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

VArious indirect estimates indicate that involuntary infertility has an incidence of 10% in Great Britain. This incidence rises to 30% in parts of Africa where tubal diseases remain unchecked. This paper outlines the endocrine causes of infertility in females and treatment of this disorder. Diagnostic tests include estimation of prolactin, follicle stimulating hormone luteinizing hormone and thyroxine. Serial measurement of estradiol and progesterone are used to assess spontaneous ovarian activity. Withdrawal bleeding after withdrawal of exogenous progesterone also indicates estrogenic status. Pituitar X-rays of anovulating women reveal tumor-mediated infertility. Anovulatory infertility may be the result of ovarian failure; gonadotropin failure (resulting from hyperprolactinemia, normoprolactinemia cases with tumors, or low gonadotropin secretion); polycystic ovary syndrome; and thyroid disease. Inadequate ovulation may result because of defective luteal phase; prolonged follicular phase; or failure of positive feedback mechanisms. Dynamic tests of pituitary-ovarian function include gonadotropin-releasing hormone, clomiphene, and estrogen provocation tests. Tests for inadequate ovulation require a control of measurements of normal women throughout the menstrual cycle to compare hormone concentrations of women affected by ovulation insufficiency rather than relying on preconceived normal values. It is preferable to compare at least the follicular phase of the cycle of infertile women with the same phase of fertilized cycles which resulted in successful pregnancies.
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PMID:Endocrinology of female infertility. 38 67

Alveoli and ducts isolated from virgin rat mammary glands synthesize basement membrane collagen (typeIV) in primary culture. Using purified antibodies to type IV collagen, prominent intracellular and extracellular fluorescence is observed in the epithelium. No fluorescence is observed with antibodies to collagen type I and III. From quantitation of the incorporation of [14c]proline-labeled proteins, 1.5 to 2.5 per cent of the newly synthesized proteins are collagen. Type IV collagen from these cultures was biochemically identified on the basis of (1) the high ratio of labeled 3-hydroxyproline to 4-hydroxyproline (1:10), (2) the gel electrophoretic pattern of the collagenase-sensitive proteins precipitated with 1.7 M NaCl, (3)the failure of the collagen to bind to diethylaminoethyl-cellulose, and(4)the immunologic cross-reactivity with mouse tumor type IV is identical with that of type IV collagen from other sources. When the supportive hormones, insulin, prolactin, hydrocortisone, progesterone, and estradiol are removed from the cultures, there is a 90 per cent reduction in the amount of [3H]proline recovered in collagen synthesis coincides with only a 30 percentdrop in the growht rate and a 20 per cent drop in total protein synthesis of the sells over the 24-hour period without hormones. Pulse-chase experimout hormones. Pulse-chase experiments revealed an enhanced turnover of collagen following hormone withdrawal. This system may be an in vitro model of collagen turnover in mammary gland in involution.
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PMID:Hormonal requirements for basement membrane collagen deposition by cultured rat mammary epithelium. 39 Feb 39

The GH3 rat pituitary tumor cell line which secretes both growth hormone (GH) and prolactin (PRL) stopped releasing PRL when transplanted to animals; furthermore, it suppressed PRL production by the hosts' pituitary glands. When the same tumor was transferred back to cell culture, PRL production resumed. The PRL to GH ratio in cell culture medium and cells ranged from 5 to 1 while in the tumor and serum of the host animals it averaged 0.09 and 0.001, respectively. To investigate further this phenomenon, female rats were transplanted with GH3 tumors (T) and compared to intact normal (N) and to thyroidectomized (Tx) rats. T animals were larger and had splanchnomegaly but smaller pituitaries and thyroids. Serum PRL concentrations in the basal state were decreased, as were levels of triiodothyronine (T3), thyroxine (T4), and free T4 index. Despite reduced serum thyroid hormone concentrations, and in contrast to Tx animals, the serum thyrotropin (TSH) level in T rats was not elevated and they did not show a supranormal TSH response to thyrotropin-releasing hormone (TRH) administration. The PRL response to TRH in T animals was completely abolished while all N and Tx animals responded by a significant increase in serum PRL. Serum corticosteroids and estrogens were normal in T rats. Pituitary content of PRL was decreased and that of TSH increased in T rats. Tx animals, however, had a reduced pituitary content of PRL, TSH, and GH. When GH3 cells were grown in cell culture media containing serum from T animals, there was a reduction of PRL content in cells and released in the medium. Addition of T3 to the T serum did not alter its suppressive effect on PRL nor did rat GH added to N serum alter PRL production and release in vitro. In a preliminary experiment, rats injected ip with 50 mug hGH in two divided doses for eighteen days, suppressed serum T4 and T3 concentrations; pituitary content of TSH was significantly increased and that of PRL slightly decreased. Injection with 250 mug oPRL or saline, on the same schedule and for the same length of time, had no significant effect on the levels of serum thyroid hormones. Thus, GH, but also possibly other substance(s) secreted by GH3 tumors in vivo a) suppress the production of tumor and pituitary PRL; b) suppress the release of TSH, causing mild hypothyroidism; c) inhibit the PRL and TSH responses to TRH; and d) decrease the production of PRL in tissue culture. Although no simple and unifying theory could explain these findings, an hypothesis implicating somatomedin is presented.
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PMID:Induction of hypothyroidism and hypoprolactinemia by growth hormone producing rat pituitary tumors. 40 84

