Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Treatment effects of RU 23908 antiandrogen (Anandron) and estrogen in low doses on hormone-dependent rat prostatic adenocarcinoma (R3327-H) were investigated. Tumor-bearing Copenhagen rats were treated for 6 weeks with 8 micrograms Anandron and 1 microgram estradiol-17 beta every two days. Reduction and counteraction of androgen synthesis and action was established by an observed decline in serum testosterone level and by changes in both histology and weight of androgen target organs. Prostate tumor growth rate was significantly retarded in rats treated with Anandron/Estradiol combination compared to untreated intact control and was equal to the slow growth rate in castrate tumor-bearing animals. Tumor histology changes during treatment correlated with the observed growth rate retardation. Areas of necrosis, metaplasia, and acellularity were more frequently observed in tumors of Anandron/Estradiol-treated compared to castrated rats. These results suggest that low doses of Anandron and estrogen can effectively be combined as a complete androgen counteracting therapy for hormone-dependent prostatic carcinoma with minimal undesired side effects.
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PMID:Efficacy and advantages in the use of low doses of Anandron and estrogen combination in the treatment of prostate cancer. 342 36

The development of learned aversions to the available diet has been shown to contribute to the anorexia and weight loss which accompany the growth of certain tumors, including the Leydig LTW(m) tumor. Estradiol infusions were found to closely mimic the effects on food intake and food preference seen after Leydig LTW(m) tumor implants. That is, reductions in food intake and the development of severe aversions to a target diet available during hormone infusions were seen. Lesions of the area postrema greatly attenuated these effects of estradiol infusions. Similar lesions have been shown to have parallel effects on the LTW(m) tumor syndrome. These findings strongly implicate the elevations of circulating estrogens which accompany the growth of LTW(m) tumors in generating the symptoms of anorexia and diet aversions.
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PMID:Estrogens and the Leydig LTW(m) tumor syndrome: anorexia and diet aversions attenuated by area postrema lesions. 346 86

Some hormones (e.g., gonadotropins and clomiphene) act indirectly on the breast by disturbing the hypothalamopituitary axis, while others, including estrogens and progestins, exert at direct effect. Numerous experimental studies have confirmed that estradiol and progesterone act synergistically in the breast, and there are often differential responses of the alveolar and ductal systems. Analysis of fibroadenomas with high epithelial cell density removed from young women at various stages of the menstrual cycle indicated that receptors in both breast and endometrial tissues are under the control of cyclic ovarian function. When breast tumor tissue were exposed to estradiol and progesterone in well-balanced combination, a cell distribution of progesterone receptors similar to that observed during a normal luteal phase was observed. On the other hand, when estradiol is administered in supraphysiological doses to female rats, changes comparable to human fibrocystic disease are noted. The anti-estrogenic mechanisms of action of progesterone and progestins in women includes a reduction of estrogen secretion in systemic circulation, inactivation of estradiol by metabolism at the target tissue, and a lowering of estrogen receptors in these tissues. The main enzyme involved in the anti-estrogenic activity is the progesterone-dependent 17 beta-hydroxysteroid dehydrogenase. In terms of benign breast disease, a context of unopposed estrogen is most likely. Since benign breast disease can be a precursor of breast cancer, caution should be exerted in prescribing mini-pills to young women. Estradiol levels in mini-pill users can remain between 50-120 pg/ml given the persistence of some gonadotrophic activity and the consequent partial follicular maturation of the ovary.
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PMID:Effects on the breast of drugs used in fertility regulation. 347 70

Estradiol and progesterone receptor concentrations have been measured and their hormonal regulation extensively studied in normal human endometrium. However, in endometrial cancer, the biochemical assays presently used face the complex problem of tumor and tissue heterogeneity. This problem may be circumvented by immunocytochemistry on tissue sections proven to be histologically malignant. The in vivo experimental model developed in our laboratory is an ideal source of tissue necessary for purification of the progesterone receptor and antibody production. Hopefully, the physiology of the receptor may be studied under ideal conditions in this experimental system.
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PMID:Sex steroid receptors in normal and malignant endometrium. 352 89

