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)

The presence of calcitonin, somatostatin-like immunoreactivity and carcinoembryonic antigen in tumor tissues (surgically obtained) and identified by the peroxidase-antiperoxidase technique, is reported in two sisters suffering from familial thyroid medullary carcinoma. C-cell hyperplasia occurred in both individuals. Preoperatively, both patients had elevated calcitonin serum levels (290 pM, 991.8 ng/l), and carcinoembryonic antigen (60 micrograms/l). No ACTH or thyroglobulin immunoreactivity could be found in the tumor tissue. After thyroidectomy, 131I-treatment and percutaneous radiation, somatostatin-like immunoreactivity and carcinoembryonic antigen plasma levels were in the normal range, whereas calcitonin was still elevated. It is proposed that calcitonin, somatostatin, and carcinoembryonic antigen are produced by the thyroid medullary carcinoma.
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PMID:Occurrence of calcitonin, somatostatin-like immunoreactivity, and carcinoembryonic antigen in two sisters suffering from familial thyroid medullary carcinoma. 288 97

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

The effects of glucocorticoids on somatostatin binding and cAMP response in the rat pancreatic acinar carcinoma AR4-2J cell line were examined. Dexamethasone treatment reduced the number of somatostatin receptors 2.5 fold without any change in receptor affinity. In addition, dexamethasone increased the sensitivity of the cells to somatostatin-inhibited cAMP formation and restored the biphasic pattern of cAMP response to somatostatin previously observed in normal pancreatic acinar cells. Such effect may be associated with the glucocorticoid-promoted cellular pancreatic differentiation of AR4-2J cells.
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PMID:Dexamethasone effects on somatostatin receptors in pancreatic acinar AR4-2J cells. 288 56

The combination of a long-acting delivery system for the agonist [D-Trp6]luteinizing hormone-releasing hormone ([D-Trp6]LH-RH) with modern somatostatin analogs was studied in the Dunning R-3327H rat prostate cancer model. Microcapsules of [D-Trp6]LH-RH releasing 25 micrograms/day were injected once a month. In the first experiment the adjunct was the somatostatin analog D-Phe-Cys-Tyr-D-Trp-Lys-Val-Cys-Thr-NH2 (RC-121), administered at a dose of 2.5 micrograms twice a day, and the therapy was continued for 70 days. Tumor volume was significantly decreased by [D-Trp6]LH-RH microcapsules or RC-121 given alone. The combination of microcapsules and analog RC-121 caused a greater inhibition of tumor growth than the single agents. Similar effects were seen when the percent increase in the tumor volume was examined. The inhibition of tumor growth caused by the [D-Trp6]LH-RH microcapsules was greater than that caused by RC-121. The combination of the two agents was again the most effective, resulting in the smallest increase in tumor volume. Tumor weights were much lower in the groups treated with microcapsules or RC-121 alone than in controls. The lowest tumor weights were obtained in the group that received the combination of [D-Trp6]LH-RH microcapsules and RC-121. Similar results were obtained in the second experiment, in which the animals were treated for a period of 83 days with microcapsules containing the somatostatin analog D-Phe-Cys-Tyr-D-Trp-Lys-Val-Cys-Trp-NH2 (RC-160) that released 5 micrograms/day and were injected twice a month alone or in combination with microcapsules of [D-Trp6]LH-RH. Microcapsules of analog RC-160 given alone significantly decreased tumor growth as measured by the final tumor volume, the percentage change from the initial tumor volume, and the reduction in tumor weight. The inhibition of tumor growth induced by [D-Trp6]LH-RH microcapsules was greater than that caused by RC-160. The most striking decrease in tumor weight and volume was obtained in animals treated with microcapsules of [D-Trp6]LH-RH combined with the delayed delivery system for RC-160. The overall response to the combination therapy could reflect the inhibition by somatostatin analogs of the proliferation of prostate cancer cells through a decrease in growth hormone and prolactin release and interference with endogenous growth factors, in addition to the main effect, which is the suppression by [D-Trp6]LH-RH of the growth of androgen-dependent tumor cells. Our results indicate that somatostatin analogs enhance the inhibitory effects of [D-Trp6]LH-RH on the growth of prostate tumors. The administration of somatostatin analogs in combination with microcapsules of [D-Trp6]LH-RH might improve clinical response in patients with advanced prostate carcinoma.
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PMID:Somatostatin analogs as adjuncts to agonists of luteinizing hormone-releasing hormone in the treatment of experimental prostate cancer. 289 Jan 64

A new human medullary carcinoma cell line has been established from a thyroid tumor removed from a 76-year-old female patient. The cultured cells grew in suspension, formed round islands and did not attach to the plastic dish. The doubling time of 48 h is the shortest recorded for C-cell lines. Ultrastructural studies disclosed that the cells had a few short profiles of rough endoplasmic reticulum, numerous ribosomes and polyribosomes, a poorly developed Golgi apparatus and small secretory granules (75 nm in mean diameter). Immunohistochemical staining for somatostatin was positive. These results show that, compared with previously established C-cell lines, this cell line has a rapid growth rate, is morphologically less differentiated, but retains a hormone production potential.
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PMID:Establishment of a new human thyroid medullary carcinoma cell line. Morphological studies. 289 Dec 16

