The effect of body size and change in BMI on endometrial cancer risk across different racial/ethnic groups has not been studied. We examined the association between body size and endometrial cancer risk and potential effect modification of other risk factors among 50,376 women in the Multiethnic Cohort Study. During 10.3 years of follow-up, 463 endometrial cancer cases were identified. Epidemiologic data were collected from the baseline questionnaire. ''BMI change'' was defined as the percentage of body mass index change from age 21 to the time of recruitment. Women who were heavier at age 21 or at baseline (weight ! 53.5 kg or ! 63.9 kg, respectively) had an increased endometrial cancer risk compared to the lowest quartile of weight during the respective periods. BMI gain ! 35% had a RR of 4.12 (95% CI: 2.69, 6.30) compared to the reference group (25% BMI change <15%). Women who averaged an annual BMI gain ! 1% had a >3.21-fold (95% CI: 2.37, 4.33) increased risk compared to women who maintained a stable adult BMI (20.25 to <10.25%). The highest risk associated with BMI gain was observed among nulliparous women and postmenopausal women who never used hormone therapy. Although African Americans and Whites showed an increase in risk after !35% BMI gain, Japanese Americans showed an increase in risk with much smaller gain (!5%). In conclusion, adult obesity and increase in adiposity are risk factors for endometrial cancer; and the risk associated with these factors may vary across racial/ethnic groups.Endometrial cancer is the fourth most common cancer among US women. 1 The role of obesity in endometrial cancer etiology is well established 2,3 ; prospective studies report obesity, defined as body mass index (BMI) !30 kg/m 2 , is associated with a 1.7-4.5 fold increase in risk. [4][5][6][7][8][9][10][11][12] Because substantial body weight gain can lead to obesity, it is believed that adult weight or BMI change, often a measure of increased adiposity, is associated with endometrial cancer risk.Among 5 prospective studies, 5,6,8,13,14 all 5 reported a positive association between weight gain during the period of young adulthood (age, 18-25 years) to age at study entry and endometrial cancer risk; however, none of these studies have investigated the role of anthropometric measures across racial/ethnic populations. The aim of this analysis was to examine the association of body size and its change over time with the risk of endometrial cancer in a multiethnic population, as well as the potential modifying effect of other risk factors on these relations. Material and Methods Study populationThe Multiethnic Cohort Study (MEC) is a prospective cohort study established to investigate the association of lifestyle and genetic factors with chronic disease. Details of the study design, recruitment, response rates and baseline characteristics of the MEC have been previously published. 15 Briefly, the cohort consists of 215,251 men and women between the ages of 45-75 years selected from 5 racial/ethnic populations: African Amer...

Purpose Older age, African ancestry, and family history of prostate cancer are well-established risk factors for prostate cancer and all are non-modifiable. Various lifestyle factors have been examined in relation to prostate cancer risk, including diet, obesity, and physical activity; however, none of them has been consistently related to risk. In the Multiethnic Cohort Study, we investigated whether lifestyle-related factors are associated with prostate cancer risk and whether such factors explain the racial/ethnic differences in risk. Methods During a mean follow-up of 13.9 years, 7,115 incident cases were identified among 75,216 white, African American, Native Hawaiian, Japanese American, and Latino men. Cox proportional hazards models were used to calculate relative risks (RR) and 95% confidence intervals (95% CI) for prostate cancer. Results Among selected lifestyle-related factors including body mass index, height, education, physical activity, and intakes of alcohol, calcium, legumes, lycopene, and selenium, only smoking (RR for current (≥20 cigarettes/day) vs. never smoking = 0.72; 95% CI: 0.63-0.83) and history of diabetes (RR for yes vs. no = 0.78; 95% CI: 0.72-0.85) were significantly associated with prostate cancer risk. Compared to whites, the risk of incident prostate cancer was two-fold higher in African Americans and 16% higher in Latinos. Additional adjustment for a history of PSA testing did not change the results. Conclusions The findings suggest that racial/ethnic differences in prostate cancer risk are not explained by the lifestyle factors examined, and that underlying genetic factors may be involved.

Common obesity risk variants have been associated with macronutrient intake; however, these associations' generalizability across populations has not been demonstrated. We investigated the associations between 6 obesity risk variants in (or near) the NEGR1, TMEM18, BDNF, FTO, MC4R, and KCTD15 genes and macronutrient intake (carbohydrate, protein, ethanol, and fat) in 3 Population Architecture using Genomics and Epidemiology (PAGE) studies: the Multiethnic Cohort Study (1993-2006) (n = 19,529), the Atherosclerosis Risk in Communities Study (1987-1989) (n = 11,114), and the Epidemiologic Architecture for Genes Linked to Environment (EAGLE) Study, which accesses data from the Third National Health and Nutrition Examination Survey (1991-1994) (n = 6,347). We used linear regression, with adjustment for age, sex, and ethnicity, to estimate the associations between obesity risk genotypes and macronutrient intake. A fixed-effects meta-analysis model showed that the FTO rs8050136 A allele (n = 36,973) was positively associated with percentage of calories derived from fat (βmeta = 0.2244 (standard error, 0.0548); P = 4 × 10(-5)) and inversely associated with percentage of calories derived from carbohydrate (βmeta = -0.2796 (standard error, 0.0709); P = 8 × 10(-5)). In the Multiethnic Cohort Study, percentage of calories from fat assessed at baseline was a partial mediator of the rs8050136 effect on body mass index (weight (kg)/height (m)(2)) obtained at 10 years of follow-up (mediation of effect = 0.0823 kg/m(2), 95% confidence interval: 0.0559, 0.1128). Our data provide additional evidence that the association of FTO with obesity is partially mediated by dietary intake.

The incidence of stomach cancer is high in certain parts of the world, particularly in China. Chronic Helicobacter pylori infection is the main risk factor, yet the vast majority of infected individuals remain unaffected with cancer, suggesting an important role of other risk factors. We conducted a population-based case-control study including 196 incident stomach cancer cases and 397 matched controls to test the hypothesis that adverse single nucleotide polymorphism (SNP) genotypes and haplotypes within genes of the DNA repair and immune regulatory pathways are associated with increased stomach cancer risk. Genomic DNA isolated from blood samples was used for genotyping, and results were obtained for 57 putatively functional SNPs in 28 genes. Odds ratios (OR) and 95% confidence intervals (95% CI) were obtained from adjusted logistic regression models. For PTGS2, a gene involved in the inflammatory response, associations with stomach cancer risk were observed for TC genotype carriers of rs5279 (OR, 0.24; 95% CI, 0.08-0.73), CT genotype carriers of the 3′-untranslated region SNP rs689470 (OR, 7.49; 95% CI, 1.21-46.20), and CTTC haplotype carriers of rs5277, rs5278, rs5279, and rs689470 (OR, 0.41; 95% CI, 0.18-0.95). For ERCC5, a gene involved in nucleotide excision repair, TC genotype carriers of rs1047768 (OR, 0.65; 95% CI, 0.41-1.03), GC genotype carriers of the nonsynonymous SNP rs2227869 (OR, 0.30; 95% CI, 0.13-0.67), and CCG haplotype carriers of rs1047768, rs17655, and rs2227869 (OR, 0.45; 95% CI, 0.20-1.04) were associated with reduced stomach cancer risk. In conclusion, PTGS2 and ERCC5 were associated with stomach cancer risk in a