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)

Immunohistochemistry was performed on biopsies of columnar mucosa from 11 patients with Barrett's esophagus and 11 patients with columnar mucosa in the cranial esophagus, the "inlet patch." Both epithelia contained endocrine cells, immunoreactive to antisera against serotonin, glucagon, somatostatin, and pancreatic polypeptide; the specialized mucosa of Barrett's esophagus contained, in addition, neurotensin-immunoreactive cells, and in the mucosa of an inlet patch we found a gastrin cell. These findings are not compatible with some of the current theories on the origin of these epithelia. The mucosa of the inlet patch has been considered to consist of heterotopic gastric mucosa. The mucosa of the adult human stomach, however, does not contain glucagon cells. These cells are only present in the early embryonic stomach, and they disappear during embryonogenesis. According to our findings, the mucosa of the inlet patch therefore represents embryonic gastric mucosa. The specialized columnar epithelium of Barrett's esophagus has been considered to have evolved from gastric mucous neck cells. However, although glucagon cells are a feature of the embryonic stomach, neurotensin-immunoreactive cells have not been found in the gastric mucosa. Our study suggests that the specialized columnar epithelium of Barrett's esophagus originates from a very immature multipotent gastrointestinal stem cell.
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PMID:Distinct immunohistochemical findings in columnar epithelium of esophageal inlet patch and of Barrett's esophagus. 229 98

In order to characterize the differentiation of endocrine cells present in Barrett's oesophagus and to determine if they express a single or multiple hormonal pattern, endoscopic biopsies were taken from both the lesion and the fundus of 45 patients and studied at the light microscopical level. Conventional histology revealed three different epithelial patterns: gastric atrophic fundic, intestinal and junctional. A mixture of these patterns was present in 28 cases (62%) and the single type was identified in 17 cases (38%). The use of three silver staining methods and antibodies to human chromogranins allowed us to identify numerous endocrine cells in all but 1 case. Eleven sera against all the most common hormones stored in the endocrine cells of the gut were used to identify the main products of the cells. The following immunoreactivities were identified: 5-hydroxytryptamine (5-HT) (in 75% of the studied cases), somatostatin (87%), motilin (31%), pancreatic polypeptide (PP) (20%), glucose-dependent insulinotropic polypeptide (20%), gastrin (15%), glucagon (15%), peptide tyrosine tyrosine (13%), secretin (7%) and neurotensin (2%). No cholecystokinin-immunoreactive cells were identified. Our results indicated that, in Barrett's epithelium, both gastric and intestinal endocrine cells differentiate, in accordance with the variability of differentiation in the non-endocrine cells present in the different types of columnar epithelium. These findings provide support for the conclusion that Barrett's epithelium arises from a pluripotential stem cell capable of both gastric and intestinal differentiation.
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PMID:A mixed pattern of endocrine cells in metaplastic Barrett's oesophagus. Evidence that the epithelium derives from a pluripotential stem cell. 244 38

Barrett's epithelium refers to the presence of ectopic mucosal types in the squamous-lined oesophagus. Previous studies have documented argentaffin and argyrophil-positive cells as well as gastrin-like immunoreactivity in oesophageal tissue extracts from patients with Barrett's mucosa. In the present study, 125 oesophageal biopsies obtained under direct vision at endoscopy from 22 patients with Barrett's oesophagus were systematically studied using fluorescence and peroxidase antiperoxidase single and double-staining immunocytochemical methods employing highly specific antibodies to localize the following peptide-containing cell types in Barrett's mucosa: gastrin, somatostatin, gastric inhibitory polypeptide, motilin, neurotensin and pancreatic glucagon. In addition, EC cells were localized using a cytochemical silver staining method. The results of this study indicate that EC cells and gastrin- and somatostatin-containing endocrine cells are detectable in Barrett's epithelium.
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PMID:Regulatory peptides in Barrett's oesophagus. 286 40

