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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PURPOSE Agent Orange exposure (AOe) is a potential risk factor for the development of prostate cancer (PCa). However, it is unknown whether AOe specifically increases the risk of lethal PCa. This study aimed to determine the association between AOe and the risk of detecting high-grade PCa (HGPCa, Gleason ≥ 7) on biopsy in a US Veteran cohort. METHODS Risk factors included clinico-demographic and laboratory data from veterans referred for an initial prostate biopsy. Outcomes were defined as the presence versus the absence of PCa, HGPCa, or low-grade PCa (LGPCa, Gleason ≤6) in biopsy specimens. Risk amongst AOe veterans relative to unexposed veterans was estimated with multivariate logistic regression. Separate models determined whether AOe was associated with an increased risk of PCa, HGPCa or LGPCa. RESULTS Of 2720 Veterans biopsied, PCa was diagnosed in 896 (32.9%); 459 (16.9%) had HGPCa. AOe was associated with a 52% increase in overall risk of PCa detection (aOR = 1.52, 95% CI: 1.07–2.13). AOe did not confer an increase in risk of LGPCa (aOR = 1.24, 95% CI: 0.81 to 1.91), although a 75% increase in risk of HGPCa (aOR = 1.75, 95% CI: 1.12 to 2.74) was observed. AOe was associated with a 2.1 fold increase (95% CI: 1.22 to 3.62, p<0.01) in Gleason 8 or higher PCa. CONCLUSION The increased risk of PCa associated with AOe is driven by an increased risk of HGPCa in men undergoing initial prostate biopsy. These findings could aid in improved PCa screening for Vietnam-era Veterans.

Despite increasing recognition of the role nutrition plays in the health of current and future generations, many women struggle to eat healthy. We used the PhotoVoice method to engage 10 rural women in identifying perceived barriers and facilitators to healthy eating in their homes and community. They took 354 photographs, selected and wrote captions for 62 images, and explored influential factors through group conversation. Using field notes and participant-generated captions, the research team categorized images into factors at the individual, relational, community/organizational, and societal levels of a socioecological model. Barriers included limited time, exposure to marketing, and the high cost of food. Facilitators included preparing food in advance and support from non-partners; opportunities to hunt, forage, and garden were also facilitators, which may be amplified in this rural environment. Nutritional interventions for rural women of childbearing age should be multi-component and focus on removing barriers at multiple socioecological levels.

Folate deficiency has been implicated in the carcinogenesis of several tumor types. The role of folate in prostate cancer remains indeterminate. We investigated folate as a risk factor for prostate cancer among 140 biopsy-confirmed prostate cancer patients, 230 age-matched clinic controls, and 250 negative prostate biopsy controls. Dietary folate intake was inversely associated with overall risk of prostate cancer as compared to clinic controls (P for a linear trend = 0.003). When stratified by disease severity, dietary folate and folate from natural sources were associated with reduced risk of high-grade cancer as compared to both clinic controls (P for a linear trend = 0.0009 and 0.02, respectively) and biopsy negative controls (P for a linear trend = 0.03 and 0.05, respectively). There was no interaction between alcohol consumption and folate intake. These analyses support an inverse association between dietary folate intake and prostate cancer risk and primarily risk of high-grade prostate cancer.