Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P61278 (somatostatin)
 22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Whilst investigating 26 members of the same family, we discovered 5 cases of multiple endocrine neoplasia type II a. The present report demonstrates the diagnostic value of basal plasma thyrocalcitonin (TCT) assays, before and after stimulation with pentagastrin, and of plasma carcinoembryonic antigen (CEA) assays. Some of the clinical features encountered were novel--e.g. in one patient the phaeochromocytoma was revealed by a haemothorax with cardiovascular collapse--and others were peculiar; thus, in 4 cases the medullary thyroid carcinoma (MTC) was less than 2 cm in diameter and without lymph node or visceral metastases, even in patients aged 87, 59 and 56. More classically, MTC, always multifocal, was clinically silent, as were the two cases of phaeochromocytoma and hyperparathyroidism. Phaeochromocytomas were difficult to diagnose. Ultrasonic tomography did not prove very helpful and the disease was transmitted as an autosomal dominant trait. Finally, MTC secreted a variety of substances (TCT, CEA, beta-endorphin, somatostatin), and HLA A2-B15 antigens were found in 3 patients.
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PMID:[Hemothorax disclosing hemorrhagic necrosis of a pheochromocytoma: circumstance for detection of multiple endocrine neoplasia type IIa. Detection of 5 familial cases]. 287 8

A continuous line of somatostatin-producing medullary thyroid carcinoma cells was established from a transplantable tumour in BALB/c mice. Virtually all of the somatostatin immunoreactivity co-chromatographed with somatostatin 14. The tumour cells replicated in spinner cultures with a doubling time of approximately 4 days, and the concentration of somatostatin released into the culture medium increased in proportion to the number of cells. Two- to threefold increases in amounts of stored and released somatostatin were observed after treatment of the cells with bromodeoxyuridine. This cell line might be valuable for studies of somatostatin regulation in normal and neoplastic C-cells, and for other studies of C-cell biology which require a mouse model.
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PMID:Establishment of a continuous somatostatin-producing line of medullary thyroid carcinoma cells from BALB/c mice. 287 21

There have been few studies of physiological importance on the regulation of somatostatin by hormones. We have studied the effect of the synthetic glucocorticoid dexamethasone on somatostatin production in the human medullary thyroid carcinoma TT cell line, a model for somatostatin production by the parafollicular cell. Dexamethasone inhibited somatostatin production in a dose-related manner with a maximal effect at a concentration of 10(-6) M. TT cells treated with dexamethasone (10(-6) M) showed an almost complete inhibition of somatostatin peptide production by 48 h of treatment. Molecular sizing chromatography demonstrated a decrease in both the probable somatostatin precursor (13,000 dalton) and the fully processed peptide. Analysis of mRNA content by hybridization revealed that dexamethasone also caused a decrease in detectable somatostatin mRNA. The hybridizable somatostatin mRNA decreased to approximately 50% of basal levels within 12 h of treatment. Northern blot hybridization showed a decrease in a single RNA species representing mature somatostatin mRNA. Dose-response experiments revealed inhibition of both peptide and mRNA at concentrations from 1 X 10(-8) to 1 X 10(-5) M dexamethasone. Four days after withdrawal from dexamethasone treatment, peptide and mRNA levels were higher than dexamethasone-treated controls. The sex steroid estradiol had no inhibitory effect on somatostatin production. These results suggest a potential regulator of somatostatin production and provide a system for the study of somatostatin gene regulation.
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PMID:The regulation of somatostatin production in human medullary thyroid carcinoma cells by dexamethasone. 287 92

We describe a 63-yr-old man with disseminated medullary carcinoma of the thyroid and pancreatic nesidioblastosis and microadenosis with pancreatic polypeptide (PP) hypersecretion. His major symptoms were watery diarrhea, flushing, and abdominal bloating; these and the elevated plasma PP levels did not change after resection of the distal two thirds of the pancreas, which contained a 2-cm mass of nesidioblastotic tissue. Postoperatively, a long-acting somatostatin analog, SMS 201-995 (100 micrograms/day), normalized PP secretion acutely and chronically (7 months) and ameliorated his symptoms. The analog had no side-effects and did not alter glucose tolerance, calcitonin hypersecretion, or growth of the medullary carcinoma, but it did inhibit GH secretion. After withdrawal from therapy for 1 month, PP hypersecretion and all symptoms except diarrhea recurred. The coexistence of medullary carcinoma of the thyroid and PP cell nesidioblastosis represents a new variant of the overlap syndromes between multiple endocrine neoplasia types I and II. Patients with medullary carcinoma and unexplained watery diarrhea should have fasting gastroenteropancreatic hormone assays done to screen for a potential gastrointestinal or pancreatic origin for the diarrhea.
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PMID:Medullary carcinoma of the thyroid, pancreatic nesidioblastosis and microadenosis, and pancreatic polypeptide hypersecretion: a new association and clinical and hormonal responses to long-acting somatostatin analog SMS 201-995. 288 96

We have identified a system, the TT human medullary thyroid carcinoma cell line, which we found to contain 31.3 +/- 27.7 ng of somatostatin 28(1-12) immunoreactivity/mg protein. Radioimmunoassay of gel filtration fractions showed that the major form of immunoreactive somatostatin 28(1-12) had a molecular weight of 1,500 daltons. During reversed-phase high pressure liquid chromatography, this 1,500-dalton species coeluted with synthetic somatostatin 28(1-12). Somatostatin 28(1-12) containing forms larger than 7,000 daltons were also observed. Further studies will be required to elucidate the route of processing of prosomatostatin. The fact that the products of prosomatostatin processing in these cells are similar to those in normal tissues indicates that the TT medullary thyroid carcinoma cell line constitutes a useful model for human somatostatin gene expression.
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PMID:Somatostatin 28(1-12) in a somatostatin-secreting human medullary thyroid carcinoma cell line. 288 45

