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  • 1
    Keywords: CANCER ; LUNG ; lung cancer ; LUNG-CANCER ; EPIDEMIOLOGY ; RISK ; GENE ; GENES ; METABOLISM ; ASSOCIATION ; FREQUENCY ; polymorphism ; POLYMORPHISMS ; SUSCEPTIBILITY ; FREQUENCIES ; DELETION ; MALIGNANCIES ; GLUTATHIONE ; meta-analysis ; smoking ; INVOLVEMENT ; TOBACCO ; CHROMOSOMAL LOCALIZATION ; FACTOR-I ; lung neoplasms ; glutathione-S-transferase ; GLUTATHIONE S-TRANSFERASE ; MALIGNANCY ; TOBACCO-SMOKE ; GSTT1 ; METAANALYSIS ; ENVIRONMENTAL TOBACCO-SMOKE ; INTERVAL ; GENETIC-POLYMORPHISM ; pooled analysis ; CANDIDATE ; odds ratio ; tobacco smoke ; RISK-FACTOR ; E ; CHEMICALS ; genetic predisposition to disease ; ENVIRONMENTAL-FACTORS ; ADENOCARCINOMA SUSCEPTIBILITY ; disease susceptibility ; EPOXIDE HYDROLASE ; ETHYLENE-OXIDE ; GSTP1 POLYMORPHISMS ; INDIVIDUAL SENSITIVITY ; TISSUE DISTRIBUTION
    Abstract: Lung cancer is the most common malignancy in the Western world, and the main risk factor is tobacco smoking. Polymorphisms in metabolic genes may modulate the risk associated with environmental factors. The glutathione S-transferase theta 1 gene (GSTT1) is a particularly attractive candidate for lung cancer susceptibility because of its involvement in the metabolism of polycyclic aromatic hydrocarbons found in tobacco smoke and of other chemicals, pesticides, and industrial solvents. The frequency of the GSTT1 null genotype is lower among Caucasians (10-20%) than among Asians (50-60%). The authors present a meta- and a pooled analysis of case-control, genotype-based studies that examined the association between GSTT1 and lung cancer (34 studies, 7,629 cases and 10,087 controls for the meta-analysis; 34 studies, 7,044 cases and 10,000 controls for the pooled analysis). No association was observed between GSTT1 deletion and lung cancer for Caucasians (odds ratio (OR) = 0.99, 95% confidence interval (CI): 0.87, 1.12); for Asians, a positive association was found (OR = 1.28, 95% CI: 1.10, 1.49). In the pooled analysis, the odds ratios were not significant for either Asians (OR = 0.97, 95% CI: 0.83, 1.13) or Caucasians (OR = 1.09, 95% CI: 0.99, 1.21). No significant interaction was observed between GSTT1 and smoking on lung cancer, whereas GSTT1 appeared to modulate occupational-related lung cancer
    Type of Publication: Journal article published
    PubMed ID: 17000715
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  • 2
    Keywords: CANCER ; CELLS ; SYSTEM ; SYSTEMS ; EXPOSURE ; HISTORY ; RISK ; GENE ; GENES ; PATIENT ; IMPACT ; CARCINOGENESIS ; polymorphism ; POLYMORPHISMS ; single nucleotide polymorphism ; NO ; SNP ; etiology ; PROSTATE-CANCER ; PATHOGENESIS ; DAMAGE ; GENOTYPES ; NATURAL-HISTORY ; OXIDATIVE STRESS ; SUPEROXIDE ; mesothelioma ; ASBESTOS EXPOSURE ; OXYGEN ; molecular epidemiology ; SINGLE ; ONCOLOGY ; REGRESSION ; RE ; SINGLE NUCLEOTIDE POLYMORPHISMS ; SNPs ; GSTM1 ; CANCER SUSCEPTIBILITY ; analysis ; GENOTYPE ; single-nucleotide ; technique ; TUMOR NECROSIS FACTOR ; USA ; INCREASED RISK ; UNIT ; manganese ; XENOBIOTIC METABOLISM ; LOGISTIC-REGRESSION ; GENETIC-SUSCEPTIBILITY ; superoxide dismutase ; genetic glutathione transferase
    Abstract: Individual response to oxidative stress, due to exposure to asbestos fibres plays a significant role in the malignant pleural mesothelioma (MPM) etiology. The differential impact on MPM risk of polymorphic alleles of glutathione-S-transferases (GSTs) and manganese superoxide dismutase (MnSOD/SOD2) genes involved in the defence against oxidative damage has been investigated. Ninety cases of MPM and 395 controls were genotyped using the arrayed-primer extension technique. Logistic regression analysis was applied to assess the predictive role of single nucleotide polymorphisms (SNPs) potentially involved in MPM carcinogenesis after adjustment for potential confounders. An increased risk of MPM was found in subjects bearing a GSTM1 null allele (OR = 1.69, 95% Cl = 1.04-2.74; p = 0.034), and in those with the Ala/Ala genotypes at codon 16 within MnSOD (OR = 3.07, 95% CI = 1.55-6.05; p = 0.001). A stronger effect of MnSOD was observed among patients without a clear exposure to asbestos fibres. No effect was found for GSTA2, GSTA4, GSTM3, GSTP1 and GSTT1 genes. These findings, if replicated, contribute substantial evidence to the hypothesis that oxidative stress and cellular antireactive oxygen species systems are involved in the pathogenesis and in the natural history of MPM. (c) 2007 Wiley-Liss, Inc
    Type of Publication: Journal article published
    PubMed ID: 17290392
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