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

The "ovarian-dependent" rat mammary tumors, induced by 9,10 dimethyl-1,2-benzanthracene, were assayed for their estrogen receptor content by dextran-coated charcoal adsorption and sucrose gradient ultra-centrifugation. The estradiol receptors bound estrogens with a high affinity (KD approximately 0.25 nM), limited capacity and high specificity, and sediment at 8 S in a sucrose gradient. The cytosol receptors were transferred to the nucleus after binding to estrogens either in vivo or in vitro. The tumor area regressed by 70% during the first 10 days of castration while the concentration of estradiol cytosol receptors decreased from 225 to 16 fmoles/mg of protein. Three to five days after in vivo administration of estradiol (2 mug daily) or prolactin (1 mg daily) the concentration of estrogen receptors was increased in spayed rats. In biopsy experiments, prolactin, but not estradiol, was shown to increase the estrogen receptor concentration when endogenous prolactin release was blocked by CB 154. Prolactin did not modify the intracellular distribution of the estrogen receptor or its binding affinity for estrogen. The uterine estrogen receptor sites were not modified by prolactin under the same conditions. We, therefore, suggest that in mammary tumors prolactin sensitizes the action of estrogens at the target level by increasing the concentration of their available receptor sites.
 ...
PMID:Regulation of estrogen receptors in ovarian-dependent rat mammary tumors. I. Effects of castration and prolactin. 17 71

A clonal cell strain F4C1 has been established from the transplantable rat pituitary tumor MtT/F4 and has been maintained in continuous culture for two years. The cells grow with a population doubling time of 48 hours; the karyotype with a modal number of 39 chromosomes includes a pair of large metacentric marker chromosomes. F4C1 cells in culture produce growth hormone and prolactin but not adrenocorticotropin in contrast to the MtT/F4 tumor which secretes all three hormones in the host rat. The cloned cells lack specific receptors for thyrotropin-releasing hormone and do not respond to this agent with increased prolactin or decreased growth hormone production. Treatment with hydrocortisone results in a small increase in growth hormone and a small decrease in prolactin production. Tumors generated in rats from injected F4C1 cells secrete prolactin and growth hormone but not adrenocorticotropin. The results suggest that growth hormone and prolactin are produced by a single cell type in the MtT/F4 tumor.
 ...
PMID:Establishment in culture of a multihormone-secreting cell strain derived from the MtT/F4 rat pituitary tumor. 17 73

The affinity for antiserum to the multipotent lipotropic hormone (beta-LPH) was tested by immunohistochemical staining of all known cell types in normal and certain abnormal mouse, rat, and human pituitaries. Results indicate that beta-LPH has ACTH, MSH, LH and StH(GH) immunologically cross-reacting determinants. Affinities of anti-LPH for TtH and MtH (prolactin) were not detected in normal pituitaries, but thyrotropic tumor cells reacted with anti-LPH. Absorption experiments confirm that the single polypeptide hormone of the pituitary, beta-LPH, is coded for ACTH and MSH activities. The multi-functional hormone, LPH probably is secreted by the adrenotropes. In addition to ACTH and MSH, it probably contains other antigenic and biologic determinants. Some of these may accentuate its lipotropic activities; others may be incidental. These are points calling for further correlated structural, biologic, and immunologic investigations.
 ...
PMID:Multipotent lipotropic hormones. In search of a pituitary cell producing multipotent LPH. 17 14

The role of the adrenal glands in the development of fatty liver was investigated in rats bearing a transplantable pituitary mammotropic tumor which produces large quantities of ACTH and prolactin. The biochemical and histochemical and histochemical evidence obtained has demonstrated that the adrenal glands, particularly glucocorticoids, are essential for lipid accumulation in the liver of rats with tumor.
 ...
PMID:The role of the adrenal gland in the lipid accumulation process in the liver of rats bearing an acth and prolactin producing tumor. 17 3

