Association between the GCG polymorphism of the selenium dependent GPX1 gene and the risk of young onset prostate cancer

Kóte-Jarai, Zsofia; Durocher, Francine; Edwards, Stephen M.; Hamoudi, Rifat; Jackson, Rachel; Ardern‐Jones, Audrey; Murkin, A; Dearnaley, David P.; Kirby, Roger; Houlston, Richard S.; Easton, Doug; Eeles, Rosalind

doi:10.1038/sj.pcan.4500569

Cited by 40 publications

(24 citation statements)

References 11 publications

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“…There have been few investigations of potential relationships between GPX1 genetic polymorphisms and prostate cancer risk, except for one study that assessed the GPX1 GCG repeat, finding no relationships with prostate cancer risk (29). In our study, we did not find an overall relationship between GPX1 Pro200Leu polymorphism and prostate cancer.…”

Section: Discussioncontrasting

confidence: 47%

Polymorphisms in Oxidative Stress–Related Genes Are Not Associated with Prostate Cancer Risk in Heavy Smokers

Choi

Neuhouser²,

Barnett³

et al. 2007

Cancer Epidemiology, Biomarkers &Amp; Prevention

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Oxidative stress, associated with aging and inflammation, is likely to play a role in the etiology of prostate cancer. We evaluated potential associations between gene variants that result in reduced neutralization of reactive oxygen species (ROS; MnSOD Ala-16Val, CAT À262 C>T, and GPX1 Pro200Leu) and prostate cancer risk among 724 men with incident prostate cancer who participated in the Carotene and Retinol Efficacy Trial (CARET) cohort, a randomized trial for the prevention of lung cancer among men with a history of smoking and/or asbestos exposure. Odds ratios (OR) and 95% confidence intervals (95% CI) were estimated by logistic regression. Nested case-control analyses included study participants with available DNA (n = 533 cases and 1,470 controls), matched for race, age, and length of followtime. Overall, there were no associations between genotypes of MnSOD, CAT, and GPX1 and prostate cancer risk, although among men diagnosed before age 65, CAT TT genotype was associated with increased risk (OR, 2.0; 95% CI, 0.97-3.95). Further analyses stratified by factors related to environmental oxidative stress exposures did not modify associations. When calculating the number of risk alleles of MnSOD, CAT, and GPX1 hypothetically related to reduced protection against ROS, there was a nonsignificant relationship between prostate cancer and carriage of five or more risk alleles, in comparison to men with less than five risk alleles (OR, 2.0; 95% CI, 0.90-4.42). In conclusion, it does not seem that variants in MnSOD, CAT, or GPX1 have an influence on prostate cancer risk in this cohort of men who were smokers or exposed to asbestos, although it is possible that cumulative defects in protection from oxidative stress may result in increased risk of the disease. (Cancer Epidemiol Biomarkers Prev 2007;16(6):1115 -20)

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Section: Discussioncontrasting

confidence: 47%

Polymorphisms in Oxidative Stress–Related Genes Are Not Associated with Prostate Cancer Risk in Heavy Smokers

Choi

Neuhouser²,

Barnett³

et al. 2007

Cancer Epidemiology, Biomarkers &Amp; Prevention

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“…Perhaps the best candidate is GPx-1, because an association with polymorphisms and the risk of lung cancer has been reported, as has loss of heterozygosity at this locus in several cancer types (9)(10)(11)(12). In fact, an association between a polyalanine polymorphism in exon 1 and the risk of young-onset prostate cancer has been reported (28). Reduced levels of GPx-1 could conceivably influence cancer risk through its role as an antioxidant or possibly through the modulation of DNA repair and cell-survival molecules (15,29).…”

Section: Discussionmentioning

confidence: 99%

Selenoprotein deficiency accelerates prostate carcinogenesis in a transgenic model

Diwadkar‐Navsariwala

Prins²,

Swanson

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

130

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Considerable animal and human data have indicated that selenium is effective in reducing the incidence of several different types of cancer, including that of the prostate. However, the mechanism by which selenium inhibits carcinogenesis remains unknown. One possibility is that dietary selenium influences the levels of selenium-containing proteins, or selenoproteins. Selenoproteins contain selenium in the form of selenocysteine and perform a variety of cellular functions, including antioxidant defense. To determine whether the levels of selenoproteins can influence carcinogenesis independent of selenium intake, a unique mouse model was developed by breeding two transgenic animals: mice with reduced selenoprotein levels because of the expression of an altered selenocysteine-tRNA (i 6 A ؊ ) and mice that develop prostate cancer because of the targeted expression of the SV40 large T and small t oncogenes to that organ [C3(1)͞Tag]. The resulting bigenic animals (i 6 A ؊ ͞Tag) and control WT͞Tag mice were assessed for the presence, degree, and progression of prostatic epithelial hyperplasia and nuclear atypia. The selenoprotein-deficient mice exhibited accelerated development of lesions associated with prostate cancer progression, implicating selenoproteins in cancer risk and development and raising the possibility that selenium prevents cancer by modulating the levels of these selenoproteins.cancer ͉ selenium

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“…Although loss of heterozygosity at the GPx-1 locus has been associated with the development of several cancer types, including those occurring in lung, breast, and head and neck, no significant association between GPx-1 genotypes and CaP has been elucidated. Selenium, as a component of GPx, has been shown to play an important role in the manganese superoxide dismutase antioxidative pathway (14). A cohort study of Finnish male heavy smokers found that the manganese superoxide dismutase AA polymorphism was significantly associated with increased risk of CaP (15).…”

Section: Seleniummentioning

confidence: 99%

Chemoprevention of Prostate Cancer through Dietary Agents: Progress and Promise

Syed

Khan

Afaq

et al. 2007

Cancer Epidemiology, Biomarkers &Amp; Prevention

164

124

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Prostate cancer (CaP) is second only to lung cancer as the cause of cancer-related deaths in American men and is responsible for over 29,000 deaths per year. One promising approach to reduce the incidence of CaP is through chemoprevention, which has been recognized as a plausible and cost-effective approach to reduce cancer morbidity and mortality by inhibiting precancerous events before the occurrence of clinical disease. Indeed, CaP is an ideal candidate disease for chemoprevention because it is typically diagnosed in the elderly population with a relatively slower rate of growth and progression, and therefore, even a modest delay in the development of cancer, achieved through pharmacologic or nutritional intervention, could result in substantial reduction in the incidence of clinically detectable disease. In this review, we have summarized the recent investigations and mechanistic studies on CaP chemoprevention using dietary agents, such as selenium, vitamins D and E, lycopene, phytoestrogens, flavonoids, and green tea polyphenols. Well-designed trials are required to delineate the potential clinical usefulness of these agents through issues, such as determining the optimal period and route of administration, systemic bioavailability, optimal dosing and toxicity of the agent, and single or combinatorial approach. It is hoped that, combining the knowledge based on agents with targets, effective approaches for CaP chemoprevention can be established. (Cancer Epidemiol Biomarkers Prev 2007;16(11):2193 -203)

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Association between the GCG polymorphism of the selenium dependent GPX1 gene and the risk of young onset prostate cancer

Cited by 40 publications

References 11 publications

Polymorphisms in Oxidative Stress–Related Genes Are Not Associated with Prostate Cancer Risk in Heavy Smokers

Polymorphisms in Oxidative Stress–Related Genes Are Not Associated with Prostate Cancer Risk in Heavy Smokers

Selenoprotein deficiency accelerates prostate carcinogenesis in a transgenic model

Chemoprevention of Prostate Cancer through Dietary Agents: Progress and Promise

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