GSTT1, GSTM1 and GSTP1 genetic polymorphisms and interaction with tobacco, alcohol and occupational exposure in esophageal cancer patients from North India

Jain, Meenu; Kumar, Shaleen; Rastogi, Neeraj; Lal, Punita; Ghoshal, Uday C; Tiwari, Ankita; Pant, M. C.; Baiq, Mirza Q.; Mittal, Balraj

doi:10.1016/j.canlet.2005.10.034

Cited by 65 publications

(46 citation statements)

References 30 publications

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“…In the present study, only marginal increase in risk due to GSTM1 null genotype was observed. We had earlier shown GSTM1 null genotype to be a risk factor for developing adenocarcinoma (9).…”

Section: Discussionmentioning

confidence: 95%

“…Genomic DNA was prepared from frozen blood samples collected in EDTA. DNA was isolated as described elsewhere (9,10). Genotype frequencies at the GSTM3 and GSTM1 loci were determined by PCR.…”

Section: Methodsmentioning

confidence: 99%

“…Genotype frequencies at the GSTM3 and GSTM1 loci were determined by PCR. GSTM1 null polymorphism genotyping was done using method described elsewhere (9). GSTM3 reactions were carried out in a total volume of 25 AL containing 50 ng DNA template, 20 pmol GSTM3 primers (10, 11), 10 mmol/L deoxynucleotide triphosphates, 10Â buffer containing Tris-HCl (pH 8.6), 50 mmol/L KCl, 15 mmol/L MgCl 2 , and 1.5 units Taq polymerase (Bangalore Genei, Bangalore, India).…”

Section: Methodsmentioning

confidence: 99%

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Role of GSTM3 Polymorphism in the Risk of Developing Esophageal Cancer

Jain

Kumar

Lal

et al. 2007

Cancer Epidemiology, Biomarkers &Amp; Prevention

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GSTM3 is involved in detoxification of carcinogens and may be important in modulating cancer susceptibility. GSTM3 genotype frequencies were determined in peripheral blood DNA of 149 esophageal cancer patients and 200 nonmalignant controls using the PCR followed by PAGE. Patients who were heterozygous carriers of GSTM3 AB genotype had an enhanced risk for developing esophageal cancer [odds ratio (OR), 2.1; 95% confidence interval (95% CI), 1.1-3.7; P = 0.01]. In males, the risk due to GSTM3 AB genotype increased further (OR, 3.4; 95% CI, 1.7-6.8; P = 0.000). Interaction of GSTM3 AB + BB and GSTM1 null genotypes marginally modulated risk (OR, 2.3; 95% CI, 1.1-3.7; P = 0.01). Association with histology (adenocarcinoma: OR, 3.4; 95% CI, 1.1-10.9; P = 0.03) and tumor site (middle third location: OR, 2.2; 95% CI, 1.1-4.4; P = 0.01; lower third location: OR, 2.6; 95% CI, 1.2-5.6; P = 0.01) was also documented. Our results suggest that GSTM3 polymorphism may influence esophageal cancer susceptibility, in particular modulating the risk for adenocarcinoma histology and tumors of the mid and lower third region. (Cancer Epidemiol Biomarkers Prev 2007;16(1):178-81)

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Section: Discussionmentioning

confidence: 95%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Role of GSTM3 Polymorphism in the Risk of Developing Esophageal Cancer

Jain

Kumar

Lal

et al. 2007

Cancer Epidemiology, Biomarkers &Amp; Prevention

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“…Sheng-Ming Yi, Gui-Yuan Li* risk, but the available evidence for the genetic association is still weak because of disagreements among studies (Jain et al, 2006;Liu et al, 2010). Differences among study designs, methodology and insufficient power may be responsible for the inconsistent findings among those studies.…”

Section: Null Genotype Of Gstt1 Contributes To Esophageal Cancer Riskmentioning

confidence: 99%

“…With our search criterion, 15 individual case-control publications with 1,626 cases and 2,216 controls were , 2006;Deng et al, 2008;Zhang et al, 2009;Ji et al, 2010;Liu et al, 2010;Malik et al, 2010;Moaven et al, 2010;Gao et al, 2012). There were 10 English language literatures (Lin et al, 1998;Tan et al, 2000;Gao et al, 2002;Wang et al, 2003;Roth et al, 2004;Jain et al, 2006;Wang et al, 2006;Liu et al, 2010;Malik et al, 2010;Moaven et al, 2010) and 5 Chinese language ones (Yi et al, 2005;Deng et al, 2008;Zhang et al, 2009;Ji et al, 2010;Gao et al, 2012).…”

