Effect of RetinylAcetate on the Occurrenceof OvarianHormone responsiveand -nonresponsiveMammaryCancers in the Rat1

tumorigenesis by modifying endocrine status, possibly by in terfering with some aspect of ovarian or pituitary function. The inhibitory nature of either a deprival or an excess of ovarian and/or hypophysial hormone(s) on mammary carcinogenesis is well documented (4). However, it has been reported that retinyl acetate inhibits mammary carcinogenesis to a greater extent in the presence of the inhibitor of prolactin secretion, 2bromo-a-ergocryptine, than can be attributed to the action of either compound alone (15). This implies a mode of action which is at least partially divorced from pituitary effects. This study was initiated to determine whether the ovarian hormones play a role in retinyl acetate inhibition of DMBA-induced mam mary carcinogenesis. Further, the effect of retinyl acetate on the occurrence of both ovarian hormone-responsive and -non responsive tumors was evaluated.