In this study, the anti-tumor effect of E2 carrier drug on MM2 cells transplanted to C3H/He mice and its mechanism were observed. The results were as follows. The estrogen receptor on cytosol in MM2 cell and nuclei were positively confirmed, but the progesterone receptor was not. When the effect of this drug on MM2 cells was measured by the ratio of inhibition to the growth of the tumor, the effect on the group treated with a high dose of E2 carrier drug (100mg/kg) was found to be significantly higher than found with physiological saline (p less than 0.05). The main route of action is considered to be not related to the steroid receptor but to the retention of Estramustine (EM-2), Estromustine (EM-1), and Estradiol (E2) in tumor tissues. Histomorphological findings on the MM2 cells treated with E2 carrier drug revealed nuclear pyknosis and giant cell transformation. The strength of these effects seemed to depend on the size of the dose of E2 carrier drug.
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PMID:[Studies on the anti-tumor effect of the E2 carrier drug and its mechanism]. 359 76

The growth fraction (GF) of human breast adenocarcinomas was studied in order to determine whether it was influenced by certain biologic characteristics of the host and whether it was modulated by the tumor's steroid hormone receptor status. It was also examined whether steroid treatment in vitro stimulated tumor's GF. Thirty-five primary breast adenocarcinomas from patients ranging in age from 26 to 85 years were analyzed for size and estrogen receptor (E2R) and progesterone receptor (PR) status. One portion of each tumor was cultured in medium 199 under four different conditions: addition of insulin alone or with 17 beta-estradiol (E), progesterone (P), or a combination of both hormones (E + P). In six cases, a dose-response curve was established for E (10(-14) to 10(-12) mol/L) and P (10(-11) to 10(-9) mol/L). Tissues were exposed to a continuous pulse of 2.5 microCi/mL (3H)-thymidine for five days before fixation and processing for autoradiography. GF ranged from 0.0074 to 0.3852, median 0.0550, and it was arbitrarily classified as low GF, less than 0.0550; or high GF, equal or greater than 0.0550. GF was significantly higher in patients with lymph nodes free of metastatic tumor than in those with positive lymph nodes. Estradiol treatment at low doses increased GF in 40% of tumors, whereas high doses increased GF in 14%. Progesterone treatment increased GF in 30% of tumors treated with low doses and in 14% of those treated with high doses. Treatment with E + P markedly depressed the GF of 85% of the tumors. It was concluded that the GF of breast carcinomas showed a great variability, which seemed to be independent of host factors such as age, menopausal status, parity history, or smoking habits; a second conclusion was that breast tumors' GF was not stimulated by steroid hormone treatment in vitro, and its response did not correlate with their hormone receptor status.
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PMID:Influence of steroid hormones on the growth fraction of human breast carcinomas. 361 47

Bone metastases of breast cancers produce not only osteolytic but also osteosclerotic lesions. The latter are often observed after androgenic treatment of the tumor. Potential production of osteoblast stimulating activity (ObSA) in breast cancer cell lines, and possible androgen control of this activity have been investigated. Conditioned media (CM) collected from 4 breast cancer cell lines (MCF-7, ZR75, MDA-MB 231, BT20) was tested in vitro on ROS 17/2,8 osteoblast-like cells and on osteoblasts derived from human bone biopsies. The parameters monitored in osteoblasts were [3H]thymidine incorporation, alkaline phosphatase activity, and osteocalcin secretion. Serum-free media conditioned during 24 h by MCF-7 cells presented the highest ObSA. CM decreased thymidine incorporation in DNA and increased alkaline phosphatase activity in a dose-dependent manner. Bone GLA protein (osteocalcin) secretion by human osteoblasts was not increased however in the presence of CM. MCF-7 cells were cultured in the presence of dihydrotestosterone (DHT) [1-100 nM] for 5 days. Serum-free, DHT-free CM collected after an additional 24 h, contained alkaline-phosphatase stimulating activity which was DHT dose-dependent. Estradiol and 1,25(OH)2D3 failed to elicit a comparable increase of the ObSA in the CM. In conclusion, MCF-7 cells product factor(s) that interfere with bone remodeling. The DHT modulation of ObSA parallels the estradiol control of MCF-7 cells osteolytic lesions in relation with Prostaglandin E secretion. Sex hormones at physiological and pharmacological levels might thus control both osteosclerotic and osteolytic lesions observed in bone deposits of hormone dependent cancers.
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PMID:Androgens increase osteoblast-stimulating activity of human breast cancer cells in vitro. 370 24

