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We pooled risk factor and pathology data on 5,905 HR+ breast cancer cases and 26,281 controls from 11 epidemiological studies. Proliferation was determined by centralized automated measures of KI67 in tissue microarrays. Odds ratios (OR), 95% confidence intervals (CI) and <jats:italic>p<\/jats:italic>\u2010values for case\u2013case and case\u2013control comparisons for risk factors in relation to levels of grade and quartiles (Q1\u2013Q4) of KI67 were estimated using polytomous logistic regression models. Case\u2013case comparisons showed associations between nulliparity and high KI67 [OR (95% CI) for Q4 <jats:italic>vs<\/jats:italic>. Q1\u2009=\u20091.54 (1.22, 1.95)]; obesity and high grade [grade 3 <jats:italic>vs<\/jats:italic>. 1\u2009=\u20091.68 (1.31, 2.16)] and current use of combined hormone therapy (HT) and low grade [grade 3 <jats:italic>vs<\/jats:italic>. 1\u2009=\u20090.27 (0.16, 0.44)] tumors. In case\u2013control comparisons, nulliparity was associated with elevated risk of tumors with high but not low levels of proliferation [1.43 (1.14, 1.81) for KI67 Q4 <jats:italic>vs<\/jats:italic>. 0.83 (0.60, 1.14) for KI67 Q1]; obesity among women \u226550 years with high but not low grade tumors [1.55 (1.17, 2.06) for grade 3 <jats:italic>vs<\/jats:italic>. 0.88 (0.66, 1.16) for grade 1] and HT with low but not high grade tumors [3.07 (2.22, 4.23) for grade 1 <jats:italic>vs<\/jats:italic>. 0.85 (0.55, 1.30) for grade 3]. Menarcheal age and family history were similarly associated with HR+ tumors of different grade or KI67 levels. These findings provide insights into the etiologic heterogeneity of HR+ tumors.<\/jats:p>","DOI":"10.1002\/ijc.31352","type":"journal-article","created":{"date-parts":[[2018,3,1]],"date-time":"2018-03-01T07:28:46Z","timestamp":1519889326000},"page":"746-757","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":27,"title":["Etiology of hormone receptor positive breast cancer differs by levels of histologic grade and proliferation"],"prefix":"10.1002","volume":"143","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3728-6535","authenticated-orcid":false,"given":"Mustapha","family":"Abubakar","sequence":"first","affiliation":[{"name":"Division of Cancer Epidemiology and Genetics National Cancer Institute, National Institutes of Health Rockville MD"},{"name":"Division of Genetics and Epidemiology The Institute of Cancer Research London United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jenny","family":"Chang\u2010Claude","sequence":"additional","affiliation":[{"name":"Division of Cancer Epidemiology German Cancer Research Center (DKFZ) Heidelberg Germany"},{"name":"University Cancer Center Hamburg, University Medical Center Hamburg\u2010Eppendorf Hamburg Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"H. 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