Section: Characteristics Of Included Studiesmentioning

confidence: 99%

Null Genotype of GSTT1 Contributes to Esophageal Cancer Risk in Asian Populations: Evidence from a Meta-analysis

Li²

2012

Asian Pacific Journal of Cancer Prevention

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Background/Aims: Glutathione S-transferase T1 (GSTT1), a phase-II enzyme, plays an important role in detoxification of carcinogen electrophiles. Many studies have investigated the association between GSTT1 polymorphism and esophageal cancer risk in Asian populations, but its actual impact is not clear owing to apparent inconsistencies among those studies. Thus, a meta-analysis was performed to explore the effect of GSTT1 polymorphism on the risk of developing esophageal cancer. Methods: A literature search of PubMed, Embase, and Wanfang databases up to August 2012 was conducted and 15 eligible papers were finally selected, involving a total of 1,626 esophageal cancer cases and 2,216 controls. We used the pooled odds ratio (OR) with its corresponding 95% confidence interval (95%CI) to estimate the association of GSTT1 polymorphism with esophageal cancer risk. Subgroup analyses and sensitivity analyses were performed to further identify the association. Results: Meta-analysis of total studies showed the null genotype of GSTT1 was significantly associated with an increased risk of esophageal cancer in Asians (OR=1.26, 95%CI=1.05-1.52, P OR =0.015, I 2 =42.7%). Subgroup analyses by sample size and countries also identified a significant association. Sensitivity analysis further demonstrated a relationship of GSTT1 polymorphism to esophageal cancer risk in Asians. Conclusions: The present meta-analysis of available data showed a significant association between the null genotype of GSTT1 and an increased risk of esophageal cancer in Asians, particularly in China.

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Genetic polymorphisms and esophageal cancer risk

Hiyama

Yoshihara

Tanaka

et al. 2007

Intl Journal of Cancer

180

145

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The aim of this paper is to review and evaluate, in a comprehensive manner, the published data regarding the contribution of genetic polymorphisms to risk of esophageal cancer, including squamous cell carcinoma (SCC) and adenocarcinoma, in humans. All relevant studies available in MEDLINE and published before February 2007 were identified. Studies carried out in humans and that compared esophageal cancer patients with at least 1 standard control group were considered for analysis. One-hundred studies and 3 meta-analyses were identified. Eighty (80%) studies were conducted in Asian countries, particularly China including Taiwan (60 (60%) studies). The most intensively examined genes were those encoding carcinogen metabolic enzymes. The most widely studied gene was GSTM1 (15 studies), followed by ALDH2 (11 studies). ALDH2, MTHFR C677T, CYP1A1 Ile/Val, CYP1A1 MspI, CYP2E1, GSTP1, GSTM1 and GSTT1 were examined by metaanalyses and significant relations were found between ALDH2*1*2 and the CYP1A1 Val allele and increased risk of esophageal cancer. In addition, increased risk of esophageal SCC was consistently associated with the ADH2*1*2 and the p53 codon 72 Pro/Pro genotypes. Cohort studies that simultaneously consider multiple genetic and environmental factors possibly involved in esophageal carcinogenesis are needed to ascertain not only the relative contribution of these factors to tumor development but also the contributions of their putative interactions. ' 2007 Wiley-Liss, Inc.

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GSTT1, GSTM1 and GSTP1 genetic polymorphisms and interaction with tobacco, alcohol and occupational exposure in esophageal cancer patients from North India

Cited by 65 publications

References 30 publications

Role of GSTM3 Polymorphism in the Risk of Developing Esophageal Cancer

Role of GSTM3 Polymorphism in the Risk of Developing Esophageal Cancer

Null Genotype of GSTT1 Contributes to Esophageal Cancer Risk in Asian Populations: Evidence from a Meta-analysis

Genetic polymorphisms and esophageal cancer risk

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