Post-menopausal breast cancer: from estrogen to androgen receptor

Avisek Majumder _, Mahavir Singh and Suresh C. Tyagi

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Oncotarget. 2017; 8:102739-102758. https://doi.org/10.18632/oncotarget.22156

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Avisek Majumder1,2, Mahavir Singh2 and Suresh C. Tyagi2

1Department of Biochemistry and Molecular Genetics, University of Louisville School of Medicine, Louisville 40202, Kentucky, USA

2Department of Physiology, University of Louisville School of Medicine, Louisville 40202, Kentucky, USA

Correspondence to:

Avisek Majumder, email: [email protected]

Mahavir Singh, email: [email protected]

Keywords: breast cancer; androgen receptor; estrogen receptor; metastasis; post-menopausal women

Received: July 06, 2017     Accepted: September 29, 2017     Published: October 27, 2017


In the United States, breast cancer is the second leading cause of death among women, and even though different therapies can treat primary breast tumors, most breast cancer-related deaths (>95%) occur due to metastasis. A majority (~70%) of breast tumors are found to express estrogen receptor, and a significant portion (~90%) of ER-positive (ER+) breast tumors are also androgen receptor-positive (AR+). Although ER is known to promote tumorigenesis, the role and underlying mechanism(s) of AR in these closely knit processes remain controversial. Endocrine therapies are the most commonly used treatment for patients with ER+ breast tumors; but, ~30%-50% of initially responsive patients develop resistance to these therapies. Whereas 70%–90% of all breast tumors are AR+ and AR overexpression is correlated with endocrine resistance, but the precise molecular mechanism(s) for this association is yet to be studied. Multiple mechanisms have been proposed to show AR and ER interactions, which indicate that AR may preferentially regulate expression of a subset of ER-responsive genes and that may be responsible for breast cancer and its progression in affected patients. On the other hand, most of the ER+ breast tumors found in post-menopausal women (~80%); and they have very low 17β-estradiol and high androgen levels, but how these hormonal changes make someone more prone to cancer phenotype has long been a disputed issue. In this study, we have discussed multiple molecular mechanisms that we believe are central to the understanding of the overall contributions of AR in breast cancer and its metastasis in post-menopausal women.

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