Observational studies have shown that 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor (statin) use may be associated with reduced cancer risk. The purpose of this case-control study was to elucidate the association between statin use and prostate cancer risk. Prostate cancer cases (n ¼ 100), recruited upon referral for prostate biopsy, and frequency age-matched, prostate-specific antigen-normal clinic controls (n ¼ 202) were recruited from the Portland, Oregon, Veterans Affairs Medical Center. Information on any use of statins from May 1997 through August 2004 was obtained from an electronic pharmacy database. Days of use, type of statin, dose, and prescription changes were recorded. Duration and intensity were calculated for each statin type on the basis of days of use and prescribed dose. Thirty-six percent of cases and 49 percent of controls had a record of any statin use. Following adjustment for other potential risk factors, statin use was associated with a significant reduction in prostate cancer risk (odds ratio ¼ 0.38, 95% confidence interval: 0.21, 0.69). Furthermore, in analyses stratified by Gleason score, the inverse association with statin use was maintained only among men with Gleason scores of 7 (odds ratio ¼ 0.24, 95% confidence interval: 0.11, 0.53). The results of this case-control study suggest that statins may reduce the risk of total prostate cancer and, specifically, more aggressive prostate cancer.case-control studies; cholesterol; hydroxymethylglutaryl-CoA reductase inhibitors; mevalonic acid; prostatespecific antigen; prostatic neoplasms; veterans Abbreviations: CI, confidence interval; FPP, farnesylpyrophosphate; GGPP, geranylgeranyl pyrophosphate; NSAID, nonsteroidal antiinflammatory drug; OR, odds ratio; p21, M r 21,000 protein (p27 defined similarly); PVAMC, Portland Veterans Affairs Medical Center; VA, Veterans Affairs.One in six men over age 60 years will be diagnosed with prostate cancer (1). Prostate cancer is the second leading cause of cancer deaths among US men (2). Therefore, the need to identify and to develop means to prevent this common malignancy is a high priority. Recent research on the chemopreventive potential of a group of cholesterollowering drugs, 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase inhibitors (statins), has shown intriguing results (3, 4). Statins lower serum cholesterol levels by inhibiting 3-hydroxy-3-methylglutaryl coenzyme A reductase, the rate-determining enzyme in the mevalonate pathway (4). In addition to their cholesterol-lowering ability, statins have been shown to inhibit prostate and breast cancer cell proliferation and to induce tumor-specific apoptosis (4-6) in in vitro studies.While the mechanism remains unclear, clinical trials with cancer as a secondary endpoint have shown a nonsignificant inverse association between statin use and total cancer incidence (7,8). Additionally, Bjerre and LeLorier's metaanalysis (9) of five trials of statins and cardiovascular

Epidemiological studies suggest a protective effect of cruciferous vegetables on breast cancer. Sulforaphane (SFN), an active food component derived from crucifers, has been shown to be effective in breast cancer chemoprevention. This study evaluated the chemopreventive effect of SFN on selective biomarkers from blood and breast tissues. In a 2-8-week double-blinded, randomized controlled trial, 54 women with abnormal mammograms and scheduled for breast biopsy were randomized to consume a placebo or a glucoraphanin (GFN) supplement providing SFN (n = 27). Plasma and urinary SFN metabolites, peripheral blood mononuclear cell (PBMC) histone deacetylase (HDAC) activity, and tissue biomarkers (H3K18ac, H3K9ac, HDAC3, HDAC6, Ki-67, p21) were measured before and after the intervention in benign, ductal carcinoma in situ (DCIS), or invasive ductal carcinoma (IDC) breast tissues. Within the supplement group, Ki-67 (p = 0.003) and HDAC3 (p = 0.044) levels significantly decreased in benign tissue. Pre-to-post-intervention changes in these biomarkers were not significantly different between treatment groups after multiple comparison adjustment. GFN supplementation was associated with a significant decrease in PBMC HDAC activity (p = 0.04). No significant associations were observed between SFN and examined tissue biomarkers when comparing treatment groups. This study provides evidence that GFN supplementation for a few weeks is safe but may not be sufficient for producing changes in breast tissue tumor biomarkers. Future studies employing larger sample sizes should evaluate alternative dosing and duration regimens to inform dietary SFN strategies in breast cancer chemoprevention.

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