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

Since prolactin has several modes of action on prostatic growth and physiology, the effect of the antiprolactin bromocriptine on plasma kinetics and intraprostatic metabolism of testosterone was studied in patients with untreated prostatic cancer; a therapy protocol was deduced which was controlled in 27 patients with advanced inoperable prostatic adenocarcinoma. Bromocriptine resulted in a significant suppression of prolactin and testosterone as well and favored testosterone elimination from the plasma pool. Prostatic androgen uptake was enhanced and the intraprostatic metabolism altered in relation to tumor grade. Adjunctive administration of bromocriptine to 27 patients, mostly in the state of hormone resistance, resulted in an overall objective regression of 22.2% and in stable disease in 55.6% of the patients. In half of the individuals a prompt relief of bone pain from osseous metastases was observed as well as improvement of micturition and decline of phosphatase activity. This preliminary data justify further investigations under controlled and randomized conditions.
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PMID:[Bromocriptine for palliation of advanced prostatic carcinoma. Experimental and clinical profile of a drug (author's' transl)]. 8 47

An immunocytochemical technique was described to test for immunoreactive prolactin (PRL) and growth hormone (GH) in spontaneous and experimentally induced hyperplastic and neoplastic lesions of the prostate and mammary gland. The dog was used as an animal model. The specificity and validity of the immunocytochemical staining procedure and of the antisera to canine PRL and canine GH can be regarded as established for the demonstration of PRL- and GH-dependent staining respectively. In mammary and prostatic tissues, both endogenous PRL and GH as well as intracellular free binding sites (for exogenous PRL and GH) were detected immunocytochemically. The technique presented seems to be an important tool to localize putative target sites for pituitary hormones in hormone-dependent hyperplasia and neoplasia.
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PMID:Immunocytochemical technique for detection of prolactin (PRL) and growth hormone (GH) in hyperplastic and neoplastic lesions of dog prostate and mammary gland. 9 2

By optimal hormonal treatment the production of exogenously transmitted MMTV can be stimulated in vitro to different degrees, depending on cultivation conditions and origin of tumor cells. Moreover, after appropriate hormonal treatment, endogenous MMTV-Y can be rescued from primary cell cultures derived from dimethyl benzanthracene- and hormone-induced C57BL/10 mouse mammary adenocarcinoma, as determined by reverse transcriptase assay, distribution of 3H-uridine-labelled viral particles, immunofluorescence, and electron microscopy. On the contrary, all attempts to rescue MMTV-Y from cultures derived from urethane-induced C57BL/10 tumors failed. These data indicate that upon syncarcinogenic action of non-viral carcinogenes, estrogen and prolactin, the MMTV-Y genome can be expressed in mammary gland parenchymatous cells, which in turn may result in cell transformation. The full MMTV-Y gene expression occur after appropriate hormonal stimulation of the C57BL/10 mammary cancer cells in vitro.
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PMID:Hormone-responsive genes of the mouse mammary tumor virus. 9 6

Endocrine disturbances have been studied in 4 children with neurofibromatosis von Recklinghausen, aged 5.0-10.5 years. Hypothalamic precocious puberty was seen in three boys; growth hormone deficiency was diagnosed in a girl. After TRH stimulation one boy and the girl showed a diminished TSH-response. Another boy showed a relatively high basal level of TSH and an elevated TSH-response to TRH. All children were euthyroid. Two boys had a hyperprolactinemia even under basal conditions; the one with elevated TSH-response showed an excessive response of prolactin as well. In all our patients a suprasellar tumor caused the endocrine disorders described.
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PMID:[Endocrine disorders in children with neurofibromatosis von Recklinghausen (author's transl)]. 10 38

Growth hormone and prolactin were localized on thin plastic sections of rat anterior pituitary gland and mammosomatotropic tumor MtTW15 that were fixed with osmium tetroxide (alone,mixed with aldehydes, or after aldehydes). Intense immunocytochemical staining for both antigens was obtained after plastic was removed from sections with an alcoholic solution of sodium hydroxide. The results indicated that antigenic determinants of rat prolactin and growth hormone were not completely destroyed or inactivated by fixation with osmium and embedment in epoxy resin, and that removal of the polymerized epoxy resin was necessary to obtain light microscopic postembedding immunocytochemical staining of these antigens. The results also demonstrated that tissues which have been conventionally processed for morphological evaluation by electron microscopy may be suitable for postembedding immunocytochemical staining of some antigens for light microscopy.
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PMID:Immunocytochemistry with osmium-fixed tissue. I. Light microscopic localization of growth hormone and prolactin with the unlabeled antibody-enzyme method. 10 97