Since metastasizing breast cancer is hormone-related, hormonal therapy is based on control of tumor growth by elimination of the hormonal influence, hormone ablatives, or administration of steroid hormones to change the hormonal milieu of thehost organism. The time span during which hormonal therapy may be effective is extremely limited; therefore, this is not recommended for patients with an interval of less than 2 years between primary treatment and 1st manifestation of metastasis, patients with visceral metastasis, or women less than 5 years in the postmenopause. According to cooperative European and American studies remission rates for different types of endocrine therapy include: ovariectomy, 25-40%; adrenalectomy, 30-40%; hypophysectomy, 30-40%; androgen, 20%; and estrogens, 20-35%. Studies are underway concerning the use of antiestrogens (Nafoxidine and Tamoxifen) andinhibition of prolactin secretion. Investigations have shown that patients with proven estrogen receptors in the tumor tissue are particularly responsive to hormonal therapy. For patients with no determinable estrogen receptors, however, chemotherapy is perferable. Ovariectomy is recommended as the 1st measure for women in the premenopause, hormone additives for women longer than 5 years in the postmenopause, and for women in the 1st years after menopause ovariectomy in combination with a form of polychemotherapy. For patients with short free intervals polychemotherapy with another endocrine measure, for pleuracarcinosis and liver metastosis high corticosteroid dosages, and for metastases in the central nervous system radiatio treatment with high corticosteroid dosages are recommended.
 ...
PMID:[Hormone therapy of breast cancer]. 18 Mar 75

Experiments in vitro on tissue from a feminizing adrenocortical carcinoma removed from a postmenopausal patient are described. Portions of the adrenal tumor were cultured. The effects of ACTH, prolactin, and other protein hormones on the synthesis and secretion of steroid hormones by the cultured tissue were studied. Steroids were extracted from the culture medium with ethyl acetate. Steroid production was determined by high resolution-mass fragmentography and by radioimmunoassay. Results suggest that in vitro neither growth hormone (GH) nor luteinizing hormone (LH), at the concentrations used, effectively stimulated the synthesis and secretion of estradiol-17beta by the adrenal tumor tissue. However, ACTH and prolactin with insulin, appearing to influence the action of both these hormones, stimulated the output of estradiol-17beta. Steroid was being synthesized during the 3-day culture period. The tumor tissue actively synthesized and secreted into the medium estrone as well as estradiol-17beta under the influence of ACTH and prolactin with insulin. Data also suggest that LH and GH were capable of influencing the synthesis and secretion of androstenedione by the tissue explants. No DNA sulphate was present in the media from the tumor tissue cultures before or after incubation with either ACTH or prolactin. Results from studies with normal adrenal tissue in culture indicated that DNA sulphate, DHA, and androstenedione were present in the culture medium after 3 days' incubation. In this report the concentration of endogenous estrone relative to estradiol-17beta and estradiol was found to be high. The effect of protein hormones, other than ACTH, on adenylate cyclase activity of this tumor tissue indicated a lack of specificity of the membrane receptor sites. High resolution-mass fragmentography had greater specificity than radioimmunoassay.
 ...
PMID:In vitro synthesis of steroids by a feminising adrenocortical carcinoma: effect of prolactin and other protein hormones. 18 Jul 40

The role of growth hormone (GH), prolactin (PRL), and adrenocorticotropic hormone (ACTH) in the induction of the PRL receptor was investigated in hypophysectomized male rat livers and in the livers of male rats bearing a GH secreting tumor. After 7 days of sc injections, specific binding of PRL in controls and rats treated with PRL, GH, ACTH, human chorionic gonadotropin, estradiol, or testosterone was approximately 1%. Treatment with PRL plus ACTH increased specific binding to 4%; adding estradiol to this combination produced a further increase to 8%, whereas the addition of testosterone decreased hepatic binding to 1%. Combination of GH with ACTH was most effective giving a specific binding of 33%, which is similar to the 36% observed in the liver of rats bearing a GH-secreting tumor. These results suggest that GH acts synergistically with PRL and/or ACTH to increase lactogenic binding sites in the male rat liver and that sex steroids have a modulating effect on this action.
 ...
PMID:Induction of lactogenic receptors. II. Studies on the liver of hypophysectomized male rats and on rats bearing a growth hormone secreting tumor. 18 48

