Introduction

Abstract

It has long been known that the endocrine status of the host has a critical influence on the induction of cancer by nonhormone chemical compounds and on the emergence of “spontaneous” tumors in a variety of mammalian species including the human. In the absence of the specific hormone the target gland atrophies, whereas if hormone is in excess the target tissue hypertrophies. The growth-promoting, anabolic properties of sex hormones toward their target tissues has been recognized as early as 1849 when Berthold (1) reported the regression of the comb of roosters following castration and restoration of the comb by testicular implants; since then the growth-promoting properties of sex hormones toward their different target organs has been confirmed in many species. The growth-promoting properties, their ability to elicit cell proliferation, largely but not solely underlie the fact that both pituitary and gonadal hormones are capable of enhancing tumor induction in various species. Conversely, some hormones, under different experimental conditions, were found to inhibit tumor induction by chemical agents. Administered alone — without the concurrent effect of a nonhormone chemical carcinogen — certain hormones by themselves can be tumorigenic through the creation of an excess hormonal stimulus; thereby the endocrine balance appropriate for that organism is shifted away from the “normal” steady-state.