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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twenty-one renal cell carcinomas were analyzed for the presence of androgen progestin and estrogen receptors by agar gel electrophoresis and a dextran-coated charcoal assay. An androgen receptor could be demonstrated in 3 tumors, a progestin or estrogen receptor was not detectable. It was therefore concluded that renal cell carcinoma is generally not a hormone-dependent tumor, and a hormonal treatment of metastatic renal cell carcinoma as first-line therapy does not seem to be justified.
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PMID:Determination of androgen, progestin and estrogen receptors with two different assays in renal cell carcinoma. 244 3

Breast cancer was induced in female Holtzman rats by intragastric administration of 7,12-dimethylbenz[a]antracene (DMBA). At tumor maturity, biopsies of viable tissue were obtained, frozen, and then assayed for estrogen, progesterone, and androgen receptor content. By simple linear regression analysis, progesterone receptor levels significantly correlated with both estrogen and androgen receptor levels, whereas estrogen and androgen receptor levels did not correlate with each other. Multiple regression analyses further substantiated the predictive value of the progesterone receptor for the other two hormone receptors. Knowledge of breast tumor androgen receptor levels may further enhance the value of the estrogen receptor and progesterone receptor in hormonal responsiveness. Further, the progesterone receptor may be the most sensitive of the steroid hormone receptors for selecting patients likely to respond to hormonal therapy.
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PMID:Correlation of estrogen, progesterone, and androgen receptors in breast cancer. 249 6

Constant release of the androgen 5 alpha-dihydrotestosterone (DHT) in ovariectomized rats bearing DMBA-induced mammary carcinoma caused a marked inhibition of tumor growth induced by 17 beta-estradiol (E2). That DHT acts through interaction with the androgen receptor is supported by the finding that simultaneous treatment with the antiandrogen Flutamide completely prevents DHT action. Particularly illustrative of the potent inhibitory effect of DHT on tumor growth are the decrease by DHT of the number of progressing tumors from 69.2% to 29.2% in E2-treated animals and the increase by DHT of the number of complete responses (disappearance of palpable tumors) from 11.5% to 33.3% in the same groups of animals. The number of new tumors appearing during the 28-day observation period in E2-treated animals decreased from 1.5 +/- 0.3 to 0.7 +/- 0.2 per rat during treatment with DHT, an effect which was also reversed by the antiandrogen Flutamide. The present data demonstrate, for the first time, that androgens are potent inhibitors of DMBA-induced mammary carcinoma growth by an action independent of inhibition of gonadotropin secretion, and suggest an action exerted directly at the tumor level.
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PMID:Inhibitory effect of androgens on DMBA-induced mammary carcinoma in the rat. 251 15

Paraffin-embedded materials from 104 patients with breast cancer were assayed for the expression of estrogen receptor (ER), progesterone receptor (PR) and androgen receptor (AR) with avidin-biotin complex method. A significant positive correlation was found between SR status and cell differentiation or lymph node status. Tumors with elastosis tend to contain ER, PR and AR more frequently. Patients with positive ER, PR or AR tumors were 1.2 to 2.6 times more likely to survive than those with negative ones. The five-year survival rate increased with the increase of number and amount of positive SR. These results indicate that ER, PR and AR detected by ABC method may be used as biomarkers for tumor differentiation and have prognostic values in breast cancer.
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PMID:[Correlation of steroid hormone receptors (SR) with clinical and pathological features of human breast cancer]. 256 32

Cytosol androgen receptor content of transitional cell bladder cancer tissue was found to be substantially higher than its content in normal bladder mucosa and lower than in control benign prostatic hypertrophy tissue. Tumors arising in female patients had a lower androgen receptor content than those arising in male patients. High-grade tumors had a lower androgen receptor content than low-grade tumors.
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PMID:Androgen receptors in bladder tumors. 257 95

