Serum levels of selenium and smoking habits at age 50 influence long term prostate cancer risk; a 34 year ULSAM follow-up

BMC Cancer

Research Article

Björn Zethelius¹  Lars Holmberg²  Hans Garmo²  Birgitta Grundmark³ 

[1] Department of Public Health and Caring Sciences/Geriatrics, Uppsala University, Sweden;Medical Products Agency, Uppsala, Sweden;Department of Surgical Sciences, Uppsala University, Uppsala, Sweden;Division of Cancer Studies, King's College London, Medical School, London, UK;Regional Oncologic Centre of the Uppsala-Orebro region, Uppsala University Hospital, Uppsala, Sweden;Department of Surgical Sciences, Uppsala University, Uppsala, Sweden;Medical Products Agency, Uppsala, Sweden;Regional Oncologic Centre of the Uppsala-Orebro region, Uppsala University Hospital, Uppsala, Sweden;

关键词: Prostate Cancer;    Selenium;    Prostate Cancer Risk;    Serum Selenium;    Full Cohort;   

DOI  :  10.1186/1471-2407-11-431

 received in 2011-04-15, accepted in 2011-10-07,  发布年份 2011

来源: Springer

【 摘 要 】

BackgroundSerum selenium level (s-Se) has been associated with prostate cancer (PrCa) risk. We investigated the relation between s-Se, smoking and non-screening detected PrCa and explored if polymorphisms in two DNA repair genes: OGG1 and MnSOD, influenced any effect of s-Se.MethodsULSAM, a population based Swedish male cohort (n = 2322) investigated at age 50 for s-Se and s-Se influencing factors: serum cholesterol, erythrocyte sedimentation rate and smoking habits. At age 71 a subcohort, (n = 1005) was genotyped for OGG1 and MnSOD polymorphisms.ResultsIn a 34-year-follow-up, national registries identified 208 PrCa cases further confirmed in medical records. Participants with s-Se in the upper tertile had a non-significantly lower risk of PrCa. Smokers with s-Se in the two lower tertiles (≤80 μg/L) experienced a higher cumulative incidence of PrCa than smokers in the high selenium tertile (Hazard Ratio 2.39; 95% CI: 1.09-5.25). A high tertile selenium level in combination with non-wt rs125701 of the OGG1 gene in combination with smoking status or rs4880 related variation of MnSOD gene appeared to protect from PrCa.ConclusionsS-Se levels and smoking habits influence long-term risk of PrCa. Smoking as a risk factor for PrCa in men with low s-Se is relevant to explore further. Exploratory analyses of variations in OGG1 and MnSOD genes indicate that hypotheses about patterns of exposure to selenium and smoking combined with data on genetic variation in genes involved in DNA repair can be valuable to pursue.

【 授权许可】

CC BY   
© Grundmark et al; licensee BioMed Central Ltd. 2011