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  • American Association for Cancer Research (AACR)  (4)
  • 1
    In: Cancer Epidemiology, Biomarkers & Prevention, American Association for Cancer Research (AACR), Vol. 29, No. 6_Supplement_2 ( 2020-06-01), p. A112-A112
    Abstract: The etiology of breast cancer (BC) among young women is not well understood. Recent studies have suggested that tobacco exposure is associated with an increased risk of BC but few studies have evaluated risk among women under age 50 or racial and socioeconomic disparities in risk. We hypothesized that racial and socioeconomic differences in age at smoking initiation and lifetime cigarette smoking contribute to disparities in BC risk among young women. Data were examined from a population-based case-control study in women under 50 years of age, the Young Women’s Health History Study. In total, 1,812 women with invasive BC (1,130 Non-Hispanic (NH) White, 682 NH Black) and an area-based sample of 1,381 control women (716 NH White, 665 NH Black), frequency matched to cases by five-year age group, study site and race were identified and interviewed from the Los Angeles County and Metropolitan Detroit SEER registry areas. Lifetime smoking history (including age at initiation, duration, and frequency) were collected from structured in-person interviews. Survey-weighted multivariable logistic regression was used to evaluate the association between lifetime cigarette smoking and BC risk adjusted for matching and known BC risk factors. Additionally, cross-product interaction terms of smoking exposure by race and by socioeconomic position (SEP; based on household percent poverty) were evaluated by Wald’s test. Among controls, 36.5% reported ever smoking at least 1 cigarette a day for at least 6 months in their lifetime with White women compared to Black women (38.3% vs. 32.3%) and women of lower SEP ( & lt;150% of poverty) compared to higher SEP (≥150% of poverty) (50.4% vs. 31.5%) being more likely to have ever smoked. In adjusted models, those who ever vs. never smoked were 1.20 times as likely to develop BC; findings were marginally significant (95% confidence interval (CI): 0.99-1.46, p=0.07). No differences were found by race or SEP, nor was there a consistent association with BC risk for duration of smoking history (in pack-years) or average number of cigarettes smoked per day. Age at smoking initiation (never smoker, initiated at age & lt;25 years, initiated at age ≥25 years) was significantly positively associated with BC risk (p trend=0.02). Smoking initiated at 25 years or older was associated with a 78% increased risk of BC compared to never smokers (95% CI: 1.15-2.77). A positive association between age at initiation and BC risk was observed among White (p trend=0.048), but not Black women. A marginally significant increased risk with age at initiation was observed among women of higher SEP (p trend=0.05) but not among those of lower SEP. We found evidence that smoking is associated with an increased risk of BC in young women, especially among those who started smoking at an older age. Despite efforts to reduce smoking, the prevalence of smoking remains highest among people of low socioeconomic position, as we found. Encouraging women not to initiate smoking is important to reduce BC risk among women under age 50. Citation Format: Ugonna Ihenacho, Ann S Hamilton, Wendy J Mack, Anna H Wu, Jennifer B Unger, Dorothy R Pathak, Richard T Houang, Michael F Press, Kendra L Schwartz, Lydia Marcus, Ellen M Velie. Lifetime cigarette smoking and breast cancer risk in young women: Racial and socioeconomic disparities in risk in the Young Women’s Health History Study [abstract]. In: Proceedings of the Twelfth AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2019 Sep 20-23; San Francisco, CA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2020;29(6 Suppl_2):Abstract nr A112.