This study was undertaken to assess the prevalence and characteristic hormonal profile of endocrine cells in Barrett's mucosa and to determine to what extent this profile was shared by endocrine cells of adenocarcinomas arising therefrom. In addition, lower oesophageal carcinomas, not associated with columnar metaplasia, were examined to see if they exhibited a different hormonal profile. The patients studied comprised 43 who had had multiple oesophageal biopsies. 35 who had had oesophagogastric resection for adenocarcinoma arising in Barrett's mucosa and 26 in whom the resection showed no metaplastic epithelium adjacent to tumour. Argyrophil cells were present in 90% of biopsies and resections of Barrett's mucosa combined, irrespective of the histological type of metaplastic epithelium. By immunocytochemistry the most frequently identified substance in mucosal endocrine cells was serotonin (82%) followed by somatostatin (54%), secretin (22%) and pancreatic polypeptide (17%). Gastrin, bombesin, cholecystokinin, ACTH and substance P were not identified in metaplastic mucosa in any case. The difference in expression of serotonin by endocrine cells of tumours arising in Barrett's mucosa (31%) and those not (3.8%) was statistically significant (P less than 0.0186). Carcinoembryonic antigen (CEA) was demonstrated in 60% of oesophageal carcinomas, both endocrine positive and endocrine negative. Focal CEA expression was seen in 4.6% of biopsies and 14% of Barrett's mucosa adjacent to tumour. These results indicate a higher prevalence of endocrine cells in Barrett's mucosa than hitherto documented and suggest that serotonin may be a useful marker in distinguishing between primary oesophageal and putative gastric cancers at the gastro-oesophageal junction. The identification of CEA in oesophageal columnar epithelium is of little value in predicting the development of malignancy.
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PMID:The relationship of endocrine cells, dysplasia and carcinoembryonic antigen in Barrett's mucosa to adenocarcinoma of the oesophagus. 288 73

Four cases of esophageal carcinoma arising in metaplastic Barrett's epithelium are presented in which multidirectional differentiation was demonstrated by light and/or electron microscopy and immunohistochemistry. All tumors and adjacent mucosa produced both neutral and acidic mucins, as well as one or more hormones indigenous to the gut, including gastrin, bombesin, substance P, somatostatin, and serotonin. Gastrin and somatostatin were the peptides most frequently identified in the tumors, while somatostatin and serotonin predominated in Barrett's epithelium. Ultrastructurally, neurosecretory-type granules, 80-250 nm in diameter, were present in 2 cases; squamous features also were present in one of these cases. One patient displayed hypertrophic osteoarthropathy, which disappeared after the tumor was resected. These cases represent the majority of the Barrett-associated carcinomas in our material. Compared to the "pure" esophageal adenocarcinomas not included in this report, these tumors behaved more aggressively, with wider local involvement and nodal and systemic metastases at the time of presentation. The incidence of multidifferentiation in esophageal carcinomas is not known nor is its possible significance, particularly with regard to tumors arising in metaplastic epithelium. This group may merit further study to detect true differences, if any, between these esophageal carcinomas and their apparently more common counterparts.
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PMID:Carcinoma with multidirectional differentiation arising in Barrett's esophagus. 613 8