A gonadoliberin analog, (D-leucyl6, desglycyl-NH2(10), prolyl ethylamide9) gonadoliberin, is known to suppress ovarian function and plasma prolactin levels. Its antitumor activity was evaluated against mammary tumors induced in Sprague-Dawley rats by dimethylbenz(a)anthracene. Observations were made when the analog, referred to as A-43818, was given alone and together with estrogen replacement or perphenazine, A-43818, 10 microgram s.c. twice a day for 6 weeks, was highly effective in producing tumor remissions. All of the 11 animals survived throughout the observation period, complete regressions occurred in 8 of 13 tumors, and 2 were classified as static. None of the 16 tumors in 12 control rats regressed, and there were 4 deaths. When estradiol benzoate, 2 microgram s.c. each day, was administered with the A-43818, antitumor activity was suppressed; only 2 of 17 tumors regressed, 6 were static, and 5 of the 10 rats in this group died. Perphenazine, 1 mg i.m. daily, a dose known to cause hyperprolactinemia, also impaired the efficacy of A-43818. Three of 14 tumors regressed, 6 were static, and the rest continued to grow; 3 of the 12 rats died within 6 weeks of starting treatment.
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PMID:Modification of the effect of a gonadoliberin analog on 7,12-dimethylbenz(a)anthracene-induced rat mammary tumors by hormone replacement. 11 83

The serum levels of follicle stimulating hormone (FSH), luteinizing hormone (LH) and, prolactin (PRL) were measured before and after gonadotrophin releasing hormone (GnRH) and thyrotrophin releasing hormone (TRH) stimulation in 17 patients with endometrial cancer, in 15 patients with uterine fibroids, in 11 patients with ovarian cystadenomas or cancer and in 14 age-matched controls. The women with fibroids had a low FSH level and a diminished FSH response to GnRH but an excessive PRL response to TRH while the other patient groups did not differ from the controls. The results indicate no relation between pituitary function and endometrial or ovarian tumor.
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PMID:Pituitary gonadotrophins and prolactin in patients with endometrial cancer, fibroids or ovarian tumours. 11 72

Prolactin binding activity was studied in suspensions of cells which had been enzymatically dissociated from R3230AC mammary tumors, 7,12-dimethylbenz(a)anthracene (DMBA)-induced mammary tumors and lactating rat mammary glands. Prolactin bound specifically with high affinity (apparent binding affinity = 4.0 X 10(9) M-1) to R3230AC tumor cells. Hormone binding at room temperature was proportional to cell number and increased with time of incubation up to 120-180 min. Prolactin binding to R3230AC tumor cells from diabetic animals was reduced by about 50%. Specific prolactin binding activity was also demonstrated in preparations of cells from DMBA-induced tumors and lactating mammary gland. The levels of hormone binding in both dissociated cells and subcellular particles prepared from these tissues varied as follows: DMBA-induced tumors > lactating mammary gland > R3230AC mammary adenocarcinoma.
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PMID:Prolactin binding to dissociated cells from rat mammary tumors and mammary gland. 12 22

The R3230AC mammary adenocarcinoma was not dependent on insulin; tumor growth was equal to or greater in diabetic rats than in intact animals. However, tumor growth was reduced when daily doses of insulin were administered. Treatment with estrogen inhibited growth of the R3230AC carcinoma, either in diabetic rats or in intact animals simultaneously treated with insulin. The effects of insulin plus estrogen treatment appeared to be additive in causing inhibition of tumor growth. Tumors from diabetic rats showed few metabolic alterations as reflected by little or no changes in the activities of selected glycolytic enzymes, pyruvate kinase, phosphofructokinase, and hexokinase, nor any striking changes in the activities of glucose-6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase, representing the pentose phosphate pathway. A modest reduction in the ratio of utilization of (1-14C)glucose: (6-14C)glucose was seen in vitro by tumors from diabetic rats. It was concluded that insulin, along with estrogen and prolactin, should be considered as a hormonal factor that influences growth of this automonous, hormone-responsive adenocarcinoma.
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PMID:Influence of insulin on estrogen-induced responses in the r3230ac mammary carcinoma. 12 68

We evaluated plasma growth hormone (GH) and plasma prolactin (PRL) levels in ten patients with metastatic carcinoid tumors and the carcinoid syndrome ("active tumors") and seven patients with metastatic carcinoid tumors without the carcinoid syndrome ("inactive tumors"). The patients with active tumors had elevated serum serotonin levels and increased urinary 5-hydroxyindoleacetic acid (5-HIAA) while these values were normal in patients with inactive tumors. Forty-five per cent of patients with active tumors had elevated fasting plasma GH levels that were either not suppressed or showed a paradoxical increase in response to I.V. glucose. There was a positive correlation between the plasma GH levels and serotonin production by the tumor. Twenty-eight per cent of patients with inactive tumors had elevated fasting plasma GH levels. GH levels were decreased by the administration of serotonin antagonists in some but not all of the patients. Parachlorophenylalanine (PCPA) an inhibitor of serotonin synthesis caused a paradoxical rise in GH levels. GH release in response to insulin hypoglycemia was normal. Plasma prolactin levels were normal in most of the patients with metastatic carcinoid tumors. PCPA administration did not systematically alter plasma prolactin levels. We conclude that elevated plasma GH levels are frequently present in patients with the carcinoid syndrome. Both serotonin produced by the tumors and the tumor itself may be responsible for the elevated GH levels.
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PMID:Growth hormone and prolactin secretion in the carcinoid syndrome. 12 43


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