Molybdate-stabilized androgen receptors have been quantitated in cytosols derived from 1026 malignant breast tumors including all new cases of primary breast cancer reported in the western region of Norway during the 3-year period 1985-1987. A simple single point saturation assay using the synthetic labeled ligand methyltrienolone was evaluated for this purpose. This approach also allowed the simultaneous determination of estrogen and progesterone receptor from the same cytosol preparation. The cytosol content of albumin was also recorded in order to control for dilution by extracellular proteins. Androgen receptor was the sex hormone receptor most frequently found both in primary and secondary breast cancer. In primary tumors 84.9% (723 of 852) showed a cytosol concentration higher than 10 fmol/mg protein compared to 71.2 and 67.1% for estrogen and progesterone receptors, respectively. This incidence is about 2 times higher than previously reported for androgen receptors in the literature and may be due to the stabilizing effects of molybdate and a serine protease inhibitor on the recovery of active binding sites in cytosol. Cytosol concentration of androgen receptor is generally lower than that of the other sex hormone receptors; the average level was 65.5 fmol/mg cytosol protein compared to 86.8 and 84.7 for estrogen and progesterone receptors, respectively. Both incidence and cytosol concentrations were lower for all sex hormone receptors in soft tissue metastasis than in the primary tumor. This decrease is not likely to be due to differences in tumor cellularity since metastatic tumors appear to be more cellular as judged from a lower cytosol content of extracellular proteins (albumin). No significant differences were observed in any parameter investigated between different metastatic sites (skin, lymph nodes). Androgen receptor levels were strongly correlated to estrogen and progesterone receptor concentration in both primary and secondary cancers. Cytosol androgen receptor concentration increases with age. This increase is more significant in metastatic than in primary tumors. Evidently, tumor cellularity is a confounding factor in primary tumors since tumor cytosols from younger patients showed a higher content of extracellular proteins. Receptor levels in lymph node metastasis did not exhibit age dependence. This may suggest that locally produced factors rather than circulating levels of sex steroids modulate tumor receptor expression. In metastatic tissues androgen receptors are present with twice the frequency of progesterone receptors and one in four of these tumors express androgen receptor as their sole sex hormone receptor. This supports the view that some of the beneficial effects of high dose progestin treatment of advanced breast cancer are mediated through the androgen receptor.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Improved measurement of androgen receptors in human breast cancer. 258 56

Human prostate tumor cells, LNCaP, contain androgen receptors and respond to androgens with increased growth rate. Although other steroid hormone receptors are not detectable in LNCaP cells, progesterone and estradiol stimulate the growth of these cells. The androgen receptor shows considerable cross binding activity with progesterone and estradiol but not with the glucocorticoid triamcinolone acetonide. The latter steroid does not have any effect on cell proliferation. LNCaP cells respond to epidermal growth factor (EGF) with an increased growth rate. Steroids that stimulate LNCaP cell proliferation also increase the number of EGF receptors per cell. In conclusion, LNCaP cells are sensitive to EGF. Different steroids bind to the androgen receptor and stimulate the proliferation of human prostate tumor cells. This stimulation of growth is preceded by an increase in EGF receptor number per cell.
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PMID:Androgen receptor-mediated growth and epidermal growth factor receptor induction in the human prostate cell line LNCaP. 272 28

In order to investigate the role of estrogen receptors (ER) in the growth of human esophageal carcinoma, tumor tissues of ER-positive but androgen receptor (AR)-negative line of squamous cell carcinoma (ES-8) were transplanted in ten male and ten female nude mice. As control, those of a tumor line without both receptors (ES-13) derived from human esophageal cancer were used. The growth rates of transplanted tumors were estimated up to 5 weeks. The tumor growth of ES-8 line was significantly greater in males than it was in females. Such a difference was not observed for ES-13 line. Moreover, in order to investigate the effect of estrogen on the ER, tumor tissues of ES-8 line were transplanted in six oophorectomized female mice, and next, estradiol (E2) (500 micrograms/kg, 50 micrograms/kg, or none) was administered to five transplanted female mice of each group, respectively. The growth rates of tumors were enhanced in oophorectomized female mice, and significantly suppressed with the physiologic dose (50 micrograms/kg) of E2 compared to the control. The current results seem to indicate that the inhibitory effect of estrogen on the tumor line is mediated by ER.
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PMID:Role of estrogen receptors in the growth of human esophageal carcinoma. 273 Nov 25

