related Publications
Hepatocellular carcinoma (HCC) is one of the most serious health problems worldwide. As in many other diseases, environment and genetic factors are believed to be involved in the pathogenesis of HCC. Numerous epidemiologic investigations including case-control and cohort studies have suggested the association of glutathione S-transferase (GST) genetic polymorphisms and HCC risk. However, some studies have produced conflicting results. Therefore, we performed an updated meta-analysis to clarify this inconsistency and to establish a comprehensive picture of the association of the polymorphisms of GSTM1 and GSTT1 with HCC susceptibility. We searched PubMed, Embase, ISI Web of Science, and CNKI databases to identify eligible studies meeting the inclusion criteria up to August 30, 2013. Odds ratios (ORs) and 95% confidence intervals (CIs) were used to assess the strength of association. Finally, there were a total of 33 studies with 4,232 cases and 6,601 controls included in this meta-analysis. In the pooled analysis, significantly increased HCC risks were found for null genotype of GSTM1 (OR = 1.31, 95% CI = 1.07-1.61, P = 0.010, P heterogeneity < 10(-5)) and GSTT1 (OR = 1.47, 95% CI = 1.25-1.74, P < 10(-5), P heterogeneity < 10(-5)). Potential sources of heterogeneity were explored by subgroup analysis based on ethnicity, sample size, and source of control. Significant results were found among East Asians and Indians when stratified by ethnicity, while no evidence of significant associations was observed among Caucasian and African populations. In the gene-gene interaction analysis, a statistically significant increased risk for HCC was detected for individuals with combined deletion mutations in both genes compared to those with wild genotypes (OR = 1.88, 95% CI = 1.41-2.50, P < 10(-4), P heterogeneity = 0.004). The present meta-analysis demonstrated that the GSTM1 and GSTT1 null genotype may be associated with an increased risk of HCC and that individuals having the combination of both defective GST genotypes may be more susceptible to developing HCC.

Haholu A, Berber U, Karagöz B, et al.
Is there any association of glutathione S-transferase T1 (GSTT1) and glutathione S-transferase M1 (GSTM1) gene polymorphism with gastric cancers?
Pol J Pathol. 2013; 64(4):247-52 [PubMed] Related Publications
The glutathione S-transferases (GST) are enzymes catalyzing reactions including carcinogens. GSTT1 and GSTM1 genes are polymorphic in humans. The relations between polymorphism of some GST genes and cancer have been reported. In this study, we aimed to investigate the distribution of GSTT1 and GSTM1 polymorphisms in a group of gastric cancer patients. The study group consisted of 50 patients (21 females, 29 males) with gastric adenocarcinoma from the archives of the pathology department of a training hospital. Fifty-seven healthy control subjects were included in the study as a control group. DNA was extracted from peripheral venous blood of control subjects and from the paraffin blocks of cases. Genotyping of GSTT1 and GSTM1 genes was performed with duplex polymerase chain reaction. No differences in the frequencies of GSTM1 or GSTT1 null genotypes were observed between patients and healthy subjects (GSTM1: 52% vs. 43.85%, OR = 1.27, 95% CI: 0.55-2.96; GSTT1: 38.46% vs. 28.07%, OR = 0.72, 95% CI: 0.25-1.96). Moreover, simultaneous carriage of both genotypes was almost identical in both groups. GSTM1 or GSTT1 null genotypes were not different in diffuse or intestinal type gastric cancer. Our data suggest that the GSTM1 and GSTT1 polymorphisms are not associated with gastric cancer in a small group of the Turkish population.

