Inappropriate hypergastrinaemia in asymptomatic healthy subjects infected with Helicobacter pylori.

Smith, J. T. L.; Pounder, RE; Nwokolo, CU; Lanzon-Miller, S.; Evans, Dolores G.; Graham, David Y.; Evans, D. J.

doi:10.1136/gut.31.5.522

Cited by 174 publications

(73 citation statements)

References 24 publications

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“…pylori-induced gastritis in the gastric mucosa, as shown by infiltration of monocytes and polymorphonuclear cells within the mucosa (6,23,26,33,35,36,41) is similar to that observed in humans. The increase in acid secretion reported in individuals infected by H. pylori has been attributed to inflammatory phenomena by some authors (18,36,37,47). This view has been strengthened by data showing that cytokines such as IL-6 and tumor necrosis factor stimulate gastric acid secretion by activating antral G cells (6), whereas inflammatory lipid mediators such as PAF also stimulate the parietal cell via a specific receptor (48).…”

Section: Discussionmentioning

confidence: 62%

“…Gastric acid secretion has been reported to increase 4-8 wk after eradication therapy in humans (28,52), suggesting that H. pylori inhibits acid secretion. In contrast, acid secretion in basal conditions and after stimulation with a meal or gastrin-releasing peptide (6,9,47,51) seemed to decrease after eradication therapy in other studies, suggesting that the bacterium has a stimulatory effect. These authors have also reported acid output to be higher in some H. pylori-positive patients and significantly lower in others compared with H. pylori-negative individuals (15)(16)(17)(18).…”

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confidence: 62%

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Putative effect ofHelicobacter pyloriand gastritis on gastric acid secretion in cat

Sobhani

Cañedo

Alchepo

et al. 2002

American Journal of Physiology-Gastrointestinal and Liver Physi

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Section: Discussionmentioning

confidence: 62%

mentioning

confidence: 62%

Putative effect ofHelicobacter pyloriand gastritis on gastric acid secretion in cat

Sobhani

Cañedo

Alchepo

et al. 2002

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…Studies during the past two decades have demonstrated that the GI peptide hormone gastrin might play key roles in regulating both normal as well as malignant GI growth (Rozengurt and Walsh, 2001). This is of clinical importance since an increase in serum gastrin levels is a common side effect following Helicobacter pylori (H. pylori) infection (Smith et al, 1990;Konturek et al, 2000), or the use of proton pump inhibitors (PPIs) (Lind et al, 1988). Both antral-and tumor-derived gastrin, as well as unprocessed forms (progastrin and glycine-extended gastrin) are capable of stimulating cell proliferation (Seva et al, 1994;Singh et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

Gastrin-mediated activation of cyclin D1 transcription involves β-catenin and CREB pathways in gastric cancer cells

et al. 2004

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Gastrin and its precursors promote proliferation in different gastrointestinal cells. Since mature, amidated gastrin (G-17) can induce cyclin D1, we determined whether G-17-mediated induction of cyclin D1 transcription involved Wnt signaling and CRE-binding protein (CREB) pathways. Our studies indicate that G-17 induces protein, mRNA expression and transcription of the G 1 -specific marker cyclin D1, in the gastric adenocarcinoma cell line AGSE (expressing the gastrin/cholecystokinin B receptor). This was associated with an increase in steadystate levels of total and nonphospho b-catenin and its nuclear translocation, indicating the activation of the Wnt-signaling pathway. In addition, G-17-mediated increase in cyclin D1 transcription was significantly attenuated by axin or dominant-negative (dn) T-cell factor 4(TCF4), suggesting crosstalk of G-17 with the Wnt-signaling pathway. Mutational analysis indicated that this effect was mediated through the cyclic AMP response element (CRE) (predominantly) and the TCF sites in the cyclin D1 promoter, which was also inhibited by dnCREB. Furthermore, G-17 stimulation resulted in increased CRE-responsive reporter activity and CREB phosphorylation, indicating an activation of CREB. Chromatin immunoprecipitation studies revealed a G-17-mediated increase in the interaction of b-catenin with cyclin D1 CRE, which was attenuated by dnTCF4 and dnCREB. These results indicate that G-17 induces cyclin D1 transcription, via the activation of b-catenin and CREB pathways.

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“…In addition, patients with asymptomatic H pylori infection were found to have increased gastrin levels by enzyme-linked immunosorbent assay. 83 Although hypergastrinemia is associated with the development of gastric neuroendocrine tumors and gastric adenocarcinoma, 84 both animal and human studies have shown the greater incidence of gastric carcinoids in patients with increased gastrin levels. One possible explanation for the more frequent neuroendocrine tumors over gastric adenocarcinoma in patients with hypergastrinemia may be related to the finding that although the CCK-B receptor is present on parietal cells, it is expressed more abundantly in ECL cells of the stomach.…”

Section: -63mentioning

confidence: 99%

Gastrin and gastric cancer

&NA;

1993

European Journal of Gastroenterology & Hepatology

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SUMMARYThe gastrointestinal peptide, gastrin, stimulates growth of gastric adenocarcinoma (gastric cancer) through the cholecystokinin-B receptors that are overexpressed in this malignancy. Serum gastrin levels may be increased secondary to chronic administration of proton pump inhibitors, atrophic gastritis, Helicobacter pylori infection, or from de novo gastrin expression from the gastric cancer epithelial cells. Strategies to interrupt the interaction of gastrin at the cholecystokinin-B receptor may provide a novel approach to the treatment of gastric cancer.Gastric cancer is the third leading cause of cancer-related mortality worldwide. Despite progress in understanding its development, challenges with treatment remain. Gastrin, a peptide hormone, is trophic for normal gastrointestinal epithelium. Gastrin also has been shown to play an important role in the stimulation of growth of several gastrointestinal cancers including gastric cancer. We sought to review the role of gastrin and its pathway in gastric cancer and its potential as a therapeutic target in the management of gastric cancer. In the normal adult stomach, gastrin is synthesized in the G cells of the antrum; however, gastrin expression also is found in many gastric adenocarcinomas of the stomach corpus. Gastrin's actions are mediated through the G-protein-coupled receptor cholecystokinin-B (CCK-B) on parietal and enterochromaffin cells of the gastric body. Gastrin blood levels are increased in subjects with type A atrophic gastritis and in those taking high doses of daily proton pump inhibitors for acid reflux disease. In experimental models, proton pump inhibitor-induced hypergastrinemia and infection with Helicobacter pylori increase the risk of gastric cancer. Understanding the gastrin:CCK-B signaling pathway has led to therapeutic strategies to treat gastric cancer by either targeting the CCK-B receptor with small-molecule antagonists or targeting the peptide with immune-based therapies. In this review, we discuss the role of gastrin in gastric adenocarcinoma, and strategies to block its effects to treat those with unresectable gastric cancer. (Cell Mol Gastroenterol Hepatol 2017;4:75-83; http://dx

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Inappropriate hypergastrinaemia in asymptomatic healthy subjects infected with Helicobacter pylori.

Cited by 174 publications

References 24 publications

Putative effect ofHelicobacter pyloriand gastritis on gastric acid secretion in cat

Putative effect ofHelicobacter pyloriand gastritis on gastric acid secretion in cat

Gastrin-mediated activation of cyclin D1 transcription involves β-catenin and CREB pathways in gastric cancer cells

Gastrin and gastric cancer

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