The new antiestrogen RU 16117, at doses of 8 or 24 mcg daily, had been shown to completely prevent the development of rat mammary cancer when given from the day after 7,12-dimethylbenz(a)anthracene (DMBA) administration. This study was undertaken to investigate the effect of this compound on the growth of DMBA-induced tumors which had already developed in Sprague-Dawley rats. The effect was compared with that of castration. Levels of receptors for 17beta-estradiol (E2), progesterone, and prolactin (PRL) were correlated with the response. At about 3 months after DMBA administration animals with palpable tumors were selected. The rats were then treated daily for 4 weeks with .1, .5, 2.5, or 12.5 mcg E2 or with 2, 8, or 24 mcg RU 16117 injected in .1 ml of 1% gelatin in .9% NaCl. Controls were injected with the vehicle alone. For comparison, a group of rats were ovariectomized. After 4 weeks' treatment rats were killed, blood collected, and a cytosol was prepared from tumor tissues. Binding assays and radioimmunoassays were done. 8 and 24 mcg doses of RU 16117 led to 45 and 65% inhibition of tumor number, respectively, and tumor size was markedly reduced. Lower doses had less effect. Ovariectomy had an effect similar to that of 24 mcg RU 16117. E2 doses did not change the number or size of tumors. Decreased levels of receptors for E2, progesterone, and PRL were found in the tumors remaining after ovariectomy. The 24 mcg dose of RU 16117 had a similar effect on levels of E2 and PRL receptors. It was considered likely that RU 16117 exerts its inhibitory activity at both the hypothalamic-pituitary and tumor levels.
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PMID:Potent inhibitory effect of a new antiestrogen (RU 16117) on the growth of 7,12-dimethylbenz[a]anthracene-induced rat mammary tumors. 40 79

In nine patients who had undergone trans-sphenoidal hypophysectomy, prolactin dynamics were studied with intravenous thyrotropin releasing hormone (TRH). Residual prolactin secretory reserve was demonstrated in seven. Five patients were TRH tested both before and after trans-sphenoidal hypophysectomy. Hypophysectomy did not alter base line prolactin concentration but did decrease prolactin response to TRH from 55 ng/ml to 21 ng/ml (p less than 0.001). Post-hypophysectomy L-Dopa suppressed baseline prolactin concentrations to undetectable levels. There was no correlation between alterations in prolactin dynamics and tumor response to hypophysectomy. Trans-sphenoidal hypophysectomy is not effective in ablating prolactin secretion and serious doubts are raised about the role of altered prolactin dynamics in inducing breast cancer remission.
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PMID:Prolactin dynamics following transphenoidal hypophysectomy for metastatic carcinoma of the breast. 40 30

Tests of prolactin regulation in the galactorrhea-amenorrhea syndrome were compared in 18 patients with normal pituitary fossae, seven patients with prolactin-secreting adenomas, and eight normal women. Mean basal prolactin was highest in patients with adenomas and was elevated in those with normal fossae when compared with normal subjects (278 versus 73 versus 10.2 ng/ml). Levodopa, water loading, or luteinizing hormone-releasing hormone testing were of no predictive value in the diagnosis of adenoma. Some patients with adenomas show a greater prolactin response after administration of thyrotrophin hormone-releasing hormone (TRH) than of chlorpromazine, whereas these responses are usually similar in patients with normal fossae. A mean basal prolactin level above 150 ng/ml or an increase of more than 100 ng/ml after TRH administration in a patient with hyperprolactinemia unresponsive to chlorpromazine stimulation strongly suggests a prolactin-secreting tumor. However, because some patients with tumor have prolactin levels below 150 ng/ml, or do not respond to TRH stimulation, or both, functional studies alone cannot permit the diagnosis of all adenomas before the appearance of radiographic changes.
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PMID:Galactorrhea-amenorrhea syndrome: diagnosis and therapy. 40 24