Meng YB, Cai XY, Lu WQ, et al.
Meta-analysis of the association of glutathione S-transferase T1 null/presence gene polymorphism with the risk of gastric carcinoma.
Mol Biol Rep. 2014; 41(2):639-49 [PubMed] Related Publications
A possible association of glutathione S-transferase T1 (GSTT1) null/presence gene polymorphism and an increased risk of developing gastric carcinoma is still unclear and hotly debated. This investigation was performed to assess the association of the GSTT1 null/presence gene polymorphism with the risk of gastric carcinoma via a meta-analysis to increase sample size and statistical significance. PubMed, Cochrane Library and CBM-disc (China Biological Medicine Database) were searched on March 1, 2013, association reports were identified, and eligible studies were recruited and synthesized. Fifty-two reports were found to be suitable for this meta-analysis for the association of the GSTT1 null genotype with gastric carcinoma risk. The results showed that there was a significantly increased gastric carcinoma risk when the GSTT1 null genotype was present in the overall population (OR 1.21, 95 % CI 1.11-1.32, P < 0.0001), Caucasians (OR 1.25, 95 % CI 1.05-1.48, P = 0.01), East-Asians (OR 1.18, 95 % CI 1.06-1.31, P = 0.003), and Chinese (OR 1.24, 95 % CI 1.07-1.44, P = 0.005). However, no statistically relevant association could be established for the Indian ethnic group (OR 1.33, 95 % CI 0.94-1.90, P = 0.11). In conclusion, the GSTT1 null genotype is associated with an increased gastric carcinoma risk in the overall population, Caucasians, East-Asians, and Chinese.

Tse G, Eslick GD
Cruciferous vegetables and risk of colorectal neoplasms: a systematic review and meta-analysis.
Nutr Cancer. 2014; 66(1):128-39 [PubMed] Related Publications
Evidence shows cruciferous vegetables exhibit chemoprotective properties, commonly attributed to their rich source of isothiocyanates. However, epidemiological data examining the association between cruciferous vegetable intake and colorectal neoplasms have been inconclusive. This meta-analysis examines the epidemiological evidence to characterize the association between cruciferous vegetable intake and risk of developing colorectal neoplasms. Thirty-three articles were included in the meta-analysis after a literature search of electronic databases. Subgroup analysis for individual cruciferae types (n = 8 studies) and GST polymorphism (n = 8 studies) were performed. Pooled adjusted odds ratios (ORs) comparing highest and lowest categories of dietary pattern scores were calculated. Results show a statistically significant inverse association between cruciferous vegetable intake and colon cancer [OR = 0.84; 95% confidence interval (CI): 0.72-0.98; P value heterogeneity < 0.001]. Broccoli in particular exhibited protective benefits against colorectal (CRC) neoplasms (OR = 0.80; 95% CI: 0.65-0.99; P value heterogeneity = 0.02). Stratification by GST genotype reveals that the GSTT1 null genotype confers a reduction in CRC risk (OR = 0.78; 95% CI: 0.64-0.95; P value heterogeneity = 0.32). This study provides support to the hypothesis that cruciferous vegetable intake protects against cancer of the colon. This study also demonstrates the significance of gene-diet interactions and the importance of assessing individual cruciferous vegetables.

Jia CY, Liu YJ, Cong XL, et al.
Association of glutathione S-transferase M1, T1, and P1 polymorphisms with renal cell carcinoma: evidence from 11 studies.
Tumour Biol. 2014; 35(4):3867-73 [PubMed] Related Publications
The glutathione S-transferases (GSTs) are a gene superfamily of phase II metabolic enzymes that has attracted a considerable attention as a candidate gene for renal cell carcinoma (RCC) based on its enzyme function as a key factor in biotransformation pathways. In the past decade, a number of case-control studies were conducted to investigate the association of GST genetic polymorphisms and RCC risk. However, studies on the association between GST (GSTM1, GSTT1, and GSTP1) polymorphisms and RCC remain to be conflicting. To derive a more precise estimation of the relationship, a meta-analysis of 2,189 cases and 3,817 controls from 11 case-control studies was performed. Overall, the summarized odds ratio for RCC of the GSTM1 null and GSTT1 null polymorphisms was 1.02 (95% confidence interval (CI) 0.91-1.15, P = 0.70) and 1.28 (95% CI 0.96-1.72, P = 0.09), respectively. No significant results were observed in heterozygous and homozygous genotypes when compared with wild-type genotype for GSTP1 I105V polymorphism. However, the GSTM1-GSTT1 interaction analysis showed that the dual null genotype of GSTM1/GSTT1 was significantly associated with an increased RCC risk (odds ratio (OR) = 1.42, 95% CI 1.14-1.76, P = 0.001). In the stratified analyses by ethnicity, significant gene-disease association was obtained among Asians for GSTT1 and GSTP1 polymorphisms. In our meta-analysis, the associations between variations of GSTs and RCC may vary in different ethnic populations, and the interaction between unfavorable GST genotypes may exist.

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