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

An autopsy case of a 9-year-old Japanese girl revealed a carcinoid tumor originating in the duodenum and hyperplasia of the multiple endocrine organs as manifested by ectopic ACTH syndrome, carcinoid syndrome and giantism. The tumor cells were positive for histochemical argyrophile reaction and two types of secretory granules were identified by electron microscopy. Biochemical assay revealed the production of ACTH and beta-MSH by the tumor cells. Other changes of multiple endocrine organs included acidophil dominant hyperplasia of the pituitary, diffuse hyperplasia of the thyroid, chief cell hyperplasia of the parathyroid, hyperplasia of the islets of Langerhans and the adrenal cortex. This case was considered to be a type of multiple endocrine adenomatosis including carcinoid tumor. The relationship between the carcinoid tumor and multiple endocrine adenomatosis was discussed.
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PMID:Ectopic ACTH-MSH producing carcinoid tumor with multiple endocrine hyperplasia in a child. 21 30

Hypothalamic extract stimulates the release of corticotropin (ACTH) and endorphins 2.5- to 30-fold in mouse pituitary tumor cell cultures (AtT-20/D(16v) line) and primary cell cultures from mouse anterior pituitary. ACTH and endorphin activities were measured by radioimmunoassay and immunoprecipitation. Pretreatment of tumor cell cultures with 1 muM dexamethasone reduced the stimulatory effect of the extract on release of ACTH and endorphins. Pretreatment of primary cell cultures with 10(-6) M dexamethasone reduced the stimulatory effect of both vasopressin and the extract on the release of ACTH and endorphins. Release of ACTH and endorphin was coupled in both kinds of cultures in the basal, stimulated, and inhibited states. The molecular weight forms of ACTH and endorphin in tumor cell culture medium were analyzed by sodium dodecyl sulfate/polyacrylamide gel electrophoresis. Radioimmunoassay and immunoprecipitation show that the 13,000-dalton and 4500-dalton forms of ACTH were present in about equal amounts in medium from cultures incubated with or without hypothalamic extract for 15 min, 30 min, or 2 hr. Smaller amounts of the high molecular weight forms of ACTH (20,000- to 23,000-dalton and 31,000-dalton ACTH) were observed in the culture medium at these times. The predominant forms of endorphin released after 20 min or 3 hr of incubation had molecular weights of 31,000, 11,700 (beta-lipotropic hormone-size material) and 3500 (beta-endorphin-size material). No degradation of the forms of endorphin released into the culture medium was observed after incubating the culture medium for 1.5 hr in the absence of cells. The proportions of the different forms of endorphin and ACTH present in the culture medium resembles that seen in cell extracts.
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PMID:Coordinate control of corticotropin, beta-lipotropin, and beta-endorphin release in mouse pituitary cell cultures. 21 8

Release of ACTH by a mouse pituitary tumor cell line )AtT-20/D-16v) is inhibited by 10(-8)-10(-6) M 9 alpha-fluoro-16 alpha-methyl-11 beta, 17 alpha, 21-trihydroxy-1,4-pregnadiene-3,20-dione (dexamethasone). Dexamethasone does not inhibit cell growth in this concentration range. Cortisol and corticosterone are almost as potent as dexamethasone in inhibiting ACTH release, whereas 17 beta-estradiol and testosterone have no effect. In rapidly growing cultures of tumor cells removal of dexamethasone leads to complete reversal of the inhibitory effect of the steroid on ACTH accumulation in culture medium within 4-5 days (3.5-4 generation times). The extent of reversal of the dexamethasone effect in slowly growing cultures (generation time 96-150 h) and in rapidly growing cultures (24-30 h) is proportional to the amount of growth that takes place in the absence of dexamethasone. Addition of hypothalamic extract to dexamethasone-treated cultures and to untreated cultures stimulates the release of ACTH 4- to 8-fold. The response occurs within 15 min after the addition of the extract and is dependent on the dose of the extract.
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PMID:Reversal of dexamethasone inhibition of adrenocorticotropin release in a mouse pituitary tumor cell line either by growing cells in the absence of dexamethasone or by addition of hypothalamic extract. 21 83

