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Biopsy specimens from 21 women with primary operable breast cancer were analyzed in a double blind study designed to compare fluorescent antibody methods for detection of estrogen receptors with estrogen receptors measured biochemically with a previously reported dextran coated charcoal technique (DCC). Fluorescent antibody methoids employed both direct techniques: (1) rabbit antisera to 6-O-Carboxymethyl-Oxime-17 beta Estradiol tagged with Fluorescin Istthiocyanate (FITC) and (2) indirect techniques (sheep antisera to 11-Hemisuccinate-17 beta Estradiol reacted wih FITC tagged rabbit antisheep sera). Fluorescent antibody methods showed 100 percent correlation with each other but only 67 percent correlation with the DCC assay. Fluorescence was striking when present. Molecular forms were not easily predicted. Divergent results occurred largely in specimes sparsely populated with malignant cells (18 percent) though neoplasms showing no fluorescence demonstrated elevated receptor conconcentrations with DCC (15 percent). Indirect fluorescent techniques are the simplest of those studied. Fluorescent techniques have not replaced biochemical techniques in the authors' laboratories.

The cytoplasmic receptors for 17 beta-estradiol (ER), 5 alpha-dihydrotestosterone (AR), progesterone (PR), and cortisol (GR) have been quantified in 36 specimens from the human ovary (13 disease-free, 5 benign, and 18 malignant) by a dextran-coated charcoal (DCC) technique. The occurrence of receptor-positive biopsies were: ER 46%, AR 85%, PR 54%, GR 92%, in normal tissue; ER 40%, AR 100%, PR 20%, GR 50%, in benign tumors; and ER 67%, AR 72%, PR 50%, GR 88%, in malignant lesions. Furthermore, the simultaneous occurrence of ER and PR in malignant tumors was 50% yet all four receptors were found to be present only in 44% of the cases. The findings reported here on the strong correlation existing between ER and PR presence or amount agree with previous observations on normal and neoplastic specimens from human breast and endometrial tissues.

The mechanism of hypogonadism was studied in a 63-year-old man with idiopathic hemochromatosis. Basal levels of thyroid, prolactin, cortisol, and growth hormones were normal and responded normally to appropriate provocative stimuli. Basal testosterone and gonadotropin levels were low. There was inadequate gonadotropin response to luteinizing hormone-releasing hormone and clomiphene citrate stimulation. Testosterone response to human chorionic gonadotropin was normal. Hypothalamic-pituitary dysfunction resulting in impaired gonadotropin secretion appears to be the cause of hypogonadism in hemochromatosis.