Estradiol and progestin receptors were studied in 20 patients with neuraxial Schwann cell tumors, and their presence was correlated to the clinicopathologic features and the amount of preoperative corticosteroid therapy. Based on an arbitrary cutoff value of 200 fmol per gram of tumor as indicative of a positive receptor value in breast cancer, 4 and 13 of the neurilemmoma tissue samples could be considered as positive for estrogen and progesterone receptors, respectively. Whereas there was no convincing correlation between the estrogen and progestin receptor activity and the age, sex, or menopausal status of the patients, overweight patients had significantly higher estrogen and progestin binding values. The correlation between the amount of preoperative prednisone therapy and the amount of [3H]estradiol and [3H]promegestone binding revealed no dose relationship. Correlating [3H]estradiol and [3H]promegestone content with the histologic type of the schwannomas (Antoni types A and B, respectively), we were not able to draw conclusions, because of the predominance of Antoni type A over Antoni type B tissues in our material. The necessity of nuclear receptor assays, ligand specificity testing, and in vitro studies is stressed as a prerequisite for answering the questions whether neurilemmomas contain genuine sexual steroid hormone receptors and whether these receptors are regulated via an estrogen-estrogen-receptor system as is the case in classical sexual steroid hormone target tissues.
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PMID:Estrogen and progestin receptors in acoustic and spinal neurilemmomas. Clinicopathologic correlations. 372 40

The human breast cancer cell line MCF-7 can be growth stimulated by estradiol (10(-8) M) when grown in the presence of high concentration of newborn calf serum (NCS, 10%) or high concentration of estrogen depleted fetal calf serum (FCS, 10%). Estradiol stimulated cultures grow with an increased growth rate and also the final cell number in the culture flasks is increased. Analysis of the cell cycle parameters revealed that the proportion of cells in the G1 phase is decreased and the proportion of S phase cells is increased. In comparison, the increase in growth fraction is less significant. These results show that estradiol stimulated cultures grow with a shorter cell cycle time and a shortening of the G1 transit time may explain the observed changes in cell cycle parameters. We assume that the shorter cell cycle time as well as the ability to grow without density inhibition may be prerequisites for tumor formation. MCF-7 cells can be growth inhibited by the antiestrogen tamoxifen (10(-6) M). The growth inhibition is estrogen reversible, but estradiol has no growth stimulatory effect under the described growth conditions (0.5% FCS). Growth inhibited cultures accumulate cells with a G1 amount of DNA and the majority of this accumulation is due to non cycling cells. Tamoxifen is not a cell cycle phase specific growth inhibitory agent since cells with a G2 amount of DNA are non cycling. Long term treatment with tamoxifen results in cell death, but a few colonies of cells survive more than 10 days' treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cell cycle analysis of estrogen stimulation and antiestrogen inhibition of growth of the human breast cancer cell line MCF-7. 374 66

Estradiol and progesterone receptors were studied in 14 patients with meningiomas. Estrogen receptors were detected by specific monoclonal antibodies, whereas progesterone receptors were assayed by the dextran-coated charcoal method. In 9 cases the estrogen receptors were also investigated in cultured tumor cells. Positive estrogen and progesterone receptors were found in 86% of patients. The results have been compared with 11 published series of sex steroid assays in meningiomas. The different rate of positive results in most series can be explained by preoperative glucocorticoid therapy. There is no correlation between the estrogen and progesterone receptor activity, the sex and age of the patients, and the location and histological features of the meningioma. The authors suggest that assays of antiestrogen and antiprogestin drugs in cultured cells can indicate whether this estrogen and progesterone receptor activity may be of therapeutic use.
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PMID:Estrogen and progesterone receptors in meningiomas. 376 48


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