To identify common alleles associated with different histotypes of epithelial ovarian cancer (EOC), we pooled data from multiple genome-wide genotyping projects totaling 25,509 EOC cases and 40,941 controls. We identified nine new susceptibility loci for different EOC histotypes: six for serous EOC histotypes (3q28, 4q32.3, 8q21.11, 10q24.33, 18q11.2 and 22q12.1), two for mucinous EOC (3q22.3, 9q31.1) and one for endometrioid EOC (5q12.3). We then meta-analysed the results for high-grade serous ovarian cancer with the results from analysis of 31,448 BRCA1 and BRCA2 mutation carriers, including 3,887 mutation carriers with EOC. This identified an additional three loci at 2q13, 8q24.1 and 12q24.31. Integrated analyses of genes and regulatory biofeatures at each locus predicted candidate susceptibility genes, including OBFC1, a novel susceptibility gene for low grade/borderline serous EOC.
Background:The Sister Study was designed to address gaps in the study of environment and breast cancer by taking advantage of more frequent breast cancer diagnoses among women with a sister history of breast cancer and the presumed enrichment of shared environmental and genetic exposures.Objective:The Sister Study sought a large cohort of women never diagnosed with breast cancer but who had a sister (full or half) diagnosed with breast cancer.Methods:A multifaceted national effort employed novel strategies to recruit a diverse cohort, and collected biological and environmental samples and extensive data on potential breast cancer risk factors.Results:The Sister Study enrolled 50,884 U.S. and Puerto Rican women 35–74y of age (median 56 y). Although the majority were non-Hispanic white, well educated, and economically well off, substantial numbers of harder-to-recruit women also enrolled (race/ethnicity other than non-Hispanic white: 16%; no college degree: 35%; household income <$50,000: 26%). Although all had a biologic sister with breast cancer, 16.5% had average or lower risk of breast cancer according to the Breast Cancer Risk Assessment Tool (Gail score). Most were postmenopausal (66%), parous with a first full-term pregnancy <30y of age (79%), never-smokers (56%) with body mass indexes (BMIs) of <29.9 kg/m2 (70%). Few (5%) reported any cancer prior to enrollment.Conclusions:The Sister Study is a unique cohort designed to efficiently study environmental and genetic risk factors for breast cancer. Extensive exposure data over the life-course and baseline specimens provide important opportunities for studying breast cancer and other health outcomes in women. Collaborations are welcome. https://doi.org/10.1289/EHP1923
Background: We sought to estimate the prevalence of low sexual desire and hypoactive sexual desire disorder (HSDD) in US women, focusing on their menopausal status. Methods: We performed a cross-sectional study. From a probability sample of households, 2207 US women aged 30 to 70 years and in stable relationships (Ն3 months) were interviewed by telephone. The analysis focused on 755 premenopausal women and 552 naturally and 637 surgically menopausal women. Low sexual desire was defined using the Profile of Female Sexual Function desire domain, and HSDD was defined using the Profile of Female Sexual Function and the Personal Distress Scale. Results: Prevalence of low sexual desire ranged from 26.7% among premenopausal women to 52.4% among naturally menopausal women. The prevalence of HSDD was highest among surgically menopausal women (12.5%). Compared with premenopausal women and adjusting for age, race/ethnicity, educational level, and smoking status, the prevalence ratios for HSDD were 2.3 (95% confidence interval, 1.2-4.5) for surgically menopausal women and 1.2 (0.5-2.8) for naturally menopausal women; the prevalence ratios for low sexual desire were 1.3 (0.9-1.9) and 1.5 (1.0-2.2) for surgically and naturally menopausal women, respectively. Conclusions: Prevalence of low sexual desire is elevated among surgically and naturally menopausal women vs premenopausal women. Distress about low desire (HSDD) appears to be more than twice as prevalent among surgically menopausal women vs premenopausal women, although the estimate is fairly imprecise.
BackgroundEarly-life exposures to hormonally active compounds and other factors may affect later response to estrogen or progesterone and hence may influence development of uterine leiomyomata (fibroids).ObjectivesWe evaluated associations of in utero and early-life exposures, including soy formula, with self-report of physician-diagnosed fibroids by 35 years of age.MethodsOur study included 19,972 non-Hispanic white women who were 35–59 years of age when they enrolled in the Sister Study in 2003–2007. We estimated risk ratios (RRs) and 95% confidence intervals (CIs) using log-binomial regression models for fibroid associations with adjustment for participant’s age and education, maternal age at participant’s birth, birth order, and childhood family income.ResultsGreater risk of early fibroid diagnosis was associated with soy formula during infancy (RR = 1.25; 95% CI, 0.97–1.61), maternal prepregnancy diabetes (RR = 2.05; 95% CI, 1.16–3.63), low childhood socioeconomic status (RR = 1.28; 95% CI, 1.01–1.63), and gestational age at birth (RR = 1.64; 95% CI, 1.27–2.13, for being born at least 1 month early). In utero diethylstilbestrol (DES) exposure was also associated with early fibroid diagnosis (RR = 1.42; 95% CI, 1.13–1.80), but this association was driven by women reporting probable rather than definite exposure.ConclusionsThere are plausible biological pathways by which these early-life factors could promote fibroid pathogenesis. This is the first epidemiologic study to evaluate such exposures, with the exception of in utero DES, in relation to fibroid risk, and replication of findings in other populations is needed.
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