Combined effect of glutathione S-transferase M1 and T1 genotypes on bladder cancer risk

Lee, Seung Joon; Cho, Soo Hun; Park, Sue Kyung; Kim, Soo Woong; Park, Moon Soo; Choi, Han Yong; Choi, Ji Yeob; Lee, Sang Yoon; Im, Hyoung June; Kim, Jae Yong; Yoon, Kyungho; Choi, Hwang; Shin, Sang Goo; Park, Tae Won; Rothman, Nathaniel; Hirvonen, Ari; Kang, Daehee

doi:10.1016/s0304-3835(01)00820-5

Cited by 49 publications

(33 citation statements)

References 21 publications

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“…Of the published studies, some suggested an increased risk with the GSTT1 null genotype [13,37] and others reported no association [38]. In our study, the comparison of patients and controls according to the GSTT1 genotype and tobacco status suggested an aggravating effect of wild-type GSTT1 genotype in smokers, which confirmed the study of Kim et al [39].…”

Section: Discussionsupporting

confidence: 90%

Smoking and Polymorphisms in Xenobiotic Metabolism and DNA Repair Genes are Additive Risk Factors Affecting Bladder Cancer in Northern Tunisia

Rouissi

Ouerhani

Hamrita

et al. 2011

Pathol. Oncol. Res.

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Cancer epidemiology has undergone marked development since the nineteen-fifties. One of the most spectacular and specific contributions was the demonstration of the massive effect of smoking and genetic polymorphisms on the occurrence of bladder cancer. The tobacco carcinogens are metabolized by various xenobiotic metabolizing enzymes, such as the super-families of N-acetyltransferases (NAT) and glutathione S-transferases (GST). DNA repair is essential to an individual's ability to respond to damage caused by tobacco carcinogens. Alterations in DNA repair genes may affect cancer risk by influencing individual susceptibility to this environmental exposure. Polymorphisms in NAT2, GST and DNA repair genes alter the ability of these enzymes to metabolize carcinogens or to repair alterations caused by this process. We have conducted a case-control study to assess the role of smoking, slow NAT2 variants, GSTM1 and GSTT1 null, and XPC, XPD, XPG nucleotide excision-repair (NER) genotypes in bladder cancer development in North Tunisia. Taken alone, each gene unless NAT2 did not appear to be a factor affecting bladder cancer susceptibility. For the NAT2 slow acetylator genotypes, the NAT2*5/*7 diplotype was found to have a 7-fold increased risk to develop bladder cancer (OR = 7.14; 95% CI: 1.30-51.41). However, in tobacco consumers, we have shown that Null GSTM1, Wild GSTT1, Slow NAT2, XPC (CC) and XPG (CC) are genetic risk factors for the disease. When combined together in susceptible individuals compared to protected individuals these risk factors give an elevated OR (OR = 61). So, we have shown a strong cumulative effect of tobacco and different combinations of studied genetic risk factors which lead to a great susceptibility to bladder cancer.

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Section: Discussionsupporting

confidence: 90%

Smoking and Polymorphisms in Xenobiotic Metabolism and DNA Repair Genes are Additive Risk Factors Affecting Bladder Cancer in Northern Tunisia

Rouissi

Ouerhani

Hamrita

et al. 2011

Pathol. Oncol. Res.

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“…Zinc sulphide (ZnS) is an important semiconductor material with an energy band gap of E g ¼ 3:65 eV (bulk), which is the highest among all II-VI compound semiconductors [1]. ZnS, in both bulk and thin film forms, is receiving everincreasing attention owing to its potential uses [2,3].…”

Section: Introductionmentioning

confidence: 99%

Growth of ZnS thin films obtained by chemical spray pyrolysis: The influence of precursors

López

Espinós²,

Martı́n

et al. 2005

Journal of Crystal Growth

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“…Studies have found that the GSTM1 null genotype is associated, alone and in smokers, with an increased risk of bladder cancer (30,31), but equivocal or negative results have been obtained for GSTT1 or GSTP1 genotypes (30,31). Only one study has reported, so far, the potential prognostic value of GSTM1 tissue genotype to predict recurrence of bladder cancer (32).…”

Section: Discussionmentioning

confidence: 99%

Phase II Drug-Metabolizing Polymorphisms and Smoking Predict Recurrence of Non–Muscle-Invasive Bladder Cancer: A Gene–Smoking Interaction

Lacombe

Fradet

Lévesque

et al. 2016

Cancer Prevention Research

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Cigarette smoking is the most important known risk factor for urinary bladder cancer. Selected arylamines in cigarette smoke are recognized human bladder carcinogens and undergo biotransformation through several detoxification pathways, such as the glutathione S-transferases (GST), and uridinediphospho-glucuronosyltransferases (UGT) pathways. GSTM1 deletion status and UGT1A1Ã 28 rs8175347 genotypes were assessed in 189 non-muscle-invasive bladder cancers (NMIBC) patients with pTa (77.2%) and pT1 (22.8%) tumors and a mean follow-up of 5.6 years, to investigate whether two common functional polymorphisms in GSTM1 and UGT1A1 genes and smoking history are associated with recurrence-free survival of patients with NMIBC. Ã 28 allele demonstrated a risk of recurrence of 4.95 (95% CI, 1.02-24.0) and 5.32 (95% CI, 2.07-13.7), respectively. This study establishes a connection between GSTM1, UGT1A1, and tobacco exposure as prognostic markers of NMIBC recurrence in bladder cancer patients. These findings warrant validation in larger cohorts. Cancer Prev Res; 9(2); 189-95. Ó2015 AACR.

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Combined effect of glutathione S-transferase M1 and T1 genotypes on bladder cancer risk

Cited by 49 publications

References 21 publications

Smoking and Polymorphisms in Xenobiotic Metabolism and DNA Repair Genes are Additive Risk Factors Affecting Bladder Cancer in Northern Tunisia

Smoking and Polymorphisms in Xenobiotic Metabolism and DNA Repair Genes are Additive Risk Factors Affecting Bladder Cancer in Northern Tunisia

Growth of ZnS thin films obtained by chemical spray pyrolysis: The influence of precursors

Phase II Drug-Metabolizing Polymorphisms and Smoking Predict Recurrence of Non–Muscle-Invasive Bladder Cancer: A Gene–Smoking Interaction

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