Gastric cancer: Animal studies on the risk of hypoacidity and hypergastrinemia

Fossmark, Reidar; Qvigstad, Gunnar

doi:10.3748/wjg.14.1646

Cited by 29 publications

(22 citation statements)

References 72 publications

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“…H. pylori infection is an important independent risk factor for gastric carcinogenesis. It has been confirmed that H. pylori infection can result in hypergastrinemia [14]. Asymptomatic patients with H. pylori colonization have elevated serum gastrin concentrations [15], and following the eradication of H. pylori, there is a reduction of serum gastrin concentration in fasting patients [16].…”

Section: Discussionmentioning

confidence: 97%

Human gastrin mRNA expression up-regulated by Helicobacter pylori CagA through MEK/ERK and JAK2-signaling pathways in gastric cancer cells

et al. 2011

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Background Helicobacter pylori-cytotoxin-associated protein A (CagA) and gastrin are believed to play an important role in gastric carcinogenesis, but their interaction has been incompletely clear. Methods We constructed a eukaryotic expression vector pcDNA3.1/cagA and a luciferase reporter vector pGL/ gastrin promoter, and then co-transfected them into gastric cancer AGS and SGC-7901 cells. The two kinds of gastric cancer cells were, respectively, infected with cagA-positive H. pylori NCTC11637, and then the gastrin promoter activity and gastrin mRNA level were detected with a Dual-Luciferase reporter assay system and quantitative reverse transcription polymerase chain reaction (RT-PCR), respectively. Next, after the MEK/ERK and JAK2-signaling pathway inhibitors, U0126 and AG490, were used to treat the two cell lines, or the ERK1 and JAK2 genes were knocked down by siRNAs (small interference RNAs) in the two cell lines, the gastrin promoter activity and gastrin mRNA level were observed again. Results The results indicated that CagA could activate the gastrin promoter and up-regulate gastrin mRNA expression in AGS and SGC-7901 cells, but these effects could be inhibited by the inhibitors U0126 and AG490, and the CagAinduced gastrin mRNA expression was down-regulated in the cells whose ERK1 or JAK2 gene was knocked down.

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Section: Discussionmentioning

confidence: 97%

Human gastrin mRNA expression up-regulated by Helicobacter pylori CagA through MEK/ERK and JAK2-signaling pathways in gastric cancer cells

et al. 2011

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“…Hypergastrinemia has been proposed in many models of gastric carcinogenesis and seems to be a common causative factor in otherwise different circumstances; in all species where long-term hypergastrinemia has been induced, an increased risk of gastric malignancy, with adenocarcinoma phenotype and even the signet-ring cells phenotype, was observed [37,38].…”

Section: Discussionmentioning

confidence: 99%

Gastric cancer in patients with type I gastric carcinoids

et al. 2014

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Background Atrophic body gastritis (ABG) is associated with both type I gastric carcinoids (T1-GCs) and intestinaltype gastric cancer. The occurrence of gastric cancer in ABG patients with type I gastric carcinoids has not yet been described. Aim To describe the occurrence at follow-up of gastric cancer in ABG patients with type I gastric carcinoid in a retrospective case series in a single tertiary referral center. Methods Between 1994 and 2012, 17 new cases of T1-GCs were diagnosed among a cohort of ABG patients in a single tertiary referral center for ABG. The clinical charts of these 17 T1-GC patients were retrospectively evaluated for the occurrence of gastric cancer at follow-up (median 4.2 years, range 0.5-13). Results In 4 (23.5 %)/17 T1-GCs patients (3 females, age 40-78 years), gastric cancer occurred (median follow-up 5.9 years, range 5.1-13). Three cases were intestinal-type adenocarcinomas and one a signet-ring cell diffuse gastric cancer, localized in three cases in the antrum. In two patients, it was detected on random biopsies during followup gastroscopy; in the other two, gastroscopy was performed because of new symptoms. All patients with gastric cancer had associated autoimmune features (pernicious anemia, autoimmune thyroid disease and a spared antrum) compared to 77, 46 and 54 % of those without gastric cancer, although statistical significance was not reached. Conclusions This case series shows that in patients with T1-GCs, gastric cancer may frequently occur at long-term follow-up. Thus, these patients should be monitored by a long-term surveillance program, including an accurate bioptic sampling of the antral mucosa.

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“…Achlorhydric gastritis or drug-induced inhibition of acid secretion increases the secretion of gastrin due to abolition of the negative feedback regulation [1]. Accordingly, long-term use of proton pump inhibitors has raised concerns about the ensuing hypergastrinemia [1][2][3], because hypergastrinemia increases the risk of gastric carcinogenesis in animal models [4,5]. Also cell line studies have implicated gastrin as a growth factor in gastric cancer cells [6][7][8][9][10][11][12].…”

Section: Introductionmentioning

confidence: 97%