The endocrine biology of cancers originating from the ovarian epithelium was examined with respect to three sequential indicators for estrogen action: available estrogen receptor in the cytosol, total extractable estrogen receptor from the nucleus, and endogenous tissue peroxidase--a putative postnuclear marker for estrogen-induced growth in uteri of laboratory animals and in some mammary tumor models. Cancers of human ovarian epithelium were distinguished from other ovarian tumors by a higher incidence of detectable (greater than 50 fmol/g tissue wet wt) estrogen receptor in the cytosol (P less than 0.001). Approximately one-half (14/29) of the ovarian adenocarcinoma specimens had greater than 500 fmol available estrogen receptor/g tissue wet weight in their cytosols when assayed by a 2-hour incubation with 17 beta-[2,4,6,7-3H(N)]estradiol followed by treatment with dextran-coated charcoal. With a single exception, ovarian adenomas and nondiseased specimens of premenopausal and postmenopausal ovaries (n = 24) contained less than 500 fmol available estrogen receptor/g tissue wet weight in their cytosols. With respect to extractable estrogen receptor in the nucleus, 11/14 primary and 3/9 metastatic ovarian adenocarcinomas had greater than 50 fmol/g wet weight, as assayed by exchange at 30 degrees C for 5 hours after adsorption of the extracted receptor to hydroxylapatite. Endogenous peroxidase activity, measured in vitro by guaiacol oxidation, occurred in substantially higher amounts in the primary ovarian adenocarcinomas than in benign tumors and control ovaries and could be demonstrated within ovarian adenocarcinoma cells by electron microscopy.