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Response and Resistance to the Endocrine Prevention of Breast Cancer

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Part of the book series: Advances in Experimental Medicine and Biology ((AEMB,volume 617))

Current endocrine approaches to breast cancer (BC) prevention are targeted mainly at the estrogen receptor alpha (ERα) (1). Endocrine prevention depends upon either reducing the concentration of estrogen reaching ERα+ breast epithelial cells [estrogen deprivation (ED)] by, for example, ovarian suppression in premenopausal women, or aromatase inhibition in postmenopausal women, or by blocking the interaction of estrogen with ERα by selective estrogen receptor modulators (SERMs) such as tamoxifen (Tarn) and raloxifene (Ral). Observational studies (2–11) and randomised controlled trials (12–25) indicate that treatment by ED and SERMS reduces the risk of subsequent BC by approximately 50% and that this effect is prolonged (16, 18, 20, 26). In the human breast, ERα is detectable in epithelial cells of lobules and ducts and not in the stroma (27). However, it is not clear whether normal, premalignant or malignant epithelial cells are the targets for endocrine prevention. In this chapter, we summarise the results of endocrine prevention trials to date and what is known about the response of the three types of potential target structures to estrogen stimulation and inhibition by ED and SERMS.

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Howell, A., Bundred, N.J., Cuzick, J., Allred, D.C., Clarke, R. (2008). Response and Resistance to the Endocrine Prevention of Breast Cancer. In: Li, J.J., Li, S.A., Mohla, S., Rochefort, H., Maudelonde, T. (eds) Hormonal Carcinogenesis V. Advances in Experimental Medicine and Biology, vol 617. Springer, New York, NY. https://doi.org/10.1007/978-0-387-69080-3_19

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