A case of prostatic carcinoma with the cellular patterns of an adenocarcinoma and carcinoid tumor is reported. The tumor contained ultrastructural dense core neuroendocrine granules, and immunoperoxidase staining revealed prostatic acid phosphatase, prostatic-specific antigen, chromogranin, neuron-specific enolase, serotonin, adrenocorticotrophic hormone (ACTH), somatostatin, parathormone, calcitonin, bombesin, and glucagon but no insulin. The patient had exhibited hypercalcemia that may have been related to hormone production by the tumor. The literature on the endocrine aspect of the prostate and its tumor is reviewed.
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PMID:Prostatic carcinoma with endocrine features. A report of a neoplasm containing multiple immunoreactive hormonal substances. 289 Dec 93

Immunohistochemical determinations in tissue specimens of medullary and "undifferentiated" thyroid carcinomas were carried out with antisera against calcitonin, calcitonin-gene related peptide (CGRP), somatostatin, and also thyroglobulin, using the PAP method. All 8 samples of medullary carcinoma stained positive with antisera against calcitonin and CGRP, 7 samples were also positive for somatostatin. Out of 22 cases initially diagnosed as "undifferentiated thyroid carcinoma" 3 revealed positivity for calcitonin, 2 for CGRP, and 1 for somatostatin. Congo red stain for amyloid, performed several years ago in 2 of these 3 cases, had been negative. The patients with medullary carcinoma survived longer than those with "undifferentiated" carcinoma. One patient of the latter group, but with calcitonin, CGRP, and somatostatin immunoreactivity in the tumour tissue, is now alive and well, more than 4 a after initial treatment.
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PMID:Immunohistochemical hormone content in medullary and undifferentiated thyroid carcinoma and prognosis after surgery. 289 52

The growth-inhibiting effects of the long-acting somatostatin analogue Sandostatin on the transplanted Dunning R3327-H androgen-sensitive rat prostate tumor were investigated. Recipient animals were male Copenhagen x Fischer F1 rats (N = 36). When mean tumor volume reached 700 mm3 (20 weeks following transplantation), the rats were divided into four groups: control; Sandostatin (100 micrograms/kg s.c. twice a day); castrate; castrate/Sandostatin. Tumor size was assessed by magnetic resonance imaging 21, 42, 63, 105, and 138 days subsequently. Administration of Sandostatin was interrupted between days 43 and 62. As assessed by transplant volume, Sandostatin caused a moderate (up to 50%) but highly significant (P less than 0.001) suppression of tumor growth in the intact rats; the effect was reversed when drug administration was stopped. In the castrates, in which tumor growth was markedly less than in intact rats, no significant effect of Sandostatin was seen. Analysis of the tumor growth rate demonstrated that Sandostatin led to a 19% reduction (P less than 0.05) in growth rate in intact rats and a 9% decrease (not significant) in castrates. These findings extend previous reports of partial suppression of various types of tumors in vivo with Sandostatin and other somatostatin analogues. Their relevance with regard to the possible use of Sandostatin in the treatment of prostatic carcinoma in humans is discussed.
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PMID:Partial inhibition of the growth of transplanted dunning rat prostate tumors with the long-acting somatostatin analogue sandostatin (SMS 201-995). 289 58

The presence of somatostatin-immunoreactivity in tumor tissue of adrenal pheochromocytoma and thyroid medullary carcinoma identified by peroxidase-antiperoxidase technique is reported in one case of Sipple syndrome. This patient was found to have a high concentration of somatostatin-immunoreactivity in the peripheral blood (40 ng/l, normal 0-20 ng/l). After removal of the tumors, the plasma somatostatin-immunoreactivity fell within normal range (12.5 ng/l). This seems to be the first report of Sipple syndrome that produces somatostatin-immunoreactivity in both: pheochromocytoma and thyroid medullary carcinoma.
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PMID:Coexistence of somatostatin-immunoreactivity in an adrenal pheochromocytoma and a thyroid medullary carcinoma (Sipple syndrome). 290 Jul 71

A case of multiple nonfunctional pancreatic islet cell tumor in multiple endocrine neoplasia type I (MEN I) is reported. The patient was a 41-year-old woman who had a past history of thyroid cancer (papillary carcinoma) and hyperparathyroidism due to parathyroid adenoma. Later, a nonfunctional pituitary tumor and five nonfunctional pancreatic tumors were found simultaneously and the patient was finally diagnosed as having MEN I. Following surgical enucleation, the pancreatic tumors were histopathologically diagnosed as benign islet cell tumors. One of them (tumor 3) exhibited a solid nodular pattern while the others showed gyriform patterns. They were divided histochemically and immunohistochemically into three types: two (tumors 1 and 2) produced a single hormone (glucagon), one (tumor 3) produced five (insulin, glucagon, somatostatin, gastrin and pancreatic polypeptide) and the remaining two (tumors 4 and 5) produced two (glucagon and pancreatic polypeptide). Electron microscopically, three types of endosecretory granules were found in the tumor cells of tumor 3 but only one type was found in tumor 4. However, in the tumor 4 extract, glucagon, pancreatic polypeptide, C-peptide, somatostatin, vasoactive intestinal peptide and growth hormone releasing factor were detected by radioimmunoassay. These findings suggest that these pancreatic tumors were both multicellular and multihormonal.
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PMID:Multiple nonfunctional pancreatic islet cell tumor in multiple endocrine neoplasia type I. A case report. 290 67


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