Prostate cancer is a highly heritable disease with large disparities in incidence rates across ancestry populations. We conducted a multiancestry meta-analysis of prostate cancer genome-wide association studies (107,247 cases and 127,006 controls) and identified 86 new genetic risk variants independently associated with prostate cancer risk, bringing the total to 269 known risk variants. The top genetic risk score (GRS) decile was associated with odds ratios that ranged from 5.06 [95% confidence interval (CI) 4.84–5.29] for men of European ancestry to 3.74 [95% CI 3.36–4.17] for men of African ancestry. Men of African ancestry were estimated to have a mean GRS that was 2.18-times higher [95% CI 2.14–2.22], and men of East Asian ancestry 0.73-times lower [95% CI 0.71–0.76], than men of European ancestry. These findings support the role of germline variation contributing to population differences in prostate cancer risk, with the GRS offering an approach for personalized risk prediction.

Latinos represent <1% of samples analyzed to date in genome‐wide association studies of cancer. The clinical value of genetic information in guiding personalized medicine in populations of non‐European ancestry will require additional discovery and risk locus characterization efforts across populations. In the present study, we performed a GWAS of prostate cancer (PrCa) in 2,820 Latino PrCa cases and 5,293 controls to search for novel PrCa risk loci and to examine the generalizability of known PrCa risk loci in Latino men. We also conducted a genetic admixture‐mapping scan to identify PrCa risk alleles associated with local ancestry. Genome‐wide significant associations were observed with 84 variants all located at the known PrCa risk regions at 8q24 (128.484–128.548) and 10q11.22 (MSMB gene). In admixture mapping, we observed genome‐wide significant associations with local African ancestry at 8q24. Of the 162 established PrCa risk variants that are common in Latino men, 135 (83.3%) had effects that were directionally consistent as previously reported, among which 55 (34.0%) were statistically significant with p < 0.05. A polygenic risk model of the known PrCa risk variants showed that, compared to men with average risk (25th–75th percentile of the polygenic risk score distribution), men in the top 10% had a 3.19‐fold (95% CI: 2.65, 3.84) increased PrCa risk. In conclusion, we found that the known PrCa risk variants can effectively stratify PrCa risk in Latino men. Larger studies in Latino populations will be required to discover and characterize genetic risk variants for PrCa and improve risk stratification for this population.

Background-To study the association of nutrient intake measured by baseline food frequency questionnaire and risk of subsequent prostate cancer (PCa) in the SABOR (San Antonio Biomarkers of Risk) cohort study. Methods-After IRB approval, more than 1903 men enrolled in a prospective cohort from 2000 to 2010 as part of the SABOR clinical validation site for the National Cancer Institute Early Detection Research Network. Food and nutrient intakes were calculated using a Food Frequency Questionnaire. Cox proportional hazards modeling and covariate-balanced propensity scores were used to assess the associations between all nutrients and PCa. Results-A total of 229 men were diagnosed with PCa by prostate biopsy. Among all nutrients, increased risk of PCa was associated with intake of dietary fat scaled by the total caloric intake, particularly saturated fatty acid (SFA) [HR 1.19; 95% CI, 1.07-1.32), P value <0.001, False discovery rate (FDR) 0.047] and trans fatty acid (TFA) [HR per quintile 1.21; (95% CI) (1.08-Michael A. Liss

In a population based cohort, two-thirds of men diagnosed with prostate cancer qualify for active surveillance. Less restricted criteria for surveillance may be appropriate based on similar rates of upgrading/up staging at radical prostatectomy.

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