species. may stimulate development of mammary carcinoma in male and/or female animals. In treated rats. this is usually accompanied by higher (males) or lower (females) incidences of benign mammary tumors, as compared with the corresponding controls. The speciesspecific neuroendocrine system. i.e.. estrogen-dependent stimulation of PRL seLretion appears to be of great importance in the pathogenesis of mammary tumors in mice and rats. On the other hand, stimulation of mammary tumors in dogs by certain progestogens or progestogen-estrogen combinations seem to be related to high mammary proliferative activity of these compounds in the dog and their stimulatory effect on highly mammotrophic canine GH. In total contrast to the sittiation in mice and rats. !ong-term treatment of the dog with high doses of estrogens does not stimulate mammary tumor development in spite of their ability to stimulate PRL secretion in this species. Similarly, in the monkey and man certain sex steroids (high doses) may stimulate PRL secretion. However, in the monkey. steroid-related mammary tumors are not observed. even after long-term treatmr’nt wath high doses of estrogens. progestogt ns and their combinations. Moreover, cc Intraceptive use appears to decrease the rjsk OI benign breast tumors in women. and after two decades of extensive use of contraceptive steroids, the evidence weighs against an association of these preparations with human breast cancer. These findings indicate that, with regard to the develop rr,ent of mammary tumors as an undesirable effect of contraceptive steroids. not otlly the species-specific neuroendocrine s! stem (e.g. stimulation of PRL and/or GH secretion) but also the susceptibility of certain species, strains or individuals seems to play a great role. This clearly illustrates the hmitations inherent in the extrapolation to man of data on steroid-related mamman tumors in various experimental animals.