Hazel B Nichols1, Minouk J Schoemaker2, Jianwen Cai1, Jiawei Xu1, Lauren B Wright2, Mark N Brook2, Michael E Jones2, Hans-Olov Adami3, Laura Baglietto4, Kimberly A Bertrand5, William J Blot6, Marie-Christine Boutron-Ruault7, Miren Dorronsoro8, Laure Dossus9, A Heather Eliassen10, Graham G Giles11, Inger T Gram12, Susan E Hankinson13, Judy Hoffman-Bolton14, Rudolf Kaaks15, Timothy J Key16, Cari M Kitahara17, Susanna C Larsson18, Martha Linet17, Melissa A Merritt19, Roger L Milne11, Valeria Pala20, Julie R Palmer5, Petra H Peeters21, Elio Riboli19, Malin Sund22, Rulla M Tamimi10, Anne Tjønneland23, Antonia Trichopoulou24, Giske Ursin25, Lars Vatten25, Kala Visvanathan26, Elisabete Weiderpass27, Alicja Wolk18, Wei Zheng6, Clarice R Weinberg28, Anthony J Swerdlow2, Dale P Sandler28. 1. University of North Carolina Gillings School of Global Public Health, Chapel Hill, North Carolina (H.B.N., J.C., J.X.). 2. The Institute of Cancer Research, London, United Kingdom (M.J.S., L.B.W., M.N.B., M.E.J., A.J.S.). 3. Karolinska Institutet, Stockholm, Sweden (H.A.). 4. University of Pisa, Pisa, Italy (L.B.). 5. Slone Epidemiology Center at Boston University, Boston, Massachusetts (K.A.B., J.R.P.). 6. Vanderbilt-Ingram Cancer Center and Vanderbilt University School of Medicine, Nashville, Tennessee (W.J.B., W.Z.). 7. Institut National de la Santé et de la Recherche Médicale (INSERM) U1018 and Institut Gustave Roussy Centre for Research in Epidemiology and Population Health, Villejuif, France (M.B.). 8. Public Health Direction and Biodonostia Research Institute and Centro de Investigación Biomédica en Red de Epidemiología y Salud Pública, Basque Regional Health Department, San Sebastian, Spain (M.D.). 9. International Agency for Research on Cancer, Lyon, France (L.D.). 10. Brigham and Women's Hospital, Harvard Medical School, and Harvard T.H. Chan School of Public Health, Boston, Massachusetts (A.H.E., R.M.T.). 11. Cancer Council Victoria and University of Melbourne School of Population and Global Health, Melbourne, Victoria, Australia (G.G.G., R.L.M.). 12. University of Tromsø, The Arctic University of Norway, Tromsø, Norway (I.T.G.). 13. University of Massachusetts Amherst School of Public Health and Health Sciences, Amherst, Massachusetts (S.E.H.). 14. Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland (J.H.). 15. German Cancer Research Center, Heidelberg, Germany (R.K.). 16. University of Oxford, Oxford, United Kingdom (T.J.K.). 17. National Cancer Institute, National Institutes of Health, Bethesda, Maryland (C.M.K., M.L.). 18. Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden (S.C.L., A.W.). 19. School of Public Health, Imperial College London, London, United Kingdom (M.A.M., E.R.). 20. Cancer Registry of Norway, Institute of Population-Based Cancer Research, and University of Oslo, Oslo, Norway, and University of Southern California, Los Angeles, California (V.P.). 21. University Medical Center Utrecht, Utrecht, the Netherlands (P.H.P.). 22. Umeå University, Umeå, Sweden (M.S.). 23. Danish Cancer Society Research Center, Copenhagen, Denmark (A.T.). 24. Hellenic Health Foundation, Athens, Greece (A.T.). 25. Norwegian University of Science and Technology, Trondheim, Norway (G.U., L.V.). 26. Johns Hopkins Bloomberg School of Public Health and Johns Hopkins School of Medicine, Baltimore, Maryland (K.V.). 27. Karolinska Institutet, Stockholm, Sweden, University of Tromsø, The Arctic University of Norway, Tromsø, Norway, and Folkhälsan Research Center, Helsinki, Finland (E.W.). 28. National Institute of Environmental Health Sciences, National Institutes of Health, Durham, North Carolina (C.R.W., D.P.S.).