The effects of 3-methylcholanthrene and phenobarbital treatment on the adult rat hepatic cytosolic glucocorticoid (GRc) receptor were investigated. Analyses of sucrose gradient profiles and equilibrium binding data of [3H]dexamethasone bound to the GRc revealed that administration of 3-methylcholanthrene (20-40 mg/kg daily i.p. for 2 days) to adult female Fischer F344 rats led to a significant decrease in the maximal binding capacity of the 5-7S GRc [Bmax = 209 +/- 3 (SE) fmol/mg of protein] compared to the vehicle-treated controls (Bmax = 277 +/- 13 fmol/mg) but had no significant influence on the affinity of the GRc (Kd = 0.9 +/- 0.1 nM). This response was not dependent upon the sex or rat strain (female F344 versus Sprague-Dawley). Phenobarbital treatment (80 mg/kg daily i.p. for 4 days) decreased Bmax and Kd values compared to the vehicle treated controls (P less than 0.05). 3-Methylcholanthrene treatment did not significantly alter the equilibrium parameters of [3H]methyltrienolone bound to the hepatic androgen receptor indicating that the effect was specific to the hepatic GRc. Our data suggest that carcinogens and tumor promoters cause a functional decrease of the cytosolic glucocorticoid receptor in vivo.
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PMID:Characterization of 3-methylcholanthrene effects on the rat glucocorticoid receptor in vivo. 273 Nov 75

Serum melatonin was determined over 24 hours in 35 patients with breast cancer with either a fresh primary tumor (n = 23) or a secondary tumor (n = 12) and in 28 patients with untreated benign breast disease (controls) having a fibroadenoma (n = 10), fibrocystic mastopathy (n = 14), or other breast diseases (n = 4). Circadian rhythms existed in all groups with acrophases at 2 a.m. A 50% depression of peak and amplitude occurred in the group of patients with primary breast cancer compared with age-matched controls (P less than 0.001, P less than 0.01). The peak declined with increasing tumor size: 27% at Stage T1, 53% at T2 (P less than 0.001), and 73% at T3 (P less than 0.05). In contrast, patients with secondary breast cancer, particularly those receiving antiestrogen therapy, had a melatonin peak similar to controls. These results demonstrated a transient depression of pineal melatonin secretion in primary breast cancer and indicated a dynamic role of the pineal gland in malignancy. To investigate some endocrine effects of a depressed melatonin peak, the 24-hour rhythms of prolactin (PRL) and thyroid stimulating hormone (TSH) were determined in patients with primary breast cancer and compared with patients with secondary breast cancer. The PRL had significant circadian rhythms in both groups; but acrophases occurred at midnight in patients with secondary breast cancer, and there were unusually high concentrations at noon in patients with primary breast cancer. Circadian rhythms were not seen for TSH, but the 24-hour average secretion was depressed by 45% (P less than 0.01) in patients with primary breast cancer. The abnormal concentrations of PRL and TSH in these patients could be due to a depressed melatonin peak normally serving as a central circadian synchronizer and modulator of the secretion of adenohypophysial hormones. Additionally, a positive correlation existed between the nocturnal melatonin peak and progesterone and androgen receptor concentrations in primary tumors indicating a direct involvement of melatonin in the growth control of breast cancer.
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PMID:Stage-dependent depression of melatonin in patients with primary breast cancer. Correlation with prolactin, thyroid stimulating hormone, and steroid receptors. 273 89


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