While pancreatic metaplasia has been observed in gastric mucosa of patients with chronic gastritis, it has not been described in ectopic gastric mucosa. We have identified focal clusters of cells resembling pancreatic acinar cells (CPACs) in 11 of 350 biopsies of Barrett's mucosa from 120 patients with Barrett's esophagus enrolled in a clinical efficacy trial of omeprazole versus ranitidine for treatment of gastroesophageal reflux disease. Three additional cases from our surgical files were also studied. Immunoreactivity for trypsin and chymotrypsin was present in the CPACs of all 14 cases, while stains for alpha-amylase and lipase were each positive in 12 of 13. A few cells in the CPACs were also positive for chomogranins (12 of 13 cases), serotonin (seven of 13 cases), somatostatin (three of 12), gastrin (four of 11), and pancreatic polypeptide (two of 13). No staining was seen for insulin or glucagon. Ultrastructural studies performed in one case showed features of pancreatic exocrine and endocrine (PP-type) cells in cells within CPACs. These results collectively indicate that the CPACs are aggregates of true pancreatic acinar cells admixed with a few endocrine cells. This pancreatic parenchyma in Barrett's mucosa is most likely of metaplastic origin and could be derived from the transitional zone cells or from pluripotent stem cells in the esophageal mucosa or from metaplasia of mucus cells. While the development of pancreatic metaplasia in Barrett's esophagus appears to be unrelated to drug therapy, the clinical relevance of this distinctive histological finding needs further investigation.
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PMID:Pancreatic metaplasia in Barrett's esophagus. An immunohistochemical study. 757 75

Background. Somatostatin receptors (SSTRs) are over-expressed in several tumors making it possible for imaging with labelled SSTR. A previous study showed feasibility to image oesophageal cancer with SSTR analogue (99m)Tc-depreotide. Purpose. (1) To investigate expression of the SSTRs in different types of esophageal carcinoma and (2) to correlate such an expression with (99m)Tc-depreotide uptake in these lesions. Material and Methods. Total 28 patients (17 with esophageal cancer and 11 with Barrett's esophagus) were examined with (99m)Tc-depreotide scintigraphy. The SSTR2A, SSTR2B, SSTR3, and SSTR5 were analyzed immunohistochemically in the lesion samples. Results. Among the patients with adenocarcinoma 10/11 expressed different amounts of SSTRs, while SSTRs were absent in 5/6 patients with Squamous cell carcinoma (Sqcc). There was no correlation neither between the (99m)Tc-depreotide uptake and the amount of SSTRs nor between the amount of SSTRs and differentiation grade of the tumor. Conclusions. (1) SSTRs are expressed in esophageal carcinoma and more abundantly so in adenocancer specimens; (2) in vivo (99m)Tc-depreotide uptake does not obviously correlate with the immunohistochemically detection of SSTRs of different subtypes in esophageal carcinoma.
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PMID:Quantitative assessment of (99m)tc-depreotide uptake in oesophageal cancer and precursor conditions and its reflection in immunohistochemically detected somatostatin receptors. 2255 May 83

Appropriate management of Helicobacter pylori infection of the human stomach is evolving and remains a significant clinical challenge. Acute infection results in hypochlorhydria, whereas chronic infection results in either hypo- or hyperchlorhydria, depending upon the anatomic site of infection. Acute hypochlorhydria facilitates survival of the bacterium and its infection of the stomach. Interestingly, most patients chronically infected with H. pylori manifest a pangastritis with reduced acid secretion due to bacterial virulence factors, inflammatory cytokines, and various degrees of gastric atrophy. While these patients are predisposed to develop gastric adenocarcinoma (~1%), there is increasing evidence from population studies that they are also protected from gastroesophageal reflux disease (GERD), Barrett's esophagus (BE), and esophageal adenocarcinoma (EAC). Eradication of H. pylori, in these patients, may provoke GERD in predisposed individuals and may be a contributory factor for the rising incidence of refractory GERD, BE, and EAC observed in Westernized societies. Only ~10% of chronically infected patients, mainly the young, manifest an antral predominant gastritis with increased acid secretion due to a decrease in somatostatin and increase in gastrin secretion; these patients are predisposed to develop peptic ulcer disease. H. pylori-induced changes in acid secretion, in particular hypochlorhydria, may allow ingested microorganisms to survive transit through the stomach and colonize the distal intestine and colon. Such perturbation of gut microbiota, i.e. dysbiosis, may influence human health and disease.
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PMID:Helicobacter pylori-Induced Changes in Gastric Acid Secretion and Upper Gastrointestinal Disease. 2812 56