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

This study deals with the effects of gastrin on the incidence of gastric tumors in rats induced by N-methyl-N'-nitro-N-nitrosoguanidine. Inbred Basel-Wistar rats received N-methyl-N'-nitro-N-nitrosoguanidine in drinking water (50 micrograms/ml for 32 weeks) in order to produce gastric carcinoids. A treatment with s.c. injection of pentagastrin (300 micrograms/kg, once daily for 4 weeks) was started at the beginning of N-methyl-N'-nitro-N-nitrosoguanidine treatment simultaneously, on the 4th, 8th, 16th, and 32nd week after start of N-methyl-N'-nitro-N-nitrosoguanidine treatment, respectively. At autopsy, from the 55th to 60th week after start of the experiment, only in the eighth-week group of gastrin-treated rats was the incidence of gastric carcinoid significantly higher than in the gastrin-untreated group of rats receiving N-methyl-N'-nitro-N-nitrosoguanidine alone. The incidence of adenocarcinoma in the glandular stomach also was high only in the fourth-week group of gastrin-treated rats. However, these effects could not be seen in other gastrin-treated or untreated groups of rats. The data suggest that gastrin treatment in the early stage of rat stomach carcinogenesis by N-methyl-N'-nitro-N-nitrosoguanidine is effective in increasing the development of gastric tumors.
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PMID:Enhanced effect of gastrin on rat stomach carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine. 706 97

Gastrin was administered several times to mice with transplantable hepatoma, sarcomas, colon adenocarcinoma and adenocarcinoma of small intestine. Injections of gastrin stimulated the growth of colon adenocarcinoma in mice but not of the other tumors tested. Dependence upon gastro-intestinal hormones of "spontaneous" carcinogenesis in gastro-intestinal tract and the growth of many gastro-intestinal pancreatic and liver tumors is suggested. This hormone dependence could be used for the treatment and prophylaxis of some tumors of the gastro-intestinal tract.
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PMID:Dependence of gastro-intestinal tumors on gastro-intestinal hormones: pentagastrin stimulates growth of transplanted colon adenocarcinoma in mice. 721 23

A total of 30 inbred Wistar rats were orally administered 70 microgram/ml solution of N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) for 35 weeks and then tap water for the following 20 to 30 weeks. Four of the 20 females and two of ten males developed carcinoids in the glandular stomach, but no metastasis could be found. Carcinoids developed most frequently in the fundic portion along the greater curvature. Histologically, these tumors were medullary anaplastic carcinomas containing two different endocrine cell populations. The first cell type was argentaffin having the electron-dense, somewhat pleomorphic secretory granules (437-810 nm) and the second type was argyrophil having round granules with a dense core and a pale halo (550 nm). None of these tumors showed endocrine immunoactivity for gastrin, somatostatin, insulin, glucagon, and enkephalin. One of these gastric tumors developed into scirrhous carcinoma, but differentiated adenocarcinoma could not be seen in the glandular stomach.
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PMID:Induction of carcinoids in the glandular stomach of rats by N-methyl-N'-nitro-N-nitrosoguanidine. 724 Mar 40

I have reviewed Barrett's esophagus in the light of recent advances. Barrett's esophagus is not as rare as general practitioners and gastroenterologists think. Present evidence suggests that the disorder is acquired as a complication of reflux esophagitis. The epithelium is prone to inflammation, ulceration, bleeding, stricture, and adenocarcinoma. The epithelium may contain chief and/or oxyntic cells; pepsinogens are demonstrable by agar gel electrophoresis in the mucosa and Barrett's epithelium secretes pepsin and acid, and also contains gastrin by radioimmunoassay. Pertechnetate scintigraphy in the screening of these patients may be helpful. In the treatment of these patients, anti-reflux operations stop the progressive ascent of the heterotopic epithelium, prevent inflammation, and stricture formation, and lead to healing of the mucosa. Cimetidine and bethanechol along with the conventional medical regimen for reflux esophagitis may also be helpful in healing the inflamed mucosa. Adenocarcinoma in Barrett's epithelium may have a better prognosis than gastric carcinoma which invade the esophagus or than esophageal carcinoma.
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PMID:Barrett's esophagus: an old entity rediscovered. 733 15

The only gastrin-dependent gastric endocrine cells are the fundic ECL cells. Excessive hypergastrinemia stimulates ECL cell proliferation in animals and man. The growth of other gastric endocrine cells is regulated by the gastric pH. Hypergastrinemia in man results in diffuse and linear hyperplasia of the ECL cells, while micronodular hyperplasia is correlated to the grade of corpus gastritis. ECL cell dysplasia and gastric carcinoids in man have been observed only in patients with gastrinoma as part of the MEN I syndrome and with pernicious anemia. Gastrin dependence of GI adenocarcinoma has not been established. Experimental findings may be explained by the presence of gastrin receptors and the role of gastrin as an autocrine growth factor. Epidemiological data do not support gastrin dependence of carcinoma of the stomach, the pancreas and the colon.
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PMID:The consequences of hypergastrinemia. 750 28

