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ReviewNature reviews. Gastroenterology & hepatology2025

Helicobacter pylori, microbiota and gastric cancer - principles of microorganism-driven carcinogenesis.

Jonas Wizenty, Michael Sigal

Registry-linked trialAbstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Gastroenterology & hepatology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07408271 (The Impact of Rabeprazole-based Triple Therapy Plus Bismuth for First-line Helicobacter Pylori Eradication on the Vaginal Microecology Change), which is not on this map. Cited by 48 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed, 3 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

NCT07408271 completednot on this map

The Impact of Rabeprazole-based Triple Therapy Plus Bismuth for First-line Helicobacter Pylori Eradication on the Vaginal Microecology Change: a Prospective, Randomized Controlled Trial

TypeobservationalSponsorSecond Affiliated Hospital, Zhejiang University, School of MedicineRan2023 to 2024Enrolled83ConditionsHelicobacter Pylori Infection, Helicobacter Pylori Eradication AntibioticArmsrabeprazole-based triple therapy plus bismuth H. pylori eradication therapy
3 · Its place in the literature

Who cites it

48 citing papers in PubMed, 3 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Gut microbes · 2026
    Article
  5. Article
  6. Review
  7. Advances inOncology letters · 2026
    Review
  8. Review
  9. Mesenchymal R-spondin 3 promotes an immunogenic tumor microenvironment with adaptive immune resistance in human gastric adenocarcinoma.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2026
    Article
  10. From screening to surveillance: integrated prevention ofThe Lancet regional health. Western Pacific · 2026
    Review
  11. Biomolecules · 2026
    Review
  12. Article
  13. Pronounced ethnic and sex disparities in gastric cancer burden and healthcare utilization in Inner Mongolia: a 9-year population-based cohort study.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2026
    Article
  14. Review
  15. Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors.

Jonas WizentyDepartment of Hepatology and Gastroenterology, Charité - Universitätsmedizin Berlin, Berlin, Germany.ORCID http://orcid.org/0000-0003-4261-0416
Michael SigalDepartment of Hepatology and Gastroenterology, Charité - Universitätsmedizin Berlin, Berlin, Germany. michael.sigal@charite.de.ORCID http://orcid.org/0000-0003-4772-0761

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The demonstration that Helicobacter pylori is a pathogenic bacterium with marked carcinogenic potential has paved the way for new preventive approaches for gastric cancer. Although decades of research have uncovered complex interactions of H. pylori with epithelial cells, current insights have refined our view on H. pylori-associated carcinogenesis. Specifically, the cell-type-specific effects on gastric stem and progenitor cells deep in gastric glands provide a new view on the ability of the bacteria to colonize long-term, manipulate host responses and promote gastric pathology. Furthermore, new, large-scale epidemiological data have shed light on factors that determine why only a subset of carriers progress to gastric cancer. Currently, technological advances have brought yet another revelation: H. pylori is far from the only microorganism able to colonize the stomach. Instead, the stomach is colonized by a diverse gastric microbiota, and there is emerging evidence for the occurrence and pathological effect of dysbiosis resulting from an aberrant interplay between H. pylori and the gastric mucosa. With the weight of this evidence mounting, here we consider how the lessons learned from H. pylori research inform and synergize with this emerging field to bring a more comprehensive understanding of the role of microbes in gastric carcinogenesis.

Indexed as

CarcinogenesisGastrointestinal MicrobiomeHelicobacter InfectionsHelicobacter pyloriStomach NeoplasmsDysbiosisGastric MucosaHumans

Identifiers

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.