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Unraveling the Mechanisms of Endocrine Resistance in Breast Cancer: New Therapeutic Opportunities

Authors' Affiliations: ¹ Department of Medicine and ² Markey Cancer Center, University of Kentucky, Lexington, Kentucky, ³ The Breast Center and ⁴ Department of Medicine, Baylor College of Medicine, One Baylor Plaza, BCM600, Houston, Texas

Requests for reprints: Suleiman Massarweh, Markey Cancer Center, 800 Rose Street, cc452, Lexington, KY 40536. Phone: 859-257-3608; Fax: 859-257-7715; E-mail: massarweh{at}uky.edu.

Abstract

Two thirds of breast cancers express the estrogen receptor (ER), which contributes to tumor development and progression. ER-targeted therapy is therefore widely used in breast cancer to inhibit signaling through ER and disrupt breast cancer growth. This therapeutic strategy, particularly using the antiestrogen tamoxifen, is proven to increase the cure rates in early breast cancer, improve patient outcomes in advanced disease, and reduce breast cancer incidence in the prevention setting. Despite the recent integration of more powerful endocrine agents into breast cancer care, resistance to all forms of endocrine therapy remains a major problem. New insight into ER biology and progress in understanding resistance mechanisms, mediated by molecular crosstalk between ER and various growth factor signaling pathways, are generating tremendous promise for new therapeutic opportunities to target resistance and improve breast cancer disease outcomes.

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