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)

A man of 38 years of age was found to have a type I endocrine polyadenomatosis in 1969. He was operated upon for removal of tumor of the islets of Langerhans with lymph gland metastases, and the head of the pancreas was removed. This was followed at a later date by ablation of two parathyroid adenomas. A clinically silent adenoma of the left adrenal was not removed and a silent and enclosed pituitary tumore was discovered. There were no clinical or hormonal signs of progression of the pancreatic tumor ten years later, but hypertension and behavioural disorders had developed. Catecholamine levels were normal. Selective blood aldosterone levels were just within significant values. A massive increase in prolactin secretion (more than 100 times the normal) was noted. This could be reduced by bromocriptine, and the possible role of prolactin in the behavioural disorders present is discussed.
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PMID:[Prolactin adenoma and Wermer's syndrome. A 10-year follow-up of a case with two parathyroid tumors, as adrenal adenoma, and a malignant pancreatic tumor (author's transl)]. 4 60

An unusual case of orbital tumor with high renin content and severe hypertension is described. The patient was a 15-year-old girl with juvenile hypertension (200-140 mmHg) associated with right exophthalmos and hypokalemia. The patient showed extremely high levels of plasma renin activity and plasma aldosterone concentration. No difference was present in plasma renin activity from either side of the renal veins. Preoperatively, hypertension responded to treatment with spironolactone. The tumor could not be completely removed because of intracranial metastasis and infiltration, and the hyperreninemia and secondary hyperaldosteronism persisted. The renin content in the orbital tissue was 1,403-2,225 ng/angiotensin I generated/h/g wet weight of tissue. The postmortem histopathologic diagnosis was orbital hemangiopericytoma. This is the first case of extrarenal (ectopic) renin-secreting (or -producing) hemangiopericytoma of the orbital origin. Furthermore this case is worthy of note in the point of view of the presence of the extrarenal renin-angiotensin system, particularly in the brain.
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PMID:A case of ectopic renin-secreting orbital hemangiopericytoma associated with juvenile hypertension and hypokalemia. 15 52

The formation of cellular aggregates (foci) in CV-1 cells following infection with Yaba tumor poxvirus is dependent upon cell passage level, temperatue of incubation, and calcium concentration in the medium. Resistance of older cells can be reversed by maintaining calcium at 0.1 mM or by adding cortisone acetate (1 mug/ml), hydrocortisone, or estradiol-17beta to the cultures. In susceptible cells, foci formation was inhibited slightly by methyltestosterone and inhibited completely by dexamethasone, aldosterone and progesterone. Activities and patterns of enzymes associated with cytoplasmic membranes (alkaline phosphatase, mononucleotidase, and Na+-K+-adenosine triphosphatase) and lysosomes (beta-glucuronidase and acid phosphatase) of the younger susceptible and the older resistant CV-1 cells differed. These differences apparently occurred in concert with phenotypic changes in the membranes that reduced the mobility of older resistant cells. In susceptible culture, unifected cells migrated to the infected cell and participated in foci formation. Reduction of the calcium content to 0.1 mM apparently removed some of the constraints on mobility of the resistant cells. Although the hormones may have had a similar effect, the changes in enzyme patterns indicated basic alterations in protein synthesis. The development of resistance to foci formation occurred between the 45th and 50th passage level. Hormonal reversal of this resistance resulted in enzyme profiles that reflected the pattern of young susceptible cells.
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PMID:Alterations of enzymes associated with plasma membranes and cellular organelles during infection of CV-1 cells with Yaba tumor poxvirus. 16 62

A case of a young woman with the syndrome of primary aldosteronism and malignant ovarian tumor is reported. Hormone studies revealed extremely high urinary aldosterone, undetectable plasma renin activity, elevated plasma 17beta estradiol and testosterone, and low plasma FSH and LH. Plasma cortisol and urinary 17-hydroxycorticoids were at the upper normal limits. Autopsy disclosed an ovarian tumor, histologically an arrhenoblastoma, with polymorphic aspects. The adrenal glands grossly were normal. Aldosterone was found by the double radioisotopic technique in the neoplastic tissue.
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PMID:Primary aldosteronism due to a malignant ovarian tumor. 17 Dec 76