Patients with pernicious anemia have an estimated risk of gastric adenocarcinoma that ranges from three- to fivefold greater than that of the general population. It has been reported that NK cells may be involved in immunosurveillance against tumor spread. The natural killer cell activity of peripheral blood mononuclear cells was analyzed in 22 patients with pernicious anemia and in 19 healthy controls. Levels of natural killer cell activity against K-562 target cells were similar in control subjects and patients, regardless of gastrin levels and time elapsed since diagnosis. According to quantitative flow cytometry analysis, similar percentages of phenotypically defined NK cells (CD16+) were found in peripheral blood mononuclear cells from patients and healthy controls. Our results show that in pernicious anemia patients, the percentage of NK cells present in peripheral blood mononuclear cells and their lytic activity are normal.
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PMID:Natural killer cell activity in patients with pernicious anemia. 762 80

Diffusely invasive tumors occurred in the stomach of a 9-year-old female cougar (Felis concolor) from a zoo in Japan. The tumors consisted of tubular adenocarcinoma cells, and had infiltrative growth to the submucosa and muscularis propria. Tumor cells were positive for carcinoembryonic antigen (CEA), lysozyme, epithelial membrane antigen (EMA), gastrin, alpha-1-fetoprotein (AFP), keratin, and B72.3. Mucin-like materials occurred within cytoplasmic vacuoles.
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PMID:Gastric adenocarcinoma in a cougar (Felis concolor). 776 May 1

This study was carried out to develop a scoring system for the diagnosis of gastric adenocarcinoma (GAC). A total of 686 subjects, 150 patients with GAC, 182 with gastric ulcer, 127 with duodenal ulcer, and 227 subjects with negative findings, were enrolled. Analysis of the likelihood ratio (LR) showed that patients with advanced age, ulcer in the stomach, low serum levels of pepsinogen I (PGI), low PGI x gastrin values, and low PGI/gastrin ratio were likely to have GAC. Of these indicators, the serum PGI level had the greatest weight, with a LR of 7.59 for the group with a level < 30 ng/ml. A scoring system combining serum PGI level, Helicobacter pylori seropositivity, and gastric ulcer status was derived, using a logistic regression model. This scoring system was found to be better than any one-parameter criterion for diagnosing GAC after evaluation by the area under the receiver operating characteristic curve (0.84; 95% confidence interval, 0.81-0.88) or by specificity-fixed sensitivity (sensitivity 0.82 at specificity 0.72, sensitivity 0.87 at specificity 0.66, sensitivity 0.96 at specificity 0.44). This scoring system may be potentially useful as a new model for the noninvasive diagnosis of GAC in the future.
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PMID:Diagnosis of gastric adenocarcinoma using a scoring system: combined assay of serological markers of Helicobacter pylori infection, pepsinogen I and gastrin. 777 44

There is now clear-cut evidence that polypeptide growth factors control the proliferation of the normal gastrointestinal mucosa. Epidermal growth factor (EGF) stimulates normal growth throughout the gastrointestinal tract, and accelerates the healing of ulcerated epithelium. While the effects of gastrin were at first thought to be similarly widespread, the gastrin target now appears to be restricted to the enterochromaffin-like cells in the stomach. Isolated reports suggest that several other hormones, including fibroblast growth factor and the insulin-like growth factors, have similar proliferative effects. In contrast, indirect evidence suggests that somatostatin and transforming growth factor-beta inhibit the growth of the gastrointestinal mucosa. The same growth factors profoundly affect the growth of some gastrointestinal carcinomas. Prolonged hypergastrinaemia increases the risk of development of gastric endocrine tumours, but has no effect on the incidence of gastric adenocarcinoma. Gastrin also stimulates the in vivo growth of 50% of gastric and colorectal carcinoma xenografts, but has no consistent effect on the growth of carcinoma cell lines in vitro. EGF, on the other hand, significantly stimulates proliferation of many gastrointestinal cell lines in culture. Interest has recently focused on autocrine stimulation of gastrointestinal carcinoma growth. Elevated levels of EGF receptor, and of EGF or related mRNAs, have been demonstrated in gastric carcinomas, and the growth of some gastrointestinal cell lines is inhibited by antibodies against EGF, and by antisense oligonucleotides based on EGF mRNA. Similarly gastrin/cholecystokinin antagonists inhibit the growth of several colon carcinoma cell lines, although the spectrum of antagonist potencies suggests that classical gastrin and cholecystokinin receptors are not necessarily involved. Continued research on antagonists may therefore lead to novel therapies for gastrointestinal cancers.
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PMID:Gut hormones, growth and malignancy. 790 61

Gastrin has been shown to enhance the growth of various human tumors. The present study was designed to examine the gastrin receptor gene expression in various human carcinoma cell lines and in surgically resected carcinoma tissues. By Northern blot analysis, gastrin receptor mRNA was detected in 3 out of 7 small cell lung carcinoma cell lines. Gastrin receptor mRNA was also expressed in one out of 8 colon carcinoma cell lines and 2 out of 10 colon carcinoma tissues. Moreover, one of two small cell carcinoma cell lines of the stomach clearly expressed gastrin receptor mRNA. However, none of the gastric adenocarcinoma cell lines or surgically resected gastric adenocarcinomas tested had any detectable expression of gastrin receptor gene. These findings may suggest a role of gastrin receptor in the growth and differentiation of certain human carcinomas.
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PMID:Gastrin receptor gene expression in several human carcinomas. 792 27


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