Search

We have performed 23 estrogen and 24 progesterone receptor assays on tumor specimens from 26 patients with renal cancer, ten of whom subsequently received hormonal therapy for metastatic disease. Only one of these specimens contained measurable estrogen receptor levels, three contained low, but measurable progesterone receptor levels, and the remaining specimens contained no measurable estrogen or progesterone receptors. None of ten patients with metastases showed evidence of an objective response to hormonal therapy. Our data suggest that few, if any, renal cancers have high titers of estrogen or progesterone receptors, and that those patients whose tumors have low receptor titers are unlikely to respond to hormonal therapy. [ABSTRACT FROM AUTHOR]

Management of sudden unrelenting breast growth in a young woman included use of antiestrogen hormone therapy and subcutaneous mastectomy. Later, massive breast growth again occurred during pregnancy, requiring a repeat postpartum subcutaneous mastectomy. The dramatic response to a specific antiestrogen agent and the subsequent massive regrowth of breast tissue after subcutaneous mastectomy suggests that breast tissue is extremely sensitive to circulating hormones in certain patients with macromastia. The unusual nature of this patient's recurrent macromastia warrants this review of reports of similarly affected patients and discussion of general concepts in the medical and surgical management of the disorder.

Estrogen-binding receptors (ER) and thyroid-stimulating hormone (TSH) receptors were observed in the cytosol and in a membrane particulate fraction, respectively, in most neoplastic and nonneoplastic human thyroid tissues. Fourteen of 15 thyroid neoplasms and 6 of 15 nonneoplastic thyroid specimens had estrogen receptors (assuming the sensitivity of our estrogen receptor assay is 0.2 fmole/mg protein), and 14 of 15 thyroid neoplasms and 11 of 15 nonneoplastic thyroid specimens had a high affinity, low capacity TSH receptor. Neoplastic thyroid tissue had more ER (2.35 +/- 0.70/fmole/mg protein) than nonneoplastic thyroid tissue (0.57 +/- 0.181/fmole/mg protein) removed from the same patients (P less than 0.05). The Kd for ER did not differ in nonneoplastic (0.41 +/- 0.090 nM) and neoplastic (0.311 +/- 0.048 nM) thyroid tissue. The number of TSH receptors was comparable in neoplastic (0.609 +/- 0.191 pmole/mg protein) and in nonneoplastic (0.765 +/- 0.181 pmole/mg protein) thyroid tissue removed from the same patients who had the ER studies. The maximal adenylate cyclase response to TSH was greater in the neoplastic (147 +/- 26.9 pmole/mg protein/30 min) than in nonneoplastic thyroid tissue (32.8 +/- 6.69 pmole/mg protein/30 min) (P less than 0.001) suggesting a greater metabolic responsiveness of the neoplastic thyroid tissue to TSH. No correlation was evident, however, between the number of estrogen and TSH receptors in nonneoplastic and neoplastic thyroid tissue (r = 0.226). This study demonstrates that neoplastic human thyroid tissues have both estrogen receptors and TSH receptors. The neoplastic tissue also has a greater AC response to TSH than nonneoplastic thyroid tissue.

Prompted by studies that suggested a causal relationship between sex steroids and human liver cancer, we assayed specimens of hepatoma from five patients and adjacent liver tissue from three of the same patients for estrogen receptors. After finding that the assay material contained specific cytosolic receptor proteins for estradiol, we treated a second group of five patients who had hepatomas with progestin. This therapy resulted in tumor regression in two of these patients.