A 45-year-old women had medullary tyroid carcinoma associated with Cushing's syndrome and galactorrhoea. Elevated plasma immunoreactive ACTH and cortisol were partially suppressed by intravenous dexamethasone, appreciably raised by lysine vasopressin, and urinary excretion of 17-oxogenic steroids slightly elevated by metyrapone. A large arterio-venous increase in plasma corticotrophin releasing factor-like activity across the thyroid gland was observed and tumour tissue contained corticotrophin releasing factor-like activity. Biologically active ACTH was not detected in tumour extracts before incubation with trypsin, but after trypsinization a value of 3.2 mU per gram was obtained. Arterial plasma contained biologically active ACTH (1.5 mU/100 ml) prior to trypsinization. Venous effluent from the thyroid gland contained biologically active (9.6 mU/100 ml) and immunoreactive ACTH (970 pg/ml) before trypsinization. Tumour extracts also contained prolactin production-stimulating activity. These findings can explain the Cushing's syndrome and the galactorrhoea both of which disappeared completely after thyroidectomy.
 ...
PMID:Medullary thyroid carcinoma: ectopic production of peptides with ACTH-like, corticotrophin releasing factor-like and prolactin production-stimulating activities. 18 33

Prolactin reverses the inhibitory effects of pharmacological doses of androgen on 7,12-dimethylbenz(a)anthracene-induced mammary tumor growth (Quadri, S.K., Kledzik, G.S., and Meites, J.J. Natl. Cancer Inst., 52: 875-878,1974). To determine whether this effect is due to an alteration in the ability of the tumor cell to bind prolactin, we have quantitated prolactin receptors in androgen-responsive and nonresponsive tumors. Prolactin receptors were measured with 125I-labeled ovine prolactin in a subcellular fraction which reproducibly contained 60 to 80% of the total receptor present in tumor homogenates. Prolactin binding was reversible, reached a steady state in 9 hr, and was completed by excess unlabeled prolactin. Prolactin bound to its receptor with a Kd of approximately 1 X 10(-10) M. Growing tumors were biopsied, and rats bearing regrown tumors were given injections of 4 mg testosterone propionate twice a week. Prolactin receptors were reduced in most of the tumors, which regressed after testosterone treatment by an average of 63% compared to the pretreatment biopsy specimens. Nonresponsive tumors and vehicle-injected controls showed no signifcant alterations in receptor content. This reduction of prolactin receptors is probably insufficient to account for androgen-induced mammary tumor regression.
 ...
PMID:Prolactin receptors and androgen-induced regression of 7,12-dimethylbenz(a)anthracene-induced mammary carcinoma. 18 48

Regulation of the lactogen specific binding sites of rat liver was studied in several different high lactogen states. The specific binding of [125I]iodo-hGH was determined as a measure of these sites. Hypophysectomy of pregnant rats produced a much smaller decrease in hepatic binding of [125I]iodo-hGH than was seen in nonpregnant females. Three different prolactin secreting tumors (MtT/F4, MtT/F45, MtT/W5) produced greatly elevated levels of both rPRL and hepatic binding of [125I]iodo-hGH in both male and female rats. The increased binding reflected an increase in the concentration of lactogen specific membrane binding sites. There was no change in the apparent affinity of binding. Hypophysectomy of tumor-bearing rats was not followed by a decrease in the concentration of hepatic sites. Pituitary transplants beneath the kidney capsules of hypophysectomized (hypox) rats produced elevated rPRL levels and increased [125I]iod-GH specific binding to hepatic membranes. The elevation of serum rPRL preceded the increase in hepatic binding. There was a direct correlation between rPRL levels attained by 8 days after implantation and the level of hepatic binding. Estrogen treatment did not alter this correlation. Hormonal replacement with prolactin in combination with various hormones failed to induce the lactogen specific hepatic sites in estrogen treated hypox males, and did not prevent the marked decrease in hepatic binding observed in females following hypophysectomy. It is suggested that chronic elevation of prolactin plays a role in inducing lactogen specific binding sites in rat liver. Estrogen's inductive action seems to be largely effected at the pituitary level.
 ...
PMID:Regulation of lactogen specific binding sites in rat liver: studies on the role of lactogens and estrogen. 18 50


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>