Abstract
Background: Parity is widely recognized as protective for breast cancer, but breast cancer risk may be increased shortly after childbirth. Whether this risk varies with breastfeeding, family history of breast cancer, or specific tumor subtype has rarely been evaluated. Objective: To characterize breast cancer risk in relation to recent childbirth. Design: Pooled analysis of individual-level data from 15 prospective cohort studies. Setting: The international Premenopausal Breast Cancer Collaborative Group. Participants: Women younger than 55 years. Measurements: During 9.6 million person-years of follow-up, 18 826 incident cases of breast cancer were diagnosed. Hazard ratios (HRs) and 95% CIs for breast cancer were calculated using Cox proportional hazards regression. Results: Compared with nulliparous women, parous women had an HR for breast cancer that peaked about 5 years after birth (HR, 1.80 [95% CI, 1.63 to 1.99]) before decreasing to 0.77 (CI, 0.67 to 0.88) after 34 years. The association crossed over from positive to negative about 24 years after birth. The overall pattern was driven by estrogen receptor (ER)-positive breast cancer; no crossover was seen for ER-negative cancer. Increases in breast cancer risk after childbirth were pronounced when combined with a family history of breast cancer and were greater for women who were older at first birth or who had more births. Breastfeeding did not modify overall risk patterns. Limitations: Breast cancer diagnoses during pregnancy were not uniformly distinguishable from early postpartum diagnoses. Data on human epidermal growth factor receptor 2 (HER2) oncogene overexpression were limited. Conclusion: Compared with nulliparous women, parous women have an increased risk for breast cancer for more than 20 years after childbirth. Health care providers should consider recent childbirth a risk factor for breast cancer in young women. Primary Funding Source: The Avon Foundation, the National Institute of Environmental Health Sciences, Breast Cancer Now and the UK National Health Service, and the Institute of Cancer Research.
Background: Parity is widely recognized as protective for breast cancer, but breast cancer risk may be increased shortly after childbirth. Whether this risk varies with breastfeeding, family history of breast cancer, or specific tumor subtype has rarely been evaluated. Objective: To characterize breast cancer risk in relation to recent childbirth. Design: Pooled analysis of individual-level data from 15 prospective cohort studies. Setting: The international Premenopausal Breast Cancer Collaborative Group. Participants: Women younger than 55 years. Measurements: During 9.6 million person-years of follow-up, 18 826 incident cases of breast cancer were diagnosed. Hazard ratios (HRs) and 95% CIs for breast cancer were calculated using Cox proportional hazards regression. Results: Compared with nulliparous women, parous women had an HR for breast cancer that peaked about 5 years after birth (HR, 1.80 [95% CI, 1.63 to 1.99]) before decreasing to 0.77 (CI, 0.67 to 0.88) after 34 years. The association crossed over from positive to negative about 24 years after birth. The overall pattern was driven by estrogen receptor (ER)-positive breast cancer; no crossover was seen for ER-negative cancer. Increases in breast cancer risk after childbirth were pronounced when combined with a family history of breast cancer and were greater for women who were older at first birth or who had more births. Breastfeeding did not modify overall risk patterns. Limitations: Breast cancer diagnoses during pregnancy were not uniformly distinguishable from early postpartum diagnoses. Data on human epidermal growth factor receptor 2 (HER2) oncogene overexpression were limited. Conclusion: Compared with nulliparous women, parous women have an increased risk for breast cancer for more than 20 years after childbirth. Health care providers should consider recent childbirth a risk factor for breast cancer in young women. Primary Funding Source: The Avon Foundation, the National Institute of Environmental Health Sciences, Breast Cancer Now and the UK National Health Service, and the Institute of Cancer Research.
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