Key words: prostate cancer; 25(OH)-vitamin D 3 ; serum bankVitamin D deficiency has been implicated as risk factor for prostate cancer. 1 In cell culture studies, vitamin D metabolites have had protective action against cancer development (for review see Ylikomi et al. 2 ). Normal and malignant prostate cells contain vitamin D receptor (VDR), 3-5 which mediates the antiproliferative action of 1,25(OH) 2 -vitamin D 3 . 6 In addition to the antiproliferative action of 1,25(OH) 2 -vitamin D 3 , it can cause apoptosis, 7 induce differentiation, 8 inhibit telomerase expression, 9 inhibit tumor cell invasiveness 10 and suppress tumor-induced angiogenesis. 11 Several epidemiologic studies have reported that high serum vitamin D levels or sunlight may protect against prostate cancer. 3,4,[12][13][14][15] Factors that affect prostate cancer include age, dark skin and environment, e.g., latitude and diet. 16 These factors might be linked to vitamin D availability. 17,18 Furthermore, high fish (rich in vitamin D) consumption appears to correlate with lower prostate cancer risk. 19 In addition, VDR gene polymorphism may contribute to the risk of prostate cancer. 20 -24 There is also a study showing no correlation between serum vitamin D metabolites and prostate cancer in Maryland (USA), 25 but the authors concluded that the power of their study was limited. In another study on U.S. male physicians, only a weak protection against prostate cancer was found with the highest quartile of serum 1␣,25(OH) 2 -vitamin D 3 . 26 Similarly, no correlation was found in Hawaii. 27 There are 2 physiologically interesting metabolites of vitamin D, 1␣,25(OH) 2 -vitamin D 3 , regulating calcium homeostasis for bones and muscles in extremely narrow limits, and 25(OH)-vitamin D 3 , regulating target (prostate) cell proliferation and differentiation through activation to 1␣,25(OH) 2 -vitamin D 3 in the target (prostate) cell. Serum 25(OH)-vitamin D 3 is produced by liver 25-hydroxylase, the rate of the synthesis being directly proportional to vitamin D 3 serum concentration. 28 Therefore, serum 25(OH)-vitamin D 3 reflects vitamin D availability in the organism. Serum concentration of 25(OH)-vitamin D 3 is so high that it might possess a significant biologic activity in target cells, but it is also a precursor for the biologically more active 1␣,25(OH) 2 -vitamin D 3 . Prostate as well as many other target organs can activate 25(OH)-vitamin D 3 through 1␣-hydroxylation 29,30 and inactivate it through 24-hydroxylation. 31 In an epidemiologic study, we found that low concentrations (Ͻ40 nmol/l) of 25(OH)-vitamin D in serum were associated with a 1.7-fold increased risk of prostate cancer. 3,4 Since the power of our study was limited, preventing extensive analysis of the data, and we are partners in the Nordic Specimen Banks for Cancer Causes and Control, we had an opportunity to extend our study to other Scandinavian countries located geographically at the same latitude. Our aim was to determine whether our finding could be replicated in a la...

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Background: Attendance in screening is an important determinant of cervical cancer. Previous experience on high-risk human papillomavirus (hrHPV) DNA testing on patient-obtained samples suggests a good effect among nonattendees of screening. We assessed the effects of self-sampling on attendance in the Finnish screening program.Methods: Nonattendees after the primary invitation in one municipality (Espoo) were randomized to receive either a self-sampling kit (2,397 women) or an extra invitation (6,302 women). One fourth (1,315 women) of reminder letter arm nonattendees also received a self-sampling kit as a third intervention. Main outcomes were increases in screening attendance and coverage.Results: The adjusted relative risk for participation by self-sampling as a second intervention in comparison to a reminder letter arm was 1.21 (95% CI: 1.13-1.30). Total attendance increased from 65% to 76% by selfsampling and from 65% to 74% with a reminder letter. Combining the interventions (reminder letter and then self-sampling) increased total attendance from 63% to 78%. One fifth of the participants in all three groups increased screening coverage (previous Pap smear !5 years ago or never). Self-obtained samples were more often HPV positive than provider-obtained ones (participants after primary invitation and reminder letter), 12% to 13% versus 7%.Conclusions: Self-sampling is a feasible option in enhancing the attendance at organized screening, particularly as an addition to a reminder letter.Impact: If self-sampling is used as a third intervention after two written invitations, the overall attendance in Finland could most likely reach the desired 80% to 85%. Cancer Epidemiol Biomarkers Prev; 20(9); 1960-9. Ó2011 AACR.

Androgens stimulate prostate cancer in vitro and in vivo. However, evidence from epidemiologic studies of an association between circulating levels of androgens and prostate cancer risk has been inconsistent. We investigated the association of serum levels of testosterone, the principal androgen in circulation, and sex hormone-binding globulin (SHBG) with risk in a case-control study nested in cohorts in Finland, Norway and Sweden of 708 men who were diagnosed with prostate cancer after blood collection and among 2,242 men who were not. In conditional logistic regression analyses, modest but significant decreases in risk were seen for increasing levels of total testosterone down to odds ratio for top vs. bottom quintile of 0.80 (95% CI ‫؍‬ 0.59 -1.06; p trend ‫؍‬ 0.05); for SHBG, the corresponding odds ratio was 0.76 (95% CI ‫؍‬ 0.57-1.01; p trend ‫؍‬ 0.07). For free testosterone, calculated from total testosterone and SHBG, a bell-shaped risk pattern was seen with a decrease in odds ratio for top vs. bottom quintile of 0.82 (95% CI ‫؍‬ 0.60 -1.14; p trend ‫؍‬ 0.44). No support was found for the hypothesis that high levels of circulating androgens within a physiologic range stimulate development and growth of prostate cancer.