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Polymorphisms of methylenetetrahydrofolate reductase and the risk of prostate cancer: a nested case-control study
Umeå University, Faculty of Medicine, Department of Medical Biosciences, Pathology.
Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology.
Umeå University, Faculty of Medicine, Department of Medical Biosciences, Pathology.
Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.ORCID iD: 0000-0001-9581-3845
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2006 (English)In: European Journal of Cancer Prevention, ISSN 0959-8278, E-ISSN 1473-5709, Vol. 15, no 1, 46-50 p.Article in journal (Refereed) Published
Abstract [en]

It has been proposed that folate and polymorphisms of the enzyme methylenetetrahydrofolate reductase (MTHFR), which regulates influx of folate from DNA synthesis and repair to methylation reactions, are involved in the aetiology of cancer. To relate the MTHFR 677C→T and 1298A→C polymorphisms to the risk of prostate cancer, taking into consideration prospective plasma levels of folate, vitamin B12 and homocysteine. The design was a case-control study of 223 prostate cancer cases and 435 matched controls nested within the population-based Northern Sweden Health and Disease Cohort. Neither the MTHFR 677C→T nor the MTHFR 1298A→C polymorphism was statistically significantly associated with the risk of prostate cancer in univariate analysis by conditional logistic regression. After adjustment for MTHFR 1298A→C, plasma folate, vitamin B12, homocysteine, body mass index and smoking, the odds ratios were, for the 677 CT genotype, 1.52 [95% confidence interval (CI) 1.02-2.26], and for TT, 0.91 (95% CI 0.41-2.04). Our previously reported observation of a possible increase in the risk of prostate cancer at high plasma folate levels was attributable in this study to subjects having the MTHFR 677C→T polymorphism. We found that the MTHFR 677C→T polymorphism is not likely to have a major role in the development of prostate cancer, although it may possibly increase the risk in combination with high plasma folate levels. Further investigation in larger studies is warranted.

Place, publisher, year, edition, pages
Lippincott Williams & Wilkins, 2006. Vol. 15, no 1, 46-50 p.
Keyword [en]
Adult, Case-Control Studies, Folic Acid/blood, Genotype, Homocysteine/blood, Humans, Male, Methylenetetrahydrofolate Reductase (NADPH2)/*genetics, Middle Aged, Odds Ratio, Polymorphism; Genetic, Prospective Studies, Prostatic Neoplasms/*genetics, Risk, Sweden, Vitamin B 12/blood
National Category
Cancer and Oncology
URN: urn:nbn:se:umu:diva-15281PubMedID: 16374229OAI: diva2:154953
Available from: 2008-01-11 Created: 2008-01-11 Last updated: 2015-04-22Bibliographically approved

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Van Guelpen, BethanyWirén, SaraBergh, AndersHallmans, GöranStattin, PärHultdin, Johan
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