Previous studies have shown that the sensitivity of tissues to insulin is diminished in states of glucocorticoid and GH excess and is increased when these hormones are deficient. To evaluate the role of the insulin receptor in these states, we have studied [125I]insulin binding to purified liver plasma membranes obtained from rats with a variety of perturbations of both glucocorticoids and GH. Glucocorticoid excess was produced in rats by administration of ACTH (40 U/day for 4 days) or dexamethasone (1 mg/day for 4 days). This resulted in an insulin-resistant state. Associated with this insulin resistance, there was a 50-60% decrease in insulin binding to its specific receptors in liver. Conversely, adrenalectomy, which produces an increase in insulin sensitivity, was associated with an increase in insulin binding to liver. Computer-assisted Scatchard analysis using a negative cooperative model for the inulin-receptor interaction indicated that, in contrast to our findings with obesity, the changes in insulin binding in these states were most likely due entirely to changes in receptor affinity, with no change in receptor concentration. GH administration also produced mild insulin resistance and a decrease in receptor concentration. This was associated with a reciprocal increase in receptor affinity and thus, no major alteration in insulin binding occurred at low physiological insulin concentrations. Hypophysectomized rats, on the other hand, showed an increase in receptor concentration and a decrease in affinity, and GH treatment only partially corrected these changes. Rats implanted with the MtT tumor (which secretes ACTH, GH, and PRL) have the combined effects of excess glucocorticoids and GH and are very insulin resistant. Liver membranes prepared from these rats showed a decrease in insulin binding and receptor affinity similar to that observed in other states of glucocorticoid excess. Further, adrenalectomy of the tumor-bearing rats resulted in an increase in insulin binding despite the persistence of the elevated levels of GH, ACTH, and PRL. These findings suggest that alterations in insulin receptor affinity and number may play a major role in the states of altered insulin sensitivity which accompany glucocorticoid excess and deficiency, and follow hypophysectomy. In contrast, the insulin resistance associated with GH excess is mediated at either a site on the receptor distal to the insulin-binding site (i.e. transduction) or at one or more of the intracellular reactions important in insulin action.
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PMID:Alterations in insulin binding induced by changes in vivo in the levels of glucocorticoids and growth hormone. 21 65

Implantation of MtT-F4 tumor, a mammotropic tumor that secretes large quantities of ACTH, GH and prolactin, into male Fisher rats induced the development of hyperlipidemia. Free fatty acid, triglyceride and cholesterol levels in the plasma were significantly increased at 31 days after tumor implantation. Blood glucose and glycerol levels remained normal, while uric acid concentration in the blood was significantly decreased. The lipolytic response of isolated adipose tissue cells to ACTH was significantly higher in cells derived from rats bearing an MtT-F4 tumor for 31 days than from their corresponding controls. However, the activity of adenylate cyclase in fat cells stimulated with ACTH was not significantly higher in cells derived from tumor bearing rats than in cells from control rats.
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PMID:Development of hyperlipidemia associated with increased lipolytic response of isolated adipose tissue cells following prolonged stimulation by an ectopic pituitary tumor. 21 11

In a middle-aged woman with virilizing adenoma, 2 mg dexamethasone increased urinary excretion of 17-ketosteroids (17-KS) and 17-hydroxycorticosteroids, whereas 8 mg dexamethasone increased urinary excretion only of 17-KS. With discontinuation of dexamethasone, 17-KS excretion returned to the predexamethasone level. Dexamethasone depressed the basal level of cAMP synthesis and basal testosterone production by the normal adrenal tissue in vitro. Dexamethasone also depressed the increase of cAMP produced by ACTH in the normal tissue. In contrast, dexamethasone increased basal cAMP synthesis and stimulated testosterone secretion in the tumor tissue. ACTH and dexamethasone were additive in their effects on cAMP and testosterone in the tumor tissue. It is suggested that dexamethasone acted directly on the adrenal tumor to stimulate steroid secretion in this patients.
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PMID:Virilizing adrenal adenoma stimulated by dexamethasone in a middle-aged woman. 21 5