    Type of Medium: Online Resource
    ISSN: 1055-9965 , 1538-7755
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2020
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  • 2
    In: Cancer Epidemiology, Biomarkers & Prevention, American Association for Cancer Research (AACR), Vol. 29, No. 12_Supplement ( 2020-12-01), p. PO-200-PO-200
    Abstract: Previous studies have found that tobacco exposure is associated with an increased risk of premenopausal breast cancer (BC) overall and some studies suggest that risk is only increased for Luminal A BC. Few studies have described the association between tobacco exposure and BC risk with characterization of the human epidermal growth factor receptor 2 (HER2) subtype. This analysis explored associations between smoking over the life course and BC risk overall and by BC subtype among a socioeconomically diverse population of young non-Hispanic (NH) Black and White women. Data were examined from a population-based case-control study in women under 50 years of age, the Young Women’s Health History Study. In total, 1,812 women with invasive BC (1,130 NH White, 682 NH Black) and an area-based sample of 1,381 (716 NH White, 665 NH Black) control women, frequency matched to cases by five-year age group, study site and self-reported race were identified from the Los Angeles County and Metropolitan Detroit SEER registry areas. Lifetime smoking histories were collected from in-person interviews. Sample-weighted logistic regression analysis was conducted to estimate the association between lifetime cigarette smoking status (never versus ever smoker) and BC risk adjusted for known BC risk factors and study site. Multinomial logistic regression analysis was conducted for analyses by BC subtype. Heterogeneity in the odds ratio (OR) estimates by BC subtype and cross-product interaction terms of smoking status by race and by household percent poverty (HHP) were evaluated by the Wald test. In adjusted models, BC risk overall was not significantly associated with ever smoking at least 1 cigarette a day for 6 months or more (OR 1.18; 95% confidence interval (CI) 0.97- 1.43). By BC subtype, ever smokers displayed a statistically significant 30% increase in Luminal A BC risk compared to never smokers (OR 1.30; 95% CI 1.03-1.64) and a 90% increased risk of HER2-type BC (OR 1.90; 95% CI 1.17-3.08). Smoking was not associated with risk of Luminal B or Triple Negative BC. Associations between ever smoking and BC risk significantly differed by BC subtype (Pheterogeneity=0.02). Statistical interactions by race or by HHP were not observed. However, we noted that in stratified models the association between smoking and risk for HER2-type BC was higher among NH White compared to NH Black women and among women with HHP ≥150% compared to HHP & lt;150%. For Luminal A BC, the association with smoking did not differ by race and risk was higher among women with HHP & lt;150% compared to HHP ≥150%. Although other studies have identified an association between smoking and Luminal A BC, this may be the first study to identify an association between smoking and hormone receptor negative, HER2-type BC risk. An increased risk for HER2-type BC among NH White women and women with HHP ≥150% was suggested. Research in HER2-type BC is a relatively new and evolving field as HER2 expression was often underreported in the pathology reports of cases diagnosed before 2005. Citation Format: Ugonna N. Ihenacho, Ann S. Hamilton, Wendy J. Mack, Anna H. Wu, Jennifer B. Unger, Dorothy R. Pathak, Richard T. Houang, Michael F. Press, Kendra L. Schwartz, Lydia Marcus, Ellen M. Velie. Increased risk of luminal A and HER2-type breast cancer with lifetime cigarette smoking among non-Hispanic Black and White women in the Young Women’s Health History Study [abstract]. In: Proceedings of the AACR Virtual Conference: Thirteenth AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2020 Oct 2-4. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2020;29(12 Suppl):Abstract nr PO-200.
    Type of Medium: Online Resource
    ISSN: 1055-9965 , 1538-7755
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2020
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  • 3
    In: Clinical Cancer Research, American Association for Cancer Research (AACR), Vol. 21, No. 19 ( 2015-10-01), p. 4440-4450
    Abstract: Purpose: Preclinical model systems should faithfully reflect the complexity of the human pathology. In hepatocellular carcinoma (HCC), the tumor vasculature is of particular interest in diagnosis and therapy. By comparing two commonly applied preclinical model systems, diethylnitrosamine induced (DEN) and orthotopically implanted (McA) rat HCC, we aimed to measure tumor biology noninvasively and identify differences between the models. Experimental Design: DEN and McA tumor development was monitored by MRI and PET. A slice-based correlation of imaging and histopathology was performed. Array CGH analyses were applied to determine genetic heterogeneity. Therapy response to sorafenib was tested in DEN and McA tumors. Results: Histologically and biochemically confirmed liver damage resulted in increased 18F-fluorodeoxyglucose (FDG) PET uptake and