The 2 most important hormones in mammary tumonigene sis in mice and rats are believed to be PRL2 and estrogen (11). Growth of mammary tumors in rats can be maintained at least temporarily by PAL even in the absence of the ovaries and adnenals (15), but estrogen has no growth promoting action on mammary tumors in the absence of the pituitary (18). Whereas low doses of estrogen can be stimu latory to mammary tumor development and growth in the intact rat (5), lange doses of estrogen have an inhibitory effect despite their ability to increase blood PAL levels (5, 11). Recent studies have suggested that high doses of es trogen may interfere directly with the stimulatory action of PAL on mammary tumor tissue (12). Welsch et al. (21) reported that, whereas PAL stimulated DNA synthesis in rat mammary tumor organ cultures, high doses of estrogen inhibited DNA synthesis and also suppressed PAL-induced DNA synthesis. PAL receptors have been shown to be present in carcino gen-induced mammary adenocarcinomas, and a direct rela tionship has been reported between the growth response of these cancers to PAL and the number of PAL receptors in the cancer tissue (7). Since the binding of PAL to its necep ton is believed to initiate PAL-dependent cellular events, it was of interest to determine the effect of large doses of estrogen on PAL-binding activity in mammary tumor tissue.