Background

Serum 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.

Methods

ULSAM, 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.

Results

In 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.

Conclusions

S-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.

Background

Associations between Metabolic Syndrome (MetS) components and prostate cancer development have not been studied comprehensively; results have been divergent. Using the National Cholesterol Education Program Adult Treatment panel III (NCEP) and International Diabetes Federation (IDF) definitions of the MetS we investigated such associations taking competing risks of death into consideration.

Methods

In the prospective Uppsala Longitudinal Study of Adult Men (ULSAM) of 2322 Caucasian men with 34 years of follow-up baseline MetS-measurements at age 50 were used. Cumulative incidence of prostate cancer and death with/without the MetS were calculated. Competing risk of dying was taken into account by calculating the conditional probability of prostate cancer with/without the MetS.

Results

Two-hundred-and- thirty-seven prostate cancers were identified. Prostate cancer probability by age 80 with baseline MetS compared to without the MetS was non-significantly higher, 5.2 percent-units (CI -0.8%-11.3%, (NCEP), 2.7 percent-units (CI -2.7%-8.0%) (IDF), cumulative incidence proportions of death was significantly higher, 19.3 percent-units (CI 13.4%-25.3%) (NCEP), 15.3 percent-units (CI 9.5%-21.1%) (IDF) and conditional probability of prostate cancer considering death from other causes was significantly higher, 7.3 percent-units (CI 0.2%-14.5%) odds ratio(OR) of 1.64 (CI 1.03-2.23). (NCEP), and non-significantly higher 5.0 percent-units (CI -1.6%-11.6%) OR 1.43 (CI 0.89-1.90). (IDF).

Conclusions

The MetS by the NCEP definition is associated with prostate cancer taking the competing risk of early death from other causes into account.

Impact

The results further highlight the public health impact of the increasing prevalence of MetS, and the importance of considering competing risks when studying risk factors for cancer.