TY - JOUR
T1 - Biology and etiology of young-onset breast cancers among premenopausal African American women
T2 - Results from the AMBER Consortium
AU - Chollet-Hinton, Lynn
AU - Olshan, Andrew F.
AU - Nichols, Hazel B.
AU - Anders, Carey K.
AU - Lund, Jennifer L.
AU - Allott, Emma H.
AU - Bethea, Traci N.
AU - Hong, Chi Chen
AU - Cohen, Stephanie M.
AU - Khoury, Thaer
AU - Zirpoli, Gary R.
AU - Borges, Virginia F.
AU - Rosenberg, Lynn A.
AU - Bandera, Elisa V.
AU - Ambrosone, Christine B.
AU - Palmer, Julie R.
AU - Troester, Melissa A.
N1 - Funding Information:
C.K. Anders reports receiving commercial research grants from Novartis, Sanofi, Cascadian, Nektar, Tesaro, toBBB, GERON, Angiochem, Merrimack, PUMA, Lily, Merck, and Oncothyreon and is a consultant/advisory board member for Novartis, Sanofi, toBBB, GERON, Angiochem, Merrimack, Lily, Genentech, Nektar, and Kadmon. No potential conflicts of interest were disclosed by the other authors.
Funding Information:
This work was supported by grants from the National Cancer Institute (NCI) at the NIH [NCI P01-CA151135 (to C.B. Ambrosone, J.R. Palmer, A.F. Olshan); the NCI Specialized Program of Research Excellence (SPORE) in Breast Cancer at UNC (NIH/NCI P50-CA58223, to A.F. Olshan and M.A. Troester); NIH U01 CA179715 (to A.F. Olshan and M.A. Troester); Lineberger Comprehensive Cancer Center (LCCC) core grant (NIH/NCI P30-CA16086); NCI P30-CA016086 to the Translational Pathology Laboratory; R01-CA058420 (to L.A. Rosenberg); UM1-CA164974 (to J.R. Palmer and L.A. Rosenberg); R01-CA098663 (to J.R. Palmer); R01-CA100598 (to C.B. Ambrosone); R01-CA185623 (to E.V. Bandera and C.C. Hong); and the University of North Carolina LCCC Cancer Control and Education Program training grant (NIH/NCI 5R25CA057726-25, to L. Chollet-Hinton)], the Department of Defense Breast Cancer Research Program, the University Cancer Research Fund of North Carolina and Susan G. Komen for the Cure Foundation (to A.F. Olshan and M.A. Troester), and the Breast Cancer Research Foundation (to C.B. Ambrosone). The authors gratefully acknowledge the support of all AMBER staff and participants.
Funding Information:
CA16086); NCI P30-CA016086 to the Translational Pathology Laboratory; R01-CA058420 (to L.A. Rosenberg); UM1-CA164974 (to J.R. Palmer and L.A. Rosenberg); R01-CA098663 (to J.R. Palmer); R01-CA100598 (to C.B. Ambrosone); R01-CA185623 (to E.V. Bandera and C.C. Hong); and the University of North Carolina LCCC Cancer Control and Education Program training grant (NIH/NCI 5R25CA057726-25, to L. Chollet-Hinton)], the Department of Defense Breast Cancer Research Program, the University Cancer Research Fund of North Carolina and Susan G. Komen for the Cure Foundation (to A.F. Olshan and M.A. Troester), and the Breast Cancer Research Foundation (to C.B. Ambrosone).
Funding Information:
This work was supported by grants from the National Cancer Institute (NCI) at the NIH [NCI P01-CA151135 (to C.B. Ambrosone, J.R. Palmer, A.F. Olshan); the NCI Specialized Program of Research Excellence (SPORE) in Breast Cancer at UNC (NIH/NCI P50-CA58223, to A.F. Olshan and M.A. Troester); NIH U01 CA179715 (to A.F. Olshan and M.A. Troester); Line-berger Comprehensive Cancer Center (LCCC) core grant (NIH/NCI P30-
Publisher Copyright:
©2017 AACR.