Eight ergot alkaloids and ergoline derivatives, effective prolactin inhibitors, were tested for activity against DMBA-induced rat mammary carcinomas. Compounds were administered daily, 5 times/week for 4 weeks, and rats were observed for an additional 4 weeks. Groups treated with androgen and estrogen were used as positive controls. Those ergot compounds and ergolines that proved to be highly effective in reducing tumor size or in inducing regression of tumors to nonpalpability were Deprenon (D-6-methyl-8-ergolin-I-ylacetic acid amide) and ergocryptine; effective to an intermediate degree were Dironyl [N-(D-6-methyl-8-isoergolin-I-yl)-N',N'-diethylurea], ergocornine, and Lysenyl [N-(D-6-methyl-8-isoergolenyl)-N',N'-diethyl-urea]; and effective to a minimal degree were Lergotrile (2-chloro-6-methylergoline-8beta-acetonitrile), CB-154, and 6605-VUFB (D-6-methyl-8-cyanomethylergolin-I). Remission of many individual carcinomas was brief, and duration of complete regression (all tumors in the rat were nonpalpable) was less than 10 weeks.
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PMID:Comparative effects of a series of prolactin inhibitors, 17beta-estradiol and 2alpha-methyldihydrotestosterone propionate, on growth of 7,12-dimethylbenz(a)anthracene-induced rat mammary carcinomas. 40 89

Growth rates of 7,12-dimethylbenz(a)anthracene-induced mammary tumors and the specific 125I-labeled prolactin binding to membrane fractions prepared from livers and tumors were studied in rats made diabetic by streptozotocin injection. Growth was inhibited in a majority of tumors and prolactin binding was reduced in both tumors and livers from diabetic animals. Prolactin binding to individual tumors varied over a wide range in both intact and diabetic animals. Scatchard analysis of binding data revealed that the apparent affinity of prolactin binding to liver and tumor membranes was similar (Ka approximately 3.0 X 10(9) M-1) and was not affected by diabetes. We suggest that the reduction in prolactin binding to tumors may render these tissues less responsive to prolactin and thereby explain, at least in part, the observed inhibition of tumor growth in diabetic rats. However, some tumors in diabetic animals regressed despite relatively high levels of prolactin binding activity. Therefore, additional factors most certainly play important roles in the mechanism(s) by which the growth of 7,12-dimethylbenz(a)anthracene-induced tumors is impaired in the diabetic rat.
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PMID:Prolactin binding to 7,12-dimethylbenz(a)anthracene-induced mammary tumors and liver in diabetic rats. 40 90

60 women were given 200 mcg thyrotropin releasing hormone (TRH) iv to assess its stimulus to prolactin (PRL) release as a diagnostic tool. It has been suggested that a blunted response to TRH in hyperprolactinemic women may be indicative of a pituitary tumor. The group included 6 normal women, 18 with hypothalamic amenorrhea, 31 with idiopathic amenorrhea galactorrhea, and 11 with pituitary tumor. Following TRH administration, serum PRL increased 614.6% in normal women, 296% in the amenorrheic, 282.1% in the nontumoral galactorrheic, and 34% in the patients with pituitary tumors. TRH response above baseline PRL levels was significant (p .001) in all but the tumor patients. Increase above baseline PRL was also greater in menstruating women than in amenorrheic (p .001). It is suggested that there is diminished PRL secretion after TRH in amenorrheic women regardless of the presence of galactorrhea or hyperprolactinemia and that a blunted response may be helpful in separating patients with pituitary tumor from those with galactorrhea of other causes.
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PMID:Prolactin responsiveness to TRH in amenorrheic women with and without galactorrhea. 41 10

Several procedures were utilized to study the effects of prolactin on dopamine synthesis in the medial basal hypothalamus of the rat. Elevation of serum prolactin was produced by the administration of trifluoperazine (5 mg/kg, i.p.) and resulted in a significant increase in the conversion of [3',5'-3H]tyrosine to dopamine when measured in slices of medial basal hypothalamus and striatum. Hypophysectomy abolished this effect of trifluoperazine in the medial basal hypothalamus but not in the striatum. In addition, the synthesis of dopamine was significantly elevated in slices of medial basal hypothalamus obtained from rats bearing pituitary tumor implants that secreted microgram quantities of prolactin. In contrast, the in vitro synthesis of dopamine in the striatum of such rats was increased by the secretory products in one tumor line but decreased in another compared to that observed in control animals. It is suggested that the ability of prolactin to accelerate the synthesis of dopamine in the medial basal hypothalamus might constitute a short loop feedback system that finely regulates prolactin secretion.
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PMID:Effect of prolactin on dopamine synthesis in medial basal hypothalamus: evidence for a short loop feedback. 42 Nov 24


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