Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P01350 (gastrin)
 9,683 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An endocrine cell carcinoma of the extrahepatic bile duct in a 79-year-old man is described. The patient had complaints of jaundice and epigastric pain due to a small tumor located at the confluence of the common hepatic duct with the cystic duct. Microscopically, the tumor showed a well differentiated tubular adenocarcinoma and was confined to the mucosa. Numerous tumor cells showed argyrophil and/or argentaffin reactions. Immunoperoxidase staining revealed that the tumor tissue contained somatostatin-, gastrin-and serotonin-immunoreactive cells. From these findings the tumor was diagnosed as endocrine cell carcinoma. Four years later he remains well without any evidence of recurrence or metastasis. The histogenesis of endocrine cells in the biliary tract is briefly discussed.
 ...
PMID:Endocrine cell carcinoma of extrahepatic bile duct. 352 8

A series of 30 gastric endocrine tumours has been revised in the light of available available cytologic and clinicopathologic information. Among 24 well differentiated endocrine tumours-16 with and 8 without chronic atrophic gastritis (CAG)-3 gastrin cell tumours have been distinguished from 21 argyrophil carcinoids, 15 of which showed light- and/or electronmicroscopy patterns of enterochromaffin-like (ECL) cell tumours, 2 of EC cell tumours and 1 of D1/P cell tumour. One case of mixed carcinoid/adenocarcinoma and 5 cases of endocrine carcinomas, 4 poorly and 1 moderately differentiated, were also identified. Achlorhydria, due to type A CAG or HCl-suppressing drugs, and bombesin hyperstimulation are among possible factors inducing G cell hyperfunction and/or hyperplasia. Hypergastrinaemia is among causative agents of argyrophil ECL cell hyperplasias and, possibly, of tumours of the oxynticopeptic mucosa, while chronic inflammation and gland atrophy with or without concomitant hypergastrinaemia are important factors in inducing both hyperplastic and tumour argyrophil growths in CAG mucosa.
 ...
PMID:Gastric carcinoids and related endocrine growths. 353 79

The effects of coffee on exocrine pancreatic secretion are unknown but may be important, because a link between chronic stimulation of pancreatic secretion and experimental chemical carcinogenesis and an association between coffee drinking and human pancreatic adenocarcinoma have been reported. We measured exocrine pancreatic trypsin and gastric acid secretions collected through orogastroduodenal tubes and serum gastrin in eight non-coffee drinkers and eight coffee drinkers. During fasting, after one interdigestive cycle control period, one of four 250-ml samples [plain water, water plus caffeine (4.6 mg/kg), decaffeinated coffee (127.9 mg/kg), caffeinated coffee (127.9 mg/kg)] was administered through the orogastric tube. Caffeinated and decaffeinated coffee (p = 0.008), caffeine (p = 0.03), and an unidentified substance(s) in coffee other than caffeine (p = 0.008) were associated with increased interdigestive exocrine pancreatic trypsin secretion. In addition, we also confirmed that coffee and caffeine stimulated gastric acid secretion (p = 0.02) and decaffeinated coffee raised serum gastrin concentrations (p = 0.005). If an association between coffee and pancreatic carcinogenesis exists, chronic stimulation of the exocrine pancreas by secretagogues could result in a gland susceptible to carcinogenesis.
 ...
PMID:The acute effects of coffee and caffeine on human interdigestive exocrine pancreatic secretion. 357

