Dietary patterns reflect combinations of dietary exposures, and here we examine these in relation to prostate cancer risk. In a case-control study, 80 incident primary prostate cancer cases and 334 urology clinic controls were enrolled from 1997 through 1999 in Kingston, Ontario, Canada. Food-frequency questionnaires were completed prior to diagnosis and assessed intake in the 1-year period 2-3 years prior to enrollment. Among controls, dietary intake was used in principal components analyses to identify patterns that were then evaluated with all subjects in relation to prostate cancer risk using unconditional logistic regression, controlling for age. Prostate cancer is one of the most common cancer types in developed countries, with an estimated 20,100 new cases in 2004 in Canada. 1 Higher incidence rates occur in North America, Great Britain, Western Europe and Australia than in Asia, Latin America and Africa. 2 While genetic susceptibility is an established risk factor for prostate cancer, 2-5 the wide international variation in incidence points primarily to an environmental etiology. 6,7 The role of diet has been investigated in several epidemiologic studies, including dietary fat intake, vitamin A, carotenoids, fruits, vegetables, dairy products and soy products. 2,3,[7][8][9][10][11][12][13][14][15][16] The most consistent dietary component associated with prostate cancer risk is fat intake, 2 an association that is apparent despite differences in the quality of the study methods and assessment of dietary intake. [2][3][4]7,8,16 Recent attention has turned to a group of phytochemicals, particularly the isoflavones found in soybeans, 10,15 since Asians, with lower prostate cancer rates, have high consumption of soy products. Hypotheses regarding exposure to cadmium from foods such as shellfish and the risk of prostate cancer have not been substantiated by epidemiologic investigations. 2 Epidemiologic evidence supports an association between dietary factors and the risk of prostate cancer, but there are few consistent findings at a specific level. This is due in part to differences in measures of dietary intake, lack of variability in nutrient intakes among the population being studied and lack of control in the analysis for several possible confounders, including energy intake and lifestyle factors such as physical activity and smoking. 2,17,18 Further, potential associations between diet and prostate cancer risk may be concealed or lost when individual food items or nutrients are analyzed for their association with risk, as opposed to looking at groupings of habitually consumed foods. The metabolic and physiologic effects of combinations of foods on total risk are also unaccounted for when the conventional method of nutrient or individual food item analysis is used. 19 A broader consideration of patterns of food use may provide a more comprehensive assessment of the role of dietary factors on prostate cancer risk, given that foods are generally eaten in combination and together may have a greater impact on...

Although bacillus Calmette-Guerin (BCG) has been recognized as an effective therapy for superficial bladder cancer, dose-response studies are not available. Such studies are important because the administration of the vaccine is not devoid of significant side effects when the standard dose of 120 mg. is used. It has been speculated that smaller doses may be equally effective but carry fewer side effects. A controlled study comparing 2 doses of BCG was conducted as an initial step to explore this possibility. A total of 97 patients with a diagnosis of superficial (stages TIS, Ta and T1) bladder cancer was assigned to receive either 60 or 120 mg. BCG intravesically weekly for 6 weeks. The higher dose resulted in a better response for stages TIS, Ta (for prophylaxis of recurrence) and T1. However, the differences were not statistically significant. When stage TIS and Ta tumors coexisted, a significantly better response was recorded for the high dose. The overall success for the 2 treatments was 67% and 37% for the high and low doses, respectively. These differences reached statistical significance (p less than 0.02). Side effects were significantly less in number and severity in patients receiving the smaller dose of the vaccine.

A case-control study was conducted to determine the association between plasma organochlorine levels and prostate cancer risk. Male clinic patients scheduled for prostate core biopsy or seeing their urologist for other conditions from 1997 through 1999 in Kingston, Ontario were eligible, excluding those with an earlier cancer. Age frequency matched controls (n ¼ 329) were compared with 79 incident prostate cancer cases. Before knowledge of diagnosis, the patients completed a questionnaire and donated 15 ml of blood for the measurement of 14 PCBs, and 13 organochlorine pesticides by gas chromatography. At least 70% of patients had detectable levels of nine PCB congeners and seven pesticides, and these chemicals were included in the risk analysis adjusted for total lipids. Geometric means for these PCB congeners, total PCBs, and p,p'-DDE are slightly lower for cases than controls, whereas the levels of p,p'-DDT and other pesticides are virtually equal. Adjusting for age and other confounders in multivariable logistic regression, odds ratios (ORs) are consistently below 1.0 for PCB congeners and total PCBs. For pesticides, most ORs are very close to the null. This study suggests that longterm low-level exposure to organochlorine pesticides and PCBs in the general population does not contribute to increased prostate cancer risk.