Tumors derived from a hormonal target organ are assumed to be stimulated by the same hormone that stimulates the normal target tissue. In spite of attempts to acquire direct indications of a correlation between hormones and cancer, none have been definitive because studies of total and free hormone levels have given contradictory results. For this reason, attention has shifted to the study of plasma binding and transport of hormones, that is, of the proteins responsible for modulation of the hormone effect and thus of hormone bioavailability. The data reviewed indicate that in-depth study of the transport and binding system of sex steroids would give new information about the endocrine characteristics of cancer patients.
The data relating to plasma steroid binding and transport (usually measured with dehydrotestosterone) are controversial. The plasma E2 binding of 79 breast carcinoma patients, 19 premenopausal and 60 postmenopausal, were compared to 46 controls, 21 premenopausal and 25 postmenopausal. In this study the authors removed the endogenous steroids with charcoal, incubated the plasma with 17-8-E2 in non-saturation conditions, and used ammonium sulfate to precipitate the complex. The authors chose 17-8-E2 as ligand because the plasma steroid binding system has not been shown to be homogeneous and because this binding function may vary independently for the different steroids. In these patients, the E2 binding was significantly (P < 0.01) increased (85 2 11 pg/ml and 73 + 13 pg/ml in premenopausal and postmenopausal) compared to the normal controls (59 f 7 pg/ml and 58 f 5 pg/ml in premenopausal and postmenopausal women. It is still unclear whether this is a primary increase of the binding capacity or a reaction of the host for sequestering excess circulating E2. However, the small percentage of false-positives and false-negatives suggests that E2 binding could be used as a tumor marker in breast carcinoma. Cancer 63:305-308, 1989. T IS THEORETICALLY POSSIBLE that a tumor Of a hor-I mone-dependent organ reacts to the same hormonal stimulus as the normal tissue, and some clinical data seem compatible with the hypotesis that endocrine factors cause or at least maintain breast carcinoma. However, despite many attempts to correlate endocrine status with the development of a tumor in a hormone-dependent organ, no general agreement has been reached, arid it has even been suggested that in breast carcinoma a relative excess of estrogens not balanced by progesterone caluld be present only in specific periods of life. ' Numerous studies have been performed on the role of estrogens in breast carcinoma. An increase in the total estrogen concentration has been found only by some authors and only under particular conditions such as the menopause.2 Many workers, but not all, agree that the free E2 fraction is increased.2-" For this reason various research programs have been developed in the last years wiith the aim of overcoming the limitations-the wide scattering of values-of hormone measurements based 011 hormone molecular concentrations in biological fluids. One approach has been the attempt to determine the hormone binding capacity (the quantity of labeled hor
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