Five peptide hormones including calcitonin (CT) and gastrin-releasing peptide (GRP), serotonin (5HT), CEA, nervous tissue specific proteins and monoclonal antibody Leu-7 were immuno-histochemically studied on 60 cases of medullary thyroid carcinoma (MTC). In addition, localization of varied products in the tumor cells and its relations with the clinical features in some cases were evaluated. MTC contains a variety of products in many cases, and CT and CEA were positive in all cases. In 50 of the 57 cases (87.7%), GRP was positive, which suggested that GRP could be a novel tumor marker for this tumor. Furthermore, in tumor cells and C-cell hyperplastic foci, identical cells were sometimes revealed to possess both CT and GRP. Existence of somatostatin (SS), substance-P (SP), beta-MSH, 5 HT, Leu-7 and NSE in the tumor cells were confirmed. NSE was positive in 32 of the 47 cases (61.8%) which could confirm that MTC possesses neuroendocrine nature. In two cases of autopsy in which the tumors were highly malignant in clinical course and undifferentiated in histology, most tumor cells showed poor stainability for peptide hormones, suggesting that specific qualities as neuroendocrine tumor had been lost. In familial cases, the tumor tended to contain multiple substances.
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PMID:[Immuno-histochemical study of medullary thyroid carcinoma]. 289 90

Four patients with advanced endocrine malignancies were treated with a somatostatin analogue (SMS 201-995) for palliation of hormone-induced symptoms during 3-6 months. Two had the carcinoid syndrome (one midgut and one foregut), one had medullary thyroid carcinoma and an ectopic ACTH syndrome, and one patient had a metastatic gastrinoma. The carcinoid patients had excellent symptomatic relief with a low dose of the drug, 50 micrograms subcutaneously twice daily, in one case despite progression of tumour disease and biochemical tumour markers. These findings indicate an action of the drug not only on hormonal release but also at peripheral sites. The patient with medullary thyroid carcinoma had relief of gastrointestinal symptoms when the drug dose was increased (100 micrograms twice daily). The levels of ACTH in peripheral blood were reduced, but not the calcitonin levels. The gastrinoma patient had undergone a major pancreatic resection (Whipple procedure) and was treated with omeprazole. SMS 201-995 reduced the peripheral gastrin levels acutely, but during the treatment fasting gastrin values increased, and the tumour growth progressed. Treatment was stopped owing to elevated fasting glucose level, increased steatorrhoea, and clinical attacks of cholangitis. Special attention is advocated for patients with major pancreatic resection and biliary reconstruction, who may be susceptible to physiological effects of somatostatin (or its analogues)--that is, impaired insulin release and decreased motility.
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PMID:The use of a long-acting somatostatin analogue in the treatment of advanced endocrine malignancies with gastrointestinal symptoms. 289 Nov 86

A 47-year-old man with multiple endocrine neoplasia (MEN) type 2a syndrome in whom metaiodobenzylguanidine (MIBG) concentrated in lesions from metastatic medullary carcinoma of the thyroid is reported. A somatostatin analogue (Sandostatin SMS 201-995) alleviated the symptoms of flushing and diarrhea associated with the elevated calcitonin levels but it did not alter either the course of the disease or the MIBG images. A review of the literature is presented of the noncatecholamine secreting tumors associated with MIBG uptake. Similarities between this case and metastatic carcinoid syndrome are discussed.
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PMID:Iodine-131 MIBG uptake in metastatic medullary carcinoma of the thyroid. A patient treated with somatostatin. 289 64

We have measured the effects of intravenous infusion of calcitonin gene-related peptide at doses of 2.5, 10, and 50 pmol/kg.min on net jejunal water and solute fluxes and on plasma somatostatin concentrations in dogs. The hemodynamic effects and the pharmacokinetics of the peptide were also assessed. Using the triple-lumen perfusion technique in unsedated restrained animals it was shown that the highest dose of the peptide stimulated a transient net jejunal water and electrolyte secretion, and induced diarrhea in 4 of 6 animals receiving it. The peptide also induced dose-dependent tachycardia, hypotension, and increases in plasma immunoreactive somatostatin. All three doses of calcitonin gene-related peptide produced plasma immunoreactive peptide levels within the elevated range previously measured in human patients with medullary thyroid carcinoma. Calcitonin gene-related peptide may have a major role in the pathogenesis of secretory diarrhea in medullary thyroid carcinoma.
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PMID:Calcitonin gene-related peptide: enteric and cardiovascular effects in the dog. 290 Jul 92

We have studied the clinical and thyroid immunohistological features of 19 patients with sporadic medullary thyroid carcinoma and 16 patients with the hereditary syndrome multiple endocrine neoplasia 2a (MEN 2a). Both groups were identified by family screening using serum calcitonin determinations before and after pentagastrin stimulation. Pheochromocytoma and hyperparathyroidism were associated both with multiple endocrine neoplasia 2a and some cases of sporadic medullary thyroid carcinoma. Hereditary medullary thyroid carcinoma was invariably associated with C-cell hyperplasia, but C-cell hyperplasia was also associated with some sporadic tumours. All tumours were positive for calcitonin and carcinoembryonic antigen (by immunohistological staining) (CEA) and most tumours stained for somatostatin. C-cell hyperplasia also stained for calcitonin, CEA and somatostatin. We conclude that sporadic and familial medullary thyroid carcinoma cannot always be discriminated by clinical or immunohistological methods. Family screening is essential in the diagnosis of hereditary medullary thyroid carcinoma.
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PMID:Familial and sporadic medullary thyroid carcinoma: clinical and immunohistological findings. 290 73


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