Characteristics of [3H]progesterone-binding components were studied in cell-free preparations of two hormonally responsive tumors: the R3230AC mammary adenocarcinoma and 9,10-dimethyl-1,2-benzanthracene-induced mammary tumor of the rat. Progesterone-binding macromolecules from cytosols of both mammary neoplasms exhibited sedimentation coefficients of 3.5 to 4.0 S on sucrose gradients of either low or high ionic strength. From Scatchard analyses of titration data, apparent dissociation constants of 4 to 6 X 10(-8) M were determined for ligand-binding protein complexes from either tumor. Specific progesterone-binding capacities varied considerably, ranging from 150 to 650 fmoles/mg of cytosol protein. Optimal binding of [3H]progesterone was reached by 2 to 3 hr at 3 degrees, pH 7.4, and then decreased rapidly. Specificity studies indicated that cortisol, corticosterone, and triamcinolone acetonide competed effectively for [3H]progesterone-binding. This suggested that [3H] progesterone was bound largely to a macromolecule distinct from transcortin, which does not bind glucocorticoids containing 9alpha-fluoro groups. Aldosterone, as well as several androgens and estrogens, were weak competitors of binding except at high concentrations. The nature of the inhibition of progesterone-binding sites by triamcinolone acetonide and corticosterone was competitive. Concurrent titrations of [3H]progesterone and [3H]triamcinolone acetonide-binding sites demonstrated that their binding capacities were similar, considering the relative stabilities of the complexes. These results, which indicated that progesterone and glucocorticoids compete for the same binding site, suggest that these hormones may influence mammary gland differentiation and development by a common mechanism.
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PMID:Characteristics of progesterone-binding components in neoplastic mammary tissues of the rat. 17 35

Approximately one-third of patients with metastatic breast carcinoma respond to surgical ablative therapy but the morbidity associated with these procedures has limited their use to highly selected patients. Consequently, a chemical method of adrenal suppression was developed using a potent inhibitor of adrenal steroid synthesis, aminoglutethimide, in combination with a synthetic glucocorticoid, dexamethasone. While this regimen effectively blocked adrenal function, it was complicated by a drug interaction in which aminoglutethimide accelerated the metabolism and reduced the bioavailability of dexamethasone. To overcome this problem, a new regime using aminoglutethimide and hydrocortisone, a glucocorticoid less susceptible to altered metabolism, was developed. Kinetic studies confirmed that aminoglutethimide does not interact with hydrocortisone to alter its rate of metabolism. Hormone measurements established that 1000 mg of aminoglutethimide and 40 mg of hydrocortisone daily suppressed DHA-sulfate, androstenedione, estrone, estradiol and aldosterone to a greater extent than the prior protocol using aminoglutethimide and 2-3 mg of dexamethasone. Patients experienced objective tumor regression with equal frequency while receiving the aminoglutethimide-hydrocortisone regimen or aminoglutethimide and dexamethasone and the overall rate of response in 50 evaluable patients was 38%. Side effects occurred frequently in the first few weeks of treatment but disappeared nearly uniformly thereafter. The present aminoglutethimide-hydrocortisone regimen is simple, non-toxic, effective in inhibiting estradiol synthesis and capable of inducing tumor regression as frequently as previously reported with adrenalectomy.
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PMID:Kinetic, hormonal and clinical studies with aminoglutethimide in breast cancer. 19 81

A 16-month-old black male infant had unusual thirst, polyuria, hyponatremia, and hypertension. His polyuria was unresponsive to vasopressin therapy, and his high blood pressure was not effectively controlled by antihypertensive drugs. Radiographic examinations revealed an occult Wilms tumor in the right kidney. After removal of the tumor, the signs and symptoms were relieved. The tumor had a renin activity about 280 times that of the adjacent renal cortex, and many intracytoplasmic secretory granules were found on electron microscopy. The pathogenesis of these clinical manifestations appears to be mediated through the physiologic pathways of renin-angiotensin II and renin-aldosterone.
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PMID:Polydipsia, polyuria, and hypertension associated with renin-secreting Wilms tumor. 20 43

A case of a feminizing adrenocortical tumor associated with Cushing's syndrome in a 29 year old male is presented. The ultrastructural features are compared with adrenal tumors secreting aldosterone, glucocorticoids of androgens. As in adrenal carcinomas, this tumor demonstrates nuclear pleomorphism with enlarged nucleoli and nuclear pseudoinclusions. The cytoplasmic organelles show some parallels between feminizing and androgen-secreting adrenal tumors. Different types of mitochondria occur with varying amounts of smooth endoplasmic reticulum. Numerous microbodies are present. Histological and ultrastructural signs indicating probably malignancy are discussed and it is noted that most of the feminizing adrenal tumors are carcinomata. Neither local recurrence nor distant metastases have yet been detected in this case, two years after excision of the tumor.
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PMID:Feminizing adrenocortical tumor. Histological and ultrastructural study. 20 8

