ABSTRACT
This chapter focuses on endogenous and exogenous sources of steroid hormones and their role in carcinogenesis of hormone-responsive tissue. It reviews multigenic models that are being used to understand the etiology of breast and prostate cancers and that may serve as examples to establish new models for other hormone-dependent cancers. The major carcinogenic consequence of hormonal exposure at the end organ is cellular proliferation. The emergence of a malignant phenotype depends on a series of somatic mutations that occur during cell division, but the specific genes involved in progression are unknown at this time. The primary sex steroid hormones are estrogens and progestins for women and androgens for men. Steroid hormones, including estrogens, androgens, progestins, mineralocorticoids, and glucorticoids, are synthesized in a tightly controlled system involving cytochrome P450 enzymes and dehydrogenases. Roughly 95% of total circulating hormones reach the appropriate cells bound to “carrier” proteins such as sex-hormone binding globulin and albumin.
