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

Ductal pancreatic cancers were induced with N-nitrosobis(2-oxopropyl)amine (BOP) in female Syrian golden hamsters. The animals were then treated for 2 months with 5-fluorouracil (5-FU) and with sustained delivery systems of the LH-RH agonist D-Trp-6-LH-RH antagonist (Ac-D-Nal(2)'-D-Phe(4Cl)2-D-Pal(3)3-D-Cit6,D-Ala10)LH- RH(SB-75) and somatostatin analog D-Phe-Cys-Tyr-D-Trp-Lys-Val-Cys-Trp-NH2 (RC-160), and with some combinations thereof. In the first experiment, the treatment with D-Trp-6-LH-RH plus 5-FU resulted in 52% inhibition of tumorous pancreas weight, a smaller number of tumor nodules on histology, a marked increase of programmed cell death (apoptosis) and a reduced number of AgNOR (argyrophilic nucleolar organizer region) in tumor cells, as compared with controls. The inhibitory effects of this combination were greater than those obtained with 5-FU and D-Trp-6-LH-RH treatment alone. In the 2nd experiment, a 76% inhibition of tumorous pancreas weight, a significant decrease in the number of tumor nodules, an increased amount of stroma, enhanced apoptosis and decreased AgNORs were observed after therapy with somatostatin analog RC-160 plus 5-FU. Most of these tumor inhibition parameters were superior to those in the group treated with 5-FU alone, and in some cases slightly better than those treated with RC-160 alone. Both LH-RH antagonist SB-75 and somatostatin analog RC-160 caused a significant inhibition of tumors, and their combination had the strongest tumor inhibitory effect, with the best survival of animals, the lowest tumorous pancreas weight and the highest apoptosis index among groups. Our results suggest that the combinations of LH-RH analogs with somatostatin analogs or of either type of analog with 5-FU may be superior to single agents in the therapy of pancreatic cancer.
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PMID:Effect of combination treatment with analogs of luteinizing hormone-releasing hormone (LH-RH) or somatostatin and 5-fluorouracil on pancreatic cancer in hamsters. 167 45

Proliferation of adipose tissue adjacent to intrasplenic transplants of whole isogeneic neonatal rat pancreas has consistently been noted. In this study over a period of 18 months there was a progressive increase in the amount of fatty tissue in the vicinity of surviving transplants. Immunohistochemistry demonstrated the presence of insulin, glucagon, somatostatin and pancreatic polypeptide within islet cells in long term grafts. Electron microscopy demonstrated a close association between islets and lipid droplets. Ductal elements within the transplants survived and showed close association with endocrine cells, but exocrine pancreatic tissue degenerated rapidly. Radioimmunoassay of extracts from surviving transplants in isogeneic rats confirmed the presence of high levels of insulin and glucagon after transplantation. In contrast, allogeneic intrasplenic transplants of rat pancreas failed to survive and showed no evidence of adipose tissue proliferation. Furthermore, isogeneic intrasplenic transplants of both adult rat fat and adrenal gland also failed to demonstrate adipocyte proliferation. It would appear that the presence of both adipocytes and pancreatic endocrine cells, particularly B cells, are required for the proliferation of adipocytes at the graft site.
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PMID:A histological study of intrasplenic transplanted neonatal rat pancreas and of adjacent adipose tissue proliferation. 703 13

To determine the variety of chemotherapy drugs administrable for malignant pancreatic neoplasm as a result of typification with endoscopic ultrasonography-fine needle aspiration (EUS-FNA). A retrospective assessment, in one center, over a period of 1 year. Only malignant pancreatic neoplasm diagnosed by EUS-FNA was recorded. Benign (serous cystic neoplasm) and potentially malignant lesions (mucinous cystic neoplasm and intraductal papillary-mucinous neoplasm) were excluded. Medical data were recorded and Oncological Pharmacy records were studied. Ductal adenocarcinoma were detected in 17 patients (N = 17/22), 2 of them with adenocarcinoma in signet ring and 1 with mucinous adenocarcinoma. The primary therapies used were as follows: Whipple pancreaticoduodenectomy (3), biliary stent by endoscopic retrograde cholangiopancreatography (3), radiological transhepatic percutaneous stent (2), intestinal bypass (2), and a gastric stent (1). The adjuvant drugs used were gemcitabine (10), erlotinib (3), and cetuximab (1), and also radiotherapy was used (1). An unresectable squamous cell carcinoma (N = 1) of the tail was detected, and gemcitabine + vinorelbine + fluorouracil + cisplatin used. Nonfunctioning neuroendocrine tumors were seen in 3 (N = 3) cases and long-acting somatostatin analogues were used (1); the remaining 2 patients showed resectable tumors and were resected accordingly. A metastasis to the pancreatic head in a hepatocellular carcinoma was found in 1 patient (N = 1), allowing specific treatment with sorafenib. Histopathologic analysis with EUS-FNA implies a variety of different treatments. Optimal management was achieved as a result of improved diagnosis, with the advent of new molecular genetic diagnostic methods facilitating the design of specific new therapy and neoadjuvant targeting strategies.
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PMID:Types of pancreatic cancer in EUS-FNA and chemotherapy. 2001 88

Glucagon-like-peptide-1 (GLP1) analogs may induce thyroid or pancreatic diseases in animals, raising questions about their use in diabetic patients. There is, however, controversy regarding expression of GLP1 receptors (GLP1R) in human normal and diseased thyroid and pancreas. Here, 221 human thyroid and pancreas samples were analyzed for GLP1R immunohistochemistry and compared with quantitative in vitro GLP1R autoradiography. Neither normal nor hyperplastic human thyroids containing parafollicular C cells express GLP1R with either method. Papillary thyroid cancer do not, and medullary thyroid carcinomas rarely express GLP1R. Insulin- and somatostatin-producing cells in the normal pancreas express a high density of GLP1R, whereas acinar cells express them in low amounts. Ductal epithelial cells do not express GLP1R. All benign insulinomas express high densities of GLP1R, whereas malignant insulinomas rarely express them. All ductal pancreatic carcinomas are GLP1R negative, whereas 6/20 PanIN 1/2 and 0/12 PanIN 3 express GLP1R. Therefore, normal thyroid, including normal and hyperplastic C cells, or papillary thyroid cancer are not targets for GLP1 analogs in humans. Conversely, all pancreatic insulin- and somatostatin-producing cells are physiological GLP1 targets, as well as most acini. As normal ductal epithelial cells or PanIN 3 or ductal pancreatic carcinomas do not express GLP1R, it seems unlikely that GLP1R is related to neoplastic transformation in pancreas. GLP1R-positive medullary thyroid carcinomas and all benign insulinomas are candidates for in vivo GLP1R targeting.
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PMID:Glucagon-like-peptide-1 receptor expression in normal and diseased human thyroid and pancreas. 2521 24