Kinetic and molecular properties of components binding [3H]triamcinolone acetonide were studied using 105,000g supernatants of lactating mammary gland, R3230AC, and dimethylbenz[a]anthracene (DMBA) induced mammary tumors of the rat. Using a dextran-coated charcoal adsorption procedure, the relationship between specific glucocorticoid binding and protein concentration was linear in the range of 0.5-4.0 mg/reaction. These cytoplasmic macromolecules bound [3H]triamcinolone acetonide with limited capacity (50-400 fmol/mg of cytosol protein) and high affinity, Kd approximately 10(-8)-10(-9) M. Optimal binding was obtained when homogenizations were made in Tris buffers, at pH 7.4, containing monothioglycerol. Time course of association of [3H]triamcinolone acetonide and its binding sites showed maximal binding by 6-8 hr at 3 degrees which remained unchanged up to 24 hr. The rate constant of association at 3 degrees was in the range of 2-4 x 10(5) M-1 min-1. The rate constant of dissociation of bound [3H]triamcinolone acetonide could not be calculated accurately since the reaction was essentially irreversible for 5 hr at 3 degrees. Estimation of the half-life of the steroid-binding protein complexes from the Kd and the rate constant for association gave a value of 11-12 hr. From ligand specificity studies, the glucocorticoids, triamcinolone acetonide, corticosterone, cortisol, and dexamethasone competed well for [3H]triamcinolone acetonide binding sites. Progesterone, aldosterone, and the anti-glucocorticoid, cortexolone, were also good competitors while androgens and estrogens were weak inhibitors of binding. The binding compenents sedimented at 7-8 S in sucrose gradients of low ionic strength and dissociated into lower molecular weight components sedimenting at 4-5S in high ionic strength gradients. Studies in vivo using animals bearing the DMBA-induced tumor demonstrated that [3H]triamcinolone acetonide binding complexes were present in cytoplasmic and nuclear compartments. Sedimentation coefficients of the cytoplasmic and nuclear forms of these receptors labeled in vivo were 7-8S and 4-5S, respectively. These studies suggest that the molecular and kinetic binding properties of glucocorticoid receptors in neoplastic mammary tissues are similar to those of the normal mammary gland.
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PMID:Comparison of glucocorticoid-binding proteins in normal and neoplastic mammary tissues of the rat. 23 78

This study describes the effects of [des-Aspartyl(1)]-angiotensin II ([des-Asp]-AII) on blood pressure and aldosterone production in patients with primary aldosteronism due to aldosterone-producing adrenal adenoma (APA) and idiopathic adrenal hyperplasia (IHA), and in normotensive control subjects. 10 patients with primary aldosteronism, 7 with APA and 3 with IHA, and 6 normotensive control subjects were placed on a constant 150-meq sodium diet for 4 days. [des-Asp]-AII was infused for 30 min at 6, 12, and 18 pmol/kg per min. Three groups of patients were identified on the basis of aldosterone response to [des-Asp]-AII. Group I, composed of normotensive control subjects, showed incremental increases in plasma aldosterone concentration from 6+/-1 to 14+/-3 ng/100 ml (P < 0.01) with [des-Asp]-AII infusion. Group II, composed of patients with primary aldosteronism, showed incremental increases in plasma aldosterone concentration from 33+/-8 to 65+/-13 ng/100 ml (P < 0.05) with 12 pmol/kg per min of [des-Asp]-AII. Group III, also composed of patients with primary aldosteronism, showed no increase of plasma aldosterone concentration with [des-Asp]-AII. Groups I and II showed similar percentage increases in plasma aldosterone concentration (P = NS). Group III showed significantly lower aldosterone responses than group I (P < 0.01). Group II included all patients with IHA and two patients with APA. Group III included only patients with APA. The blood pressure responses to [des-Asp]-AII of subjects in group I did not differ significantly from those of groups II or III.Thus, patients with IHA and a subgroup of patients with APA showed responsiveness to [des-Asp]-AII which was limited to adrenal cortical stimulation of aldosterone biosynthesis. This suggests that adrenal responsiveness to angiotensin is a major control mechanism in some forms of primary aldosteronism. The differential adrenal responsiveness to [des-Asp]-AII in patients with APA indicates either that there are two distinct subpopulations of APA, or that alteration in tumor response to angiotensin occurs during the natural progression of the disease history.
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PMID:Activity of [des-aspartyl1]-angiotensin II in primary aldosteronism. 43 32


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