Two patients with intestinal metaplasia of the stomach, whose distribution was exclusively confined to the fundic gland area, are presented herein. The first, a 51-year-old male, had been treated for pernicious anemia for 14 years when he was found to have gastric cancer. His serum gastrin level was quite high, whereas his gastric acid output was markedly low. The polypoid cancer in the fornix of the stomach, which had been removed endoscopically, revealed tubular adenocarcinoma with its invasion limited to the mucosa. The resected stomach showed no residual carcinoma but had numerous minute foci of intestinal metaplasia, diffusely distributed but exclusively confined to the fundic gland area, by macroscopic observation using the leucine aminopeptidase-alkaline phosphatase double staining method. The intestinal metaplasias were all of the complete type, and the parietal and chief cells were almost completely lost. The second patient, a 76-year-old male without pernicious anemia, underwent total gastrectomy for two polypoid cancers in the body of the stomach. The resected specimens, in addition to two hyperplastic polyps in the transitional area, showed the same distribution of intestinal metaplasia as seen in the first patient.
 ...
PMID:Intestinal metaplasia of the stomach confined to the fundic gland area. Report of two cases. 368 36

The effects of combined administration of propranolol and tetragastrin on gastric acid secretion and the incidence and histological types of gastric adenocarcinomas induced by N-methyl-N'-nitro-N-nitrosoguanidine were investigated in inbred Wistar rats. Prolonged administration of tetragastrin, 1 but not 0.2 mg/kg body weight in depot form after treatment with N-methyl-N'-nitro-N-nitrosoguanidine significantly reduced the incidence of adenocarcinoma of the glandular stomach. The adenocarcinomas that did develop in rats treated with the higher dose of tetragastrin had high mucin-producing activity and showed little or no typical glandular structure. A combination of propranolol (2 mg/kg) and tetragastrin (1 mg/kg) did not influence the inhibitory effect of gastrin on gastric carcinogenesis. However, concomitant administration of propranolol (2 mg/kg) and tetragastrin (0.2 mg/kg) caused a significant increase in gastric acid secretion and a reduction in the incidence of gastric carcinomas. With this treatment, the incidence of adenocarcinoma was similar to that of treatment with tetragastrin (1 mg/kg). Histological examinations showed that like the cancers in control rats, the adenocarcinomas induced in these rats were all highly differentiated.
 ...
PMID:Enhancement by propranolol of the inhibitory effect of tetragastrin on gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine in Wistar rats. 379 Nov 97

We present the first reported case (to our knowledge) of duodenal gangliocytic paraganglioma (GPG) to be associated with an underlying invasive adenocarcinoma. The patient, a 71-year-old man, presented with epigastric tenderness and was found to have metastatic adenocarcinoma in two regional lymph nodes. Immunohistochemical evaluation of the GPG demonstrated positive staining for gastrin, glial-fibrillary acidic protein, glucagon, neuron-specific enolase, pancreatic polypeptide, S100 protein, somatostatin, and substance P. The clinical, pathologic, and immunohistochemical features of GPG are discussed, with a review of the literature.
 ...
PMID:Gangliocytic paraganglioma associated with duodenal adenocarcinoma. Case report with immunohistochemical evaluation. 380 Jun 4

A morphologic, histochemical, and immunocytochemical study of 20 cases of pure gastrointestinal carcinoids, adenocarcinomas, and mixed neoplasms composed of both elements, so-called composite carcinoma-carcinoid tumors (CCC), was undertaken in order to correlate the morphologic patterns with the immunocytochemical localization of carcinoembryonic antigen (CEA), serotonin, and a battery of polypeptide hormones (calcitonin, glucagon, insulin, gastrin, somatostatin, and adrenocorticotropin [ACTH]). Paraffin sections from five pure carcinoids, seven pure adenocarcinomas, and eight CCC from the stomach, small bowel, appendix, and colon were studied with mucicarmine, silver impregnation stains, and a peroxidase-anti-peroxidase technic. Of the eight CCC, all were mucin positive, four were argyrophilic, and three were argentaffin positive. CEA was present in all eight, serotonin in seven, and calcitonin in one. No other neurohormonal peptides were demonstrated. The distribution of serotonin and CEA generally corresponded to the morphologic pattern, but discordance was observed in two cases, i.e., serotonin was not always localized to areas of carcinoid and CEA not always confined to areas of carcinoma. All five pure carcinoids demonstrated intracytoplasmic localization of serotonin, whereas none contained intracytoplasmic CEA. In two cases, CEA was present within acinar lumens only. The seven colonic adenocarcinomas were argyrophil and argentaffin negative. All contained CEA within the cytoplasm and in gland lumens. None contained serotonin. None of the neurohormonal peptides was localized in either pure adenocarcinomas or carcinoids. This study reveals that among gastrointestinal neoplasms displaying morphologic patterns of adenocarcinoma and carcinoid, immunocytochemical localization of CEA and serotonin confirms their bidirectional differentiation and justifies the designation "composite carcinoma-carcinoid."
 ...
PMID:Composite carcinoma-carcinoid tumors of the gastrointestinal tract. A morphologic, histochemical, and immunocytochemical study. 389 86

