Dietary intake of fiber, whole grains and risk of colorectal cancer: An updated analysis according to food sources, tumor location and molecular subtypes in two large US cohorts.

Epidemiologic evidence relating fiber intake to colorectal cancer (CRC) remains inconclusive and data are limited on different food sources of fiber and heterogeneity by tumor subsite and molecular profile. We prospectively followed for CRC incidence 90,869 women from the Nurses' Health Study (1980-2012) and 47,924 men from the Health Professionals Follow-up Study (1986-2012), who completed a validated food frequency questionnaire every 4 years. Cox proportional hazards regression was used to examine the associations with CRC risk for total, cereal, fruit and vegetable fiber and whole grains. We also assessed the associations according to tumor subsites (proximal colon, distal colon and rectum) and molecular markers (microsatellite instability, BRAF mutation, CpG island methylator phenotype and KRAS mutation). We documented 3,178 CRC cases during 3,685,903 person-years of follow-up in the NHS and HPFS. Intake of total dietary fiber was not associated with CRC risk after multivariable adjustment in either women (hazard ratio [HR] comparing extreme deciles, 1.17; 95% CI, 0.92-1.48, ptrend = 0.55) or men (HR, 0.90; 95% CI, 0.67-1.21, ptrend = 0.47). Higher intake of cereal fiber and whole grains was associated with lower CRC risk in men with an HR of 0.75 (95% CI, 0.57-1.00) and 0.72 (95% CI, 0.54-0.96), respectively. No heterogeneity was detected by tumor subsite or molecular markers (pheterogeneity > 0.05). Higher intake of total dietary fiber within the range of a typical American diet is unlikely to substantially reduce CRC risk. The potential benefit of cereal fiber and whole grains in men warrants further confirmation.

Risk of a second primary cancer after non-melanoma skin cancer in white men and women: a prospective cohort study.

BACKGROUND: Previous studies suggest a positive association between history of non-melanoma skin cancer (NMSC) and risk of subsequent cancer at other sites. The purpose of this study is to prospectively examine the risk of primary cancer according to personal history of NMSC. METHODS AND FINDINGS: In two large US cohorts, the Health Professionals Follow-up Study (HPFS) and the Nurses' Health Study (NHS), we prospectively investigated this association in self-identified white men and women. In the HPFS, we followed 46,237 men from June 1986 to June 2008 (833,496 person-years). In the NHS, we followed 107,339 women from June 1984 to June 2008 (2,116,178 person-years). We documented 29,447 incident cancer cases other than NMSC. Cox proportional hazard models were used to calculate relative risks (RRs) and 95% confidence intervals (CIs). A personal history of NMSC was significantly associated with a higher risk of other primary cancers excluding melanoma in men (RR=1.11; 95% CI 1.05-1.18), and in women (RR=1.20; 95% CI 1.15-1.25). Age-standardized absolute risk (AR) was 176 in men and 182 in women per 100,000 person-years. For individual cancer sites, after the Bonferroni correction for multiple comparisons (n=28), in men, a personal history of NMSC was significantly associated with an increased risk of melanoma (RR=1.99, AR=116 per 100,000 person-years). In women, a personal history of NMSC was significantly associated with an increased risk of breast (RR=1.19, AR=87 per 100,000 person-years), lung (RR=1.32, AR=22 per 100,000 person-years), and melanoma (RR=2.58, AR=79 per 100,000 person-years). CONCLUSION: This prospective study found a modestly increased risk of subsequent malignancies among individuals with a history of NMSC, specifically breast and lung cancer in women and melanoma in both men and women.

Sex steroid hormone exposures and risk for meningioma.

OBJECT: The goal of this study was to investigate the risk of meningioma in relation to exogenous and endogenous sex hormones. METHODS: The study participants were female registered nurses from 11 US states who were between 30 and 55 years of age when they enrolled in the Nurses' Health Study cohort. These women completed biennial questionnaires between 1976 and 1996. All participants were free from cancer and other major medical illness at the onset of the study. The primary endpoint was meningioma as self-reported in biennial and supplemental questionnaires. During 1,213,522 person-years of follow-up review, 125 cases of meningioma were confirmed. After adjusting for age and body mass index (BMI), compared with postmenopausal women who had never used postmenopausal hormones, the relative risk (RR) for premenopausal women was 2.48 (95% confidence interval [CI] 1.29-4.77; p = 0.01) and the RR for postmenopausal women who received hormone therapy was 1.86 (95% CI 1.07-3.24; p = 0.03). The authors found no excess risk associated with past hormone use. In models that additionally controlled for hormone use and menopausal status, the authors found that, compared with women whose menarche occurred before they were 12 years of age, the RR for women whose menarche occurred at ages 12 through 14 years was 1.29 (95% CI 0.86-1.92; p = 0.21) and the RR for women whose menarche occurred after age 14 years was 1.97 (95% CI 1.06-3.66; p = 0.03). The authors also observed a tendency, albeit nonsignificant, for increased risk of meningioma in parous as opposed to nulliparous women (multivariate RR = 2.39, 95% CI 0.76-7.53; p = 0.14). A trend toward an increasing risk of meningioma with increasing BMI was also noted (p for trend = 0.06). No association was found for past or current use of oral contraceptives. CONCLUSIONS: The risk for meningiomas was increased among women exposed to either endogenous or exogenous sex hormones. An unexpected relationship with increasing age at menarche was also noted; this remains unexplained.