The etiology of breast cancer (BC) is thought to involve a complex interplay of genetic, hormonal, and environmental factors that influence the physiological status of the host. Epidemiological studies indicate estrogen (E)-dependent physiological changes can increase a women's risk of developing BC (1). These findings implicate the involvement of steroid hormones, especially E, in BC development. E exerts its mitogenic effect on mammary tissue through its interaction with estrogen receptors Several studies have shown that the proliferative effect of E on epithelial cells is indirect and may involve a paracrine regulatory mechanism (3, 4). The observation that E-dependent tumors eventually lose this E-dependence suggests the presence of other factors such as growth factors and others are involved in cellular proliferation and tumor maintenance. The role of some of these factors and their E regulation in normal mammary gland (MG) development as well as tumorigenesis has been the focus of several studies (5-8).

The source of sex steroids differ between pre- and postmenopausal women. Es is synthesized by the ovary or by extra-glandular tissues, and delivered, via the endocrine route, to breast tissue. E synthesis is catalyzed by an enzyme complex known as aromatase (ARO), whose activity results in aromatization of the A ring of androgens, to form the phenolic ring characteristic of Es (9-11). The capacity of certain BCs to synthesize Es because of the presence of intratumoral ARO has been established for almost 20 years (9). The potential clinical importance of this intracrine mechanism has led to widespread clinical and laboratory investigations with aromatase inhibitors (AIs) have been used to treat women with hormone dependent BC (11). This chapter will focus on the possibility that Es may initiate, as well as promote BC, and that these processes occur in breast tissues that overexpress ARO.

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