Gastrin is trophic for normal gastric and colonic mucosa. We examined the potential trophic effects of chronic gastrin administration on the growth of mouse colon adenocarcinoma (MC-26). Thirty-three mice bearing transplantable MC-26 colon cancers were treated with varying doses (125, 250, or 500 micrograms/kg/day) of pentagastrin. Significant increases in tumor weight and DNA content were observed. Fundic mucosal weight and DNA content in these mice showed a dose-related trophic response. The weight of control fundic mucosa was 10 mg and rose to 20, 45, and 65 mg with increasing doses of gastrin. The DNA content of control fundic mucosa was 155 micrograms and rose to 220, 340, and 480 micrograms as the dose of gastrin was increased. Pentagastrin stimulated growth of the MC-26 colon cancer, but the threshold for gastrin-stimulated tumor growth was different from that of normal mucosal growth. The hyperplastic response of the fundic mucosa was increased by increasing gastrin doses; whereas, colon cancer hyperplasia was maximal at the lowest dose tested (125 micrograms/kg/day) and did not increase further with increasing doses of hormone. Mice bearing gastrin-stimulated tumors died at a significantly greater rate than did mice with untreated tumors (80% of control mice and none of the treated mice were alive at day 55). The effects of gastrin treatment on the growth of MC-26 colon cancer persist after treatment is discontinued; mice with tumors that were treated with gastrin for either 7 or 14 days and in which the treatment was stopped were all dead by 35 or 28 days, respectively, after the end of treatment.
 ...
PMID:Gastrin stimulates growth of colon cancer. 395 54

Five normal and four malignant human colon epithelial cultures initiated and maintained in our laboratories as well as the standardized in vitro human adenocarcinoma cell line HT-29 were plated in multiwell plates and incubated at 37 degrees C for 72 hours with either phosphate-buffered saline solution or pentagastrin (5 micrograms/ml). Pentagastrin stimulated normal cells to increase (p less than 0.05) in number by an average of 65 percent compared with saline control cells, whereas malignant cells increased an average of 59 percent compared with control cells. There was no difference in the magnitude of trophic effect between the normal and malignant cells. Further studies are indicated to elucidate the role of gastrin in either initiating, promoting, or both, the growth of carcinoma of the colon.
 ...
PMID:Pentagastrin stimulates in vitro growth of normal and malignant human colon epithelial cells. 396 39

The effects of prolonged administration of tetragastrin from the beginning of intrarectal instillation of 1 ml of 0.25% N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) and after MNNG-treatment on the incidence and histology of colonic tumors were compared in inbred Wistar rats. In week 35 prolonged administration of testragastrin in depot form from the beginning of MNNG-treatment resulted in a significant reduction in the incidence of colonic tumors and a significant increase in the incidence of mucinous adenocarcinoma, unlike the well-differentiated adenocarcinoma produced in controls without gastrin. In contrast, prolonged administration of tetragastrin after MNNG-treatment had little or no influence on the incidence, size or histology of colonic tumors. Thus tetragastrin had no promoting effect on colonic tumors.
 ...
PMID:Gastrin has no promoting effect on chemically induced colonic tumors in Wistar rats. 401 15


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>