Thirteen cases of bronchopulmonary carcinomas without symptoms of hypercorticoidism, hypopotassemic alkalosis, or intolerance to an overdose of glucose are described. Repeated circadian rhythm and the suppression test with small doses of dexamethasone were practiced on each one. In 7 cases the secretion of cortisol was supressed normally with oral administration of dexametahsone. In the other 6 cases the circadian rhythm was lost and it was imposible to reduce the plasma level of cortisol with dexamethasone. The results help to point out the usefulness of these easy to perform dynamic tests as a means of diagnosing the ectopic production of ACTH by bronchopulmonary tumors. At the same time they show the relatively high incidence of production of this hormone by this type of tumors in patients who have no symptoms of classical hypercorticoidism. The determination of plasma cortisol levels using this test could be valuable in establishing the prognosis and clinical course of the disease. A normalization of the endogenous adrenal secretion of glucocorticoids would indicate a regression of the tumor in response to treatment.
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PMID:[Ectopic ACTH syndrome in bronchopulmonary tumors (author's transl)]. 21 3

Initial studies of adrenocorticotropin-sensitivity (ACTH-sensitive) and ACTH-insensitive Y-1 adrenal cortical tumor cell lines suggest a relationship between responsiveness to ACTH and the presence of gap junctions. An ACTH-sensitive clone of Y-1 cells possesses gap junctions and these junctions appear to enlarge with ACTH treatment. GAP junctions have not been observed, however, in an ACTH-insensitive clone of Y-1 tumor cells even when stimulated to produce cyclic adenosine monophosphate and steroids with cholera toxin.
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PMID:Gap junctions and ACTH sensitivity in Y-1 adrenal tumor cells. 22 Apr 67

Monolayer cultures of mouse adrenal tumor cell line Y-1 have been used to investigate the effects of glucocorticoid on cell replication, [3H]thymidine incorporation into the trichloroacetic acid-precipitated cell fraction, steroidogenesis, and the ACTH receptors of adrenocortical cells. Corticosterone at a concentration of 5.0--50 micrograms/ml inhibited cell replication and [3H]thymidine incorporation into trichloroacetic acid-precipitated cell fraction in a dose-related manner. Corticosterone at a concentration of 0.5--50 micrograms/ml inhibited ACTH-induced steroidogenesis in a dose-related manner. Steroids which do not possess glucocorticoid action did not show such inhibitory effects on cell replication and steroidogenesis of Y-1 cells. The characteristics of the ACTH receptors of these cells remained unaffected by corticosterone. Our findings suggest that synthesized or secreted glucocorticoid may play an important role in the direct regulation of proliferation and function of adrenocortical cells under physiological conditions.
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PMID:Inhibitory effects of corticosterone on cell proliferation and steroidogenesis in the mouse adrenal tumor cell line Y-1. 22 Nov 80

An 8-month old male with Cushing's disease is presented; his clinical presentation and appearance were typical of infants with glucocorticoid excess. Concentrations of cortisol, 17-hydroxyprogesterone, and adrenal androgens were strikingly elevated. High doses of dexamethasone did not suppress the excretion of urinary free cortisol or 17-hydroxycorticoids, and administration of ACTH elicited no further rise in plasma cortisol. Responses of LH, FSH, and PRL to iv LRF and TRF were appropriate for age, but neither TSH nor ACTH rose significantly. Plasma ACTH values were elevated to 700 pg/ml. An intracranial mass lesion superior and anterior to the sella turcica was demonstrated by computerized axial tomography and angiography. An inoperable pituitary adenoma was a massive surrounding fibroblastic reaction was found at craniotomy. The pathological diagnosis of an ACTH-producing pituitary adenoma was confirmed by immunohistochemistry and by the in vitro secretion of ACTH by cells cultured from the tumor.
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PMID:An infant with Cushing's disease due to an adrenocorticotropin-producing pituitary adenoma. 22 23


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