PY - 2017/12/1
Y1 - 2017/12/1
N2 - Background: African American (AA) women have higher incidence of aggressive, young-onset (<40 years) breast cancers. Young- and older-onset disease may have distinct tumor biologies and etiologies; however, studies investigating age differences among AA women have been rare and generally underpowered. Methods: We examined tumor characteristics and breast cancer risk factors associated with premenopausal young (<40) vs. older (40) AA women's breast cancer in the African American Breast Cancer Epidemiology and Risk Consortium (2,008 cases and 5,144 controls). Unconditional logistic regression models assessed heterogeneity of tumor biology and risk factor associations by age, overall, and by estrogen receptor status. Results: Premenopausal AA women <40 years had higher frequency of poorer-prognosis tumor characteristics compared with older women, including negative estrogen and progesterone receptor status, triple-negative subtype, higher grade, higher stage, and larger tumors. Adiposity (i.e., waist-to-hip ratio) and family history of breast cancer were more strongly associated with young-onset disease [case–control OR ¼ 1.46, 95% confidence interval (CI) ¼ 1.04–2.05; OR ¼ 3.10, 95% CI ¼ 2.08–4.63, respectively] compared with older-onset disease (OR ¼ 1.11, 95% CI ¼ 0.91–1.35; OR ¼ 1.57, 95% CI ¼ 1.26–1.94). Breastfeeding showed a slight inverse risk association among young women (OR ¼ 0.70, 95% CI ¼ 0.43–1.16). Oral contraceptive use was associated with increased risk regardless of age. Considering various cutoff points for young age (<40, <45, <50), age-related heterogeneity was greatest when <40 was used. Conclusions: Among premenopausal AA women, diagnosis before age 40 is associated with more aggressive breast tumor biology and some etiologic differences. Impact: Modifiable risk factors including breastfeeding, adiposity, and oral contraceptive use may be important targets for mitigating harms of young-onset breast cancer.
AB - Background: African American (AA) women have higher incidence of aggressive, young-onset (<40 years) breast cancers. Young- and older-onset disease may have distinct tumor biologies and etiologies; however, studies investigating age differences among AA women have been rare and generally underpowered. Methods: We examined tumor characteristics and breast cancer risk factors associated with premenopausal young (<40) vs. older (40) AA women's breast cancer in the African American Breast Cancer Epidemiology and Risk Consortium (2,008 cases and 5,144 controls). Unconditional logistic regression models assessed heterogeneity of tumor biology and risk factor associations by age, overall, and by estrogen receptor status. Results: Premenopausal AA women <40 years had higher frequency of poorer-prognosis tumor characteristics compared with older women, including negative estrogen and progesterone receptor status, triple-negative subtype, higher grade, higher stage, and larger tumors. Adiposity (i.e., waist-to-hip ratio) and family history of breast cancer were more strongly associated with young-onset disease [case–control OR ¼ 1.46, 95% confidence interval (CI) ¼ 1.04–2.05; OR ¼ 3.10, 95% CI ¼ 2.08–4.63, respectively] compared with older-onset disease (OR ¼ 1.11, 95% CI ¼ 0.91–1.35; OR ¼ 1.57, 95% CI ¼ 1.26–1.94). Breastfeeding showed a slight inverse risk association among young women (OR ¼ 0.70, 95% CI ¼ 0.43–1.16). Oral contraceptive use was associated with increased risk regardless of age. Considering various cutoff points for young age (<40, <45, <50), age-related heterogeneity was greatest when <40 was used. Conclusions: Among premenopausal AA women, diagnosis before age 40 is associated with more aggressive breast tumor biology and some etiologic differences. Impact: Modifiable risk factors including breastfeeding, adiposity, and oral contraceptive use may be important targets for mitigating harms of young-onset breast cancer.
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U2 - 10.1158/1055-9965.EPI-17-0450
DO - 10.1158/1055-9965.EPI-17-0450
M3 - Article
C2 - 28903991
AN - SCOPUS:85036640730
SN - 1055-9965
VL - 26
SP - 1722
EP - 1729
JO - Cancer Epidemiology Biomarkers and Prevention
JF - Cancer Epidemiology Biomarkers and Prevention
IS - 12
ER -