perfusion in DEN animals only. DEN tumors exhibited G1–3 grading compared with uniform G3 grading of McA tumors. Array comparative genomic hybridization revealed a highly variable chromosomal aberration pattern in DEN tumors. Heterogeneity of DEN tumors was reflected in more variable imaging parameter values. DEN tumors exhibited lower mean growth rates and FDG uptake and higher diffusion and perfusion values compared with McA tumors. To test the significance of these differences, the multikinase inhibitor sorafenib was administered, resulting in reduced volume growth kinetics and perfusion in the DEN group only. Conclusions: This work depicts the feasibility and importance of in depth preclinical tumor model characterization and suggests the DEN model as a promising model system of multifocal nodular HCC in future therapy studies. Clin Cancer Res; 21(19); 4440–50. ©2015 AACR. See related commentary by Weber et al., p. 4254
    Type of Medium: Online Resource
    ISSN: 1078-0432 , 1557-3265
    RVK:
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2015
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    detail.hit.zdb_id: 2036787-9
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  • 4
    In: Cancer Epidemiology, Biomarkers & Prevention, American Association for Cancer Research (AACR), Vol. 32, No. 1_Supplement ( 2023-01-01), p. C129-C129
    Abstract: Few studies have described the association between lifetime smoking exposures and young-onset breast cancer (YOBC) risk by BC subtypes including the human epidermal growth factor receptor 2 (HER2) subtype. This study explored associations between lifetime cumulative cigarette smoking exposure from both secondhand smoke (SHS) and personal smoking exposures and YOBC risk, overall and by BC subtype. Data are from the Young Women’s Health History Study, a population-based, case-control study of BC in non-Hispanic Black and White women 20-49 years of age. Invasive BC cases were identified in the Los Angeles County and Metropolitan Detroit Surveillance, Epidemiology, and End Results (SEER) registry areas, 2010-2015 (n=1,812). Controls were identified through area-based sampling and frequency matched to cases by study site, race and age (n=1,381). Lifetime cumulative cigarette exposure (LCCE) was categorized as no personal or SHS exposure, only SHS exposure in childhood, only SHS exposure in adulthood, SHS exposure in childhood & adulthood, and ever personally smoked (with or without SHS exposure). BC subtypes were defined as Luminal A, Luminal B, HER2-type, and triple negative (TN) BC. We conducted multivariable adjusted sample-weighted logistic regression analysis to estimate the association between LCCE and YOBC risk among all participants and then among women who never personally smoked by duration of SHS exposure ( & lt;15 and ≥15 years). We also conducted adjusted polytomous logistic regression analyses and the Wald test to assess heterogeneity by BC subtype. Lifetime cumulative SHS exposure only was reported by 42% of participants, and an additional 37% reported personally smoking. In adjusted models, compared to no SHS, LCCE was not significantly associated with overall YOBC risk. Suggestive differences in YOBC risk by BC subtype were observed, however (P heterogeneity=0.04), with a suggestive increased odds of HER2-type BC with ever smoking (adjusted odds ratio [aOR] 1.61; 95% confidence interval [CI] 0.91, 2.86). Among participants who never smoked, duration of childhood SHS exposure was associated with differences in YOBC risk by subtype (P heterogeneity=0.01); childhood SHS exposure of ≥15 years compared to no childhood SHS was associated with a significantly decreased odds of HER2-type BC (aOR 0.31; 95% CI 0.12, 0.83) and a suggestive increased odds of TNBC (aOR 1.43; 95% CI 0.95, 2.16) while childhood SHS exposure of & lt;15 years compared to no childhood SHS was associated with a suggestive decreased odds of Luminal A BC (aOR 0.74; 95% CI 0.54, 1.03); the latter two findings did not reach statistical significance. Our results suggest that LCCE is associated with differences in risk of YOBC by BC subtype where personal cigarette smoking may be associated with an increased risk for HER2 type YOBC while childhood SHS exposure for ≥15 years may be associated with a decreased risk of HER2 type YOBC and an increased risk of TN YOBC. These findings warrant further examination. Citation Format: Ugonna Ihenacho, Ann S. Hamilton, Wendy J. Mack, Anna H. Wu, Jennifer B. Unger, Dorothy R. Pathak, Kelly A. Hirko, Richard T. Houang, Michael F. Press, Kendra L. Schwartz, Lydia R. Marcus, Ellen M. Velie. Lifetime cumulative cigarette exposure and young-onset breast cancer risk by subtype in the Young Women’s Health History Study [abstract]. In: Proceedings of the 15th AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2022 Sep 16-19; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2022;31(1 Suppl):Abstract nr C129.
    Type of Medium: Online Resource
    ISSN: 1538-7755
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2023
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    detail.hit.zdb_id: 1153420-5
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