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NPJ Breast Cancer. 2018 Sep 21;4:33. doi: 10.1038/s41523-018-0085-3. eCollection 2018.

Androgen receptor expression in normal breast tissue and subsequent breast cancer risk.

Author information

1
1Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA 02215 USA.
2
2Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, MA 02115 USA.
3
3Department of Pathology, Stanford University School of Medicine, Stanford, CA 94035 USA.
4
4Department of Pathology, Beth Israel Deaconess Medical Center, Boston, MA 02215 USA.
5
5Harvard Medical School, Boston, MA 02215 USA.
6
6PathAI, Cambridge, MA 02141 USA.
7
7Department of Pathology, Brigham and Women's Hospital, Boston, MA 02115 USA.
8
8Division of Preventive Medicine, Department of Medicine, Brigham and Women's Hospital, Boston, MA 02115 USA.
9
9Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115 USA.
10
10Department of Biostatistics, Harvard T.H. Chan School of Public Health, Boston, MA 02115 USA.
11
11Department of Biostatistics and Epidemiology, University of Massachusetts School of Public Health and Health Sciences, Amherst, MA 01003 USA.

Abstract

Sex steroid hormone signaling is critical in the development of breast cancers, although the role of the androgen receptor remains unclear. This study evaluated androgen receptor (AR) expression in normal breast tissue as a potential marker of breast cancer risk. We conducted a nested case-control study of women with benign breast disease (BBD) within the Nurses' Health Studies. Epithelial AR expression was assessed by immunohistochemistry in normal tissue from the BBD biopsy and the percent of positive nuclei was estimated in ordinal categories of 10% for 78 breast cancer cases and 276 controls. Logistic regression models adjusting for the matching factors and BBD lesion type were used to calculate odds ratios (ORs) for the association between AR expression (tertiles: ≤10%, 11-30%, and >30%) and breast cancer risk. AR expression in normal breast tissue was not associated with subsequent breast cancer risk (ORT3vsT1 = 0.9, 95% CI = 0.4-1.8, p trend = 0.68). In comparison with low AR/low ER women, ORs of 0.4 (95% CI = 0.1-1.2) for high AR/high ER women, 1.8 (95% CI = 0.4-7.8) for low AR/high ER women, and 0.7 (95% CI = 0.3-1.6) for high AR/low ER women were observed (p interaction = 0.21). Ki67 did not modify the association between AR expression and breast cancer risk (p interaction = 0.75). There was little evidence for an overall association between AR expression in normal breast tissue and breast cancer risk. These findings did not show that the AR association varied by Ki67 expression in normal breast tissue, though there was suggestive heterogeneity by ER expression.

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