The authors describe the design and implementation of a large multiethnic cohort established to study diet and cancer in the United States. They detail the source of the subjects, sample size, questionnaire development, pilot work, and approaches to future analyses. The cohort consists of 215,251 adult men and women (age 45-75 years at baseline) living in Hawaii and in California (primarily Los Angeles County) with the following ethnic distribution: African-American (16.3%), Latino (22.0%), Japanese-American (26.4%), Native Hawaiian (6.5%), White (22.9%), and other ancestry (5.8%). From 1993 to 1996, participants entered the cohort by completing a 26-page, self-administered mail questionnaire that elicited a quantitative food frequency history, along with demographic and other information. Response rates ranged from 20% in Latinos to 49% in Japanese-Americans. As expected, both within and among ethnic groups, the questionnaire data show substantial variations in dietary intakes (nutrients as well as foods) and in the distributions of non-dietary risk factors (including smoking, alcohol consumption, obesity, and physical activity). When compared with corresponding ethnic-specific cancer incidence rates, the findings provide tentative support for several current dietary hypotheses. As sufficient numbers of cancer cases are identified through surveillance of the cohort, dietary and other hypotheses will be tested in prospective analyses. Keywords alcohol drinking; cohort studies; diet; ethnic groups; obesity; physical fitness; prospective studies; smoking Ethnic minorities in the United States have not been well represented in epidemiologic research on diet and cancer, especially in prospective cohort studies. Thus, little is known about the relation of dietary factors to cancer risk in these groups. Furthermore, while diet and other external factors are the predominant determinants of cancer risk in all these groups (1), the extent to which environmental exposures explain interethnic differences in incidence Reprint requests to Dr. Laurence Kolonel, Cancer Research Center of Hawaii, 1236 Lauhala Street, Honolulu, HI 96813. HHS Public Access Author Manuscript Author Manuscript Author ManuscriptAuthor Manuscript is not known. By including a variety of ethnic groups within a single study, and by using a common data collection methodology in all groups, interethnic comparisons of exposuredisease relations can readily be made.Hawaii has long presented special opportunities for epidemiologic research because of its diverse ethnic/cultural environment. Over the past two decades, the Los Angeles basin has also attracted large ethnic populations, including a variety of groups from Asia, and Latino migrants from Mexico and Central and South America. Together, these two areas now provide an unmatched resource for epidemiologic initiatives.Recognizing the need for dietary studies of ethnic minorities in the United States, the unique opportunities offered by Hawaii and southern California for conducting cross-ethnic a...

Genome-wide association studies (GWAS) and fine-mapping efforts to date have identified more than 100 prostate cancer (PrCa)-susceptibility loci. We meta-analyzed genotype data from a custom high-density array of 46,939 PrCa cases and 27,910 controls of European ancestry with previously genotyped data of 32,255 PrCa cases and 33,202 controls of European ancestry. Our analysis identified 62 novel loci associated (P < 5.0 × 10) with PrCa and one locus significantly associated with early-onset PrCa (≤55 years). Our findings include missense variants rs1800057 (odds ratio (OR) = 1.16; P = 8.2 × 10; G>C, p.Pro1054Arg) in ATM and rs2066827 (OR = 1.06; P = 2.3 × 10; T>G, p.Val109Gly) in CDKN1B. The combination of all loci captured 28.4% of the PrCa familial relative risk, and a polygenic risk score conferred an elevated PrCa risk for men in the ninetieth to ninety-ninth percentiles (relative risk = 2.69; 95% confidence interval (CI): 2.55-2.82) and first percentile (relative risk = 5.71; 95% CI: 5.04-6.48) risk stratum compared with the population average. These findings improve risk prediction, enhance fine-mapping, and provide insight into the underlying biology of PrCa.