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Purpose: The role of alcohol in young-onset breast cancer (YOBC) is unclear. We examined associations between lifetime alcohol consumption and YOBC in the Young Women's Health History Study, a population-based case–control study of breast cancer among Non-Hispanic Black and White women < 50 years of age. Methods: Breast cancer cases (n = 1,812) were diagnosed in the Metropolitan Detroit and Los Angeles County SEER registry areas, 2010–2015. Controls (n = 1,381) were identified through area-based sampling and were frequency-matched to cases by age, site, and race. Alcohol consumption and covariates were collected from in-person interviews. Weighted multivariable logistic regression was conducted to calculate adjusted odds ratios (aOR) and 95% confidence intervals (CI) for associations between alcohol consumption and YOBC overall and by subtype (Luminal A, Luminal B, HER2, or triple negative). Results: Lifetime alcohol consumption was not associated with YOBC overall or with subtypes (all ptrend ≥ 0.13). Similarly, alcohol consumption in adolescence, young and middle adulthood was not associated with YOBC (all ptrend ≥ 0.09). An inverse association with triple-negative YOBC, however, was observed for younger age at alcohol use initiation (< 18 years vs. no consumption), aOR (95% CI) = 0.62 (0.42, 0.93). No evidence of statistical interaction by race or household poverty was observed. Conclusions: Our findings suggest alcohol consumption has a different association with YOBC than postmenopausal breast cancer—lifetime consumption was not linked to increased risk and younger age at alcohol use initiation was associated with a decreased risk of triple-negative YOBC. Future studies on alcohol consumption in YOBC subtypes are warranted. [ABSTRACT FROM AUTHOR]

Purpose: To characterize breast cancer (BC) incidence by age at diagnosis and BC subtype among disaggregated Asian American, Native Hawaiian, and Pacific Islander (AANHPI) women and non-Hispanic White (NHW) women in Hawaiʻi. Methods: Using 1990–2014 data from the Hawaiʻi tumor registry, we estimated age-adjusted incidence rates (AAIR) of BC and the annual percent change in BC incidence by age (<50 and ≥50 years) and BC subtype (hormone receptor [HR]+/human epidermal growth factor receptor 2 [HER2]−, HR+/HER2+, HR−/HER2+, triple negative BC) for Filipino American (FA), Japanese American (JA), Native Hawaiian (NH), and NHW women. Results: Among young (<50 years) women, annual BC incidence increased 2.9% (1994–2014) among JA and 1.0% (1990–2014) among NHW women. Incidence was highest among young JA women (2010–2014 AAIR 52.0 per 100,000; 95% confidence interval [CI] 45.6, 58.9). HR+/HER2− BC, the major BC subtype, was similarly highest among young JA women (AAIR 39.5; 95% CI 33.9, 45.4). Among older (≥50 years) women, annual BC incidence increased 1.6% (1990–2014) among FA and 4.2% (2006–2014) for JA women. BC incidence was highest among older NH women (AAIR 137.6, 95% CI 128.2, 147.4), who also displayed highest incidence of two subtypes: HR+/HER2− (AAIR 106.9; 95% CI 98.6, 115.5) and HR+/HER2+ (AAIR 12.1; 95% CI 9.4, 15.1). Conclusion: We observed high and increasing BC incidence among JA women ages <50 years and high incidence among NH women ages ≥50 years. These results highlight racial and ethnic differences in BC incidence among disaggregated AANHPI populations in Hawaiʻi by age and BC subtype. [ABSTRACT FROM AUTHOR]

Purpose: To evaluate the association between lifetime personal cigarette smoking and young-onset breast cancer (YOBC; diagnosed <50 years of age) risk overall and by breast cancer (BC) subtype, and whether risk varies by race or socioeconomic position (SEP). Methods: Data are from the Young Women's Health History Study (YWHHS), a population-based case–control study of non-Hispanic Black (NHB) and White (NHW) women, ages 20–49 years (n = 1812 cases, n = 1381 controls) in the Los Angeles County and Metropolitan Detroit Surveillance, Epidemiology, and End Results (SEER) registry areas, 2010–2015. Lifetime personal cigarette smoking characteristics and YOBC risk by subtype were examined using sample-weighted, multivariable-adjusted polytomous logistic regression. Results: YOBC risk associated with ever versus never smoking differed by subtype (Pheterogeneity = 0.01) with risk significantly increased for Luminal A (adjusted odds ratio [aOR] 1.34; 95% confidence interval [CI] 1.06–1.68) and HER2-type (aOR 1.97; 95% CI 1.23–3.16), and no association with Luminal B or Triple Negative subtypes. Additionally, ≥30 years since smoking initiation (versus never) was statistically significantly associated with an increased risk of Luminal A (aOR 1.55; 95% CI 1.07–2.26) and HER2-type YOBC (aOR 2.77; 95% CI 1.32–5.79), but not other subtypes. In addition, among parous women, smoking initiated before first full-term pregnancy (versus never) was significantly associated with an increased risk of Luminal A YOBC (aOR 1.45; 95% CI 1.11–1.89). We observed little evidence for interactions by race and SEP. Conclusion: Findings confirm prior reports of a positive association between cigarette smoking and Luminal A YOBC and identify a novel association between smoking and HER2-type YOBC. [ABSTRACT FROM AUTHOR]

Background: Insulin, glucose, and other insulin-related proteins that mediate insulin signaling are associated with colorectal neoplasia risk, but associations with common genetic variation in insulin axis genes are less clear. In this study, we used a comprehensive tag single-nucleotide polymorphisms (SNPs) approach to define genetic variation in six insulin axis genes ( IGF1, IGF2, IGFBP1, IGFBP3, IRS1, and IRS2) and three genes associated with estrogen signaling ( ESR1, ESR2, and PGR). Methods: We assessed associations between SNPs and distal colorectal adenoma (CRA) risk in a case-control study of 1,351 subjects. Cases were individuals with one or more adenomas diagnosed during sigmoidoscopy, and controls were individuals with no adenomas at the sigmoidoscopy exam. We used unconditional logistic regression assuming an additive model to assess SNP-specific risks adjusting for multiple comparisons with P. Results: Distal adenoma risk was significantly increased for one SNP in IGF2 [per minor allele OR = 1.41; 95 % confidence interval (CI) = 1.16, 1.67; P = 0.005] and decreased for an ESR2 SNP (per minor allele OR = 0.78; 95 % CI = 0.66, 0.91; P = 0.041). There was no statistically significant heterogeneity of these associations by race, sex, BMI, physical activity, or, in women, hormone replacement therapy use. Risk estimates did not differ in the colon versus rectum or for smaller (<1 cm) versus larger ( >1 cm) adenomas. Conclusions: These data suggest that selected genetic variability in IGF2 and ESR2 may be modifiers of CRA risk. [ABSTRACT FROM AUTHOR]