ReviewDigestive diseases and sciences2015
Gastrin May Mediate the Carcinogenic Effect of Helicobacter pylori Infection of the Stomach.
Review in Digestive diseases and sciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
27 citing papers in PubMed, 46 citations in OpenAlex.
- Perspectives on gastric cancer: the central role of gastrin in carcinogenesis byFrontiers in oncology · 2026Review
- [Screening of differentially expressed genes in gastric cancer based on GEO database and function and pathway enrichment analysis].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024Article
- Inflammation and Digestive Cancer.International journal of molecular sciences · 2023Review
- Enteroendocrine cells and gut hormones as potential targets in the crossroad of the gut-kidney axis communication.Frontiers in pharmacology · 2023Review
- The central role of gastrin in gastric cancer.Frontiers in oncology · 2023Review
- Gastrin/CCK-B Receptor Signaling Promotes Cell Invasion and Metastasis by Upregulating MMP-2 and VEGF Expression in Gastric Cancer.Journal of Cancer · 2022Article
- Gastrin: From Physiology to Gastrointestinal Malignancies.Function (Oxford, England) · 2022Review
- Time to Classify Tumours of the Stomach and the Kidneys According to Cell of Origin.International journal of molecular sciences · 2021Review
- Gastritis, Gastric Polyps and Gastric Cancer.International journal of molecular sciences · 2021Review
- Hypergastrinemia is associated with an increased risk of gastric adenocarcinoma with proximal location: A prospective population-based nested case-control study.International journal of cancer · 2021Article
- Towards Understanding of Gastric Cancer Based upon Physiological Role of Gastrin and ECL Cells.Cancers · 2020Review
- Correct Identification of Cell of Origin May Explain Many Aspects of Cancer: The Role of Neuroendocrine Cells as Exemplified from the Stomach.International journal of molecular sciences · 2020Review
- Gastrin drives gastric cancer due to oxyntic atrophy also after Helicobacter pylori eradication.Therapeutic advances in gastroenterology · 2020Article
- Role of Autoimmune Gastritis in Gastric Cancer.Clinical and translational gastroenterology · 2019Article
- The Enterochromaffin-like [ECL] Cell-Central in Gastric Physiology and Pathology.International journal of molecular sciences · 2019Review
- Proton pump inhibitor: The dual role in gastric cancer.World journal of gastroenterology · 2019Review
- The Reduction in Gastric Atrophy afterInternational journal of molecular sciences · 2019Article
- Types of Gastric Carcinomas.International journal of molecular sciences · 2018Review
- Not only stem cells, but also mature cells, particularly neuroendocrine cells, may develop into tumours: time for a paradigm shift.Therapeutic advances in gastroenterology · 2018Review
- Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gastric cancer occurs almost exclusively in patients with gastritis. Since Helicobacter pylori (Hp) was proved to cause gastritis, Hp was also expected to play a role in gastric carcinogenesis. Despite extensive studies, the mechanisms by which Hp cause gastric cancer are still poorly understood. However, there is evidence that the anatomical site of Hp infection is of major importance. Infection confined to the antral mucosa protects against gastric cancer but predisposes to duodenal ulcer, whereas Hp infection of the oxyntic mucosa increases the risk of gastric cancer. Hp infection does not predispose to cancers in the gastric cardia. In patients with atrophic gastritis of the oxyntic mucosa, the intragastric pH is elevated and the concentration of microorganisms in the stomach is increased. This does not lead to increased risk of gastric cancer at all anatomical sites. The site specificity of Hp infection in relation to cancer risk indicates that neither Hp nor the changes in gastric microflora due to gastric hypoacidity are carcinogenic per se. However, reduced gastric acidity also leads to hypergastrinemia, which stimulates the function and proliferation of enterochromaffin-like (ECL) cells located in the oxyntic mucosa. The ECL cell may be more important in human gastric carcinogenesis than previously realized, as every condition causing long-term hypergastrinemia in animals results in the development of neoplasia in the oxyntic mucosa. Patients with hypergastrinemia will far more often develop carcinomas in the gastric corpus. In conclusion, hypergastrinemia may explain the carcinogenic effect of Hp.
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