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Introduction The objective of this study was to examine the association between calcium intake and prostate cancer risk. We hypothesized that calcium intake would be positively associated with lower risk for prostate cancer. Methods We used data from a case-control study conducted among veterans between 2007 and 2010 at the Durham Veterans Affairs Medical Center. The study consisted of 108 biopsy-positive prostate cancer cases, 161 biopsy-negative controls, and 237 healthy controls. We also determined whether these associations differed for blacks and whites or for low-grade (Gleason score <7) and high-grade prostate cancer (Gleason score ≥7). We administered the Harvard food frequency questionnaire to assess diet and estimate calcium intake. We used logistic regression models to obtain odds ratios (ORs) and 95% confidence intervals (CIs). Results Intake of calcium from food was inversely related to risk for prostate cancer among all races in a comparison of cases and biopsy-negative controls ( P = .05) and cases and healthy controls ( P = .02). Total calcium was associated with lower prostate cancer risk among black men but not among white men in analyses of healthy controls. The highest tertile of calcium from food was associated with lower risk for high-grade prostate cancer in a comparison of high-grade cases and biopsy-negative controls (OR, 0.37; 95% CI, 0.15-0.90) and high-grade cases and healthy controls (OR, 0.38; 95% CI, 0.17-0.86). Conclusion Calcium from food is associated with lower risk for prostate cancer, particularly among black men, and lower risk for high-grade prostate cancer among all men.

BACKGROUND:We examined the relationship between weight change in the year before radical prostatectomy (RP) and biochemical recurrence (BCR) and adverse pathology. METHODS:We abstracted data from 359 men undergoing RP in the SEARCH (Shared Equal Access Regional Cancer Hospital) database between [2001][2002][2003][2004][2005][2006][2007]. Logistic regression and Cox proportional hazards models were used to test the association between weight change in the year before surgery and adverse pathology and BCR, respectively. RESULTS:In all, 152 (42%) men gained weight, 193 (54%) lost weight and 14 (4%) had the same weight. Among weight gainers, median gain was 2.4 kg and among weight losers, median loss was 2.7 kg. As a continuous variable, weight change was not associated with adverse pathology or BCR (all P40.05). In secondary analysis, on multivariate analysis, men gaining X2.5 kg were at higher BCR risk (hazards ratio ¼ 1.65, 95% confidence interval (CI): 1.03-2.64, P ¼ 0.04) while weight loss X2.5 kg was not associated with BCR (hazards ratio ¼ 0.83, 95% CI: 0.54-1.29, P ¼ 0.41). CONCLUSIONS:As a continuous variable, weight change was not associated with outcome. In secondary hypothesisgenerating analyses, weight gain X2.5 kg in the year before surgery, regardless of final body mass index, was associated with increased BCR following RP. If validated, these data suggest weight gain X2.5 kg may promote prostate cancer progression.

Introduction and Objective: In multiple previous studies, we have shown that mice injected with subcutaneous prostate cancer cells (LNCaP or LAPC-4) and fed a no-carbohydrate ketogenic diet (NCKD, 84% fat, 0% carbohydrate, 16% protein) have significantly decreased tumor volume and significantly prolonged survival, compared to mice fed a western diet (WD, 40% fat, 44% carbohydrate, 16% protein). All previous studies utilized a human prostate cancer cell line, requiring the use of immunodeficient mice. We sought to replicate these previous studies to determine whether diet affected tumor progression and survival in an immunocompetent model. Methods: In this treatment model, 75 male C57bl/6 mice were initially fed WD ad libitum for a period of 14 days. After this 14 day period, all mice were injected subcutaneously with 2.5×105 TRAMP cells and randomized to one of three diets: WD, NCKD, or low-fat diet (LF, 12% fat, 72% carbohydrate, 16% protein). Mice receiving LF diet were fed ad libitum, and served as the reference group in paired-feeding protocols for mice receiving WD and NCKD. Tumor volumes were assessed twice weekly, and mice were sacrificed when tumor volumes reached 1000mm3. Survival was calculated using a Log-rank test and tumor volumes were compared among dietary groups using Kruskal-Wallis test for significance. Results: Mice fed a NCKD demonstrated a trend towards decreased tumor volumes compared to mice fed WD and LF. Median tumor volume at study day 66 for mice fed WD, LF, and NCKD were 1091.2 mm3, 1082.9 mm3, and 661.5mm3 respectively. While the tumor volumes were smaller in mice fed NCKD versus LF or WD, these differences did not reach statistical significance (WD vs. NCKD, p=0.06; LF vs. NCKD, p=0.12). There was no significant difference between tumor volumes among mice fed WD compared to LF (p=0.95). Additionally, a trend towards improved survival was seen in mice fed NCKD vs. WD (p=0.09). Conclusion: This study in an immunocompetent xenograft model supports the findings of multiple previous studies. Mice fed a NCKD demonstrated a trend towards prolonged survival and decreased tumor volume compared to mice fed WD. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 2877.