Hemstreet G P, Wittliff J L, Sarrif A M, Hall M L, McRae L J, Durant J R
Int J Cancer. 1980 Dec 15;26(6):769-75. doi: 10.1002/ijc.2910260610.
Since a number of renal-cell carcinomas regress with hormonal manipulation, we have identified and measured the levels of estrogen, progestin and glucocorticoid receptors in 47 autologous pairs of normal and neoplastic kidney tissues. High-affinity receptors for these hormones were detected in kidney tissues of both sexes by means of a dextran-coated charcoal assay. Glucocorticoid receptors were demonstrated in renal cancer tissues for the first time, and were higher in the tumor (mean 31.3 +/- SEM 5.6) than in the normal tissue (mean 18.5 +/- 3.1 fmol/mg cytosol protein). There was a significant difference in the quantities of progestin receptors (expressed as fmol/mg cytosol protein) in normal (mean 18.4 +/- SEM 3.3) versus neoplastic (mean 10.4 +/- SEM 4.0) kidney specimens (p less than 0.007). There was a significant difference between the binding affinity of the progestin receptor in the male tumors (Kd = 2.2 +/- SEM 0.9 nM, n = 10) and that of the females, (Kd = 9.3 +/- SEM 6.5 nM) (p less than 0.04). When an affinity of less than 9.9 X 10(-9) M and greater than 10 fmol/mg cytosol protein were used as criteria for classifying a tissue as positive for progestin receptors, only 17% of tumors contained these receptors while 45% of normal tissues exhibited them. According to these criteria, no differences were observed in the frequency of occurrence of either estrogen receptors or glucocorticoid receptors in tumor versus normal kidney. Data from this study suggest that the use of endocrine therapy should be re-examined in the treatment of renal-cell carcinoma.