Evidence map›Paper›PMID 25043305›Full record

ReviewOncogene2015

Helicobacter pylori infection and stem cells at the origin of gastric cancer.

E Bessède, P Dubus, F Mégraud, C Varon

Abstract readReview
PubMed Publisher
In one paragraph

Review in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
11.4field-weighted citation impact, top 1% of its field
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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

47 citing papers in PubMed, 128 citations in OpenAlex.

  1. Article
  2. RBMX2 linkseLife · 2025
    Article
  3. Immune cell changes inAnnals of medicine · 2024
    Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. The dawn of precision medicine in diffuse-type gastric cancer.Therapeutic advances in medical oncology · 2022
    Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. TAZ ControlsCells · 2020
    Article
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

4 authors at 2 institutions in 1 country.

E Bessède1] Laboratoire de Bactériologie, University of Bordeaux, Bordeaux, France [2] INSERM U853, Bordeaux, France.
P Dubus1] Laboratoire d'Histologie, University of Bordeaux, Bordeaux, France [2] EA2406 Histologie et pathologie moléculaire des tumeurs, University of Bordeaux, Bordeaux, France.
F Mégraud1] Laboratoire de Bactériologie, University of Bordeaux, Bordeaux, France [2] INSERM U853, Bordeaux, France.
C Varon1] Laboratoire de Bactériologie, University of Bordeaux, Bordeaux, France [2] INSERM U853, Bordeaux, France.
Université de Bordeaux · FRInserm · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Helicobacter pylori infection is now recognized as the main and specific infectious cause of cancer in the world. It is responsible for gastric adenocarcinomas of both intestinal and diffuse types, which are the long-term consequences of the chronic infection of the gastric mucosa. Case-control studies have shown an association between the two, recognized as early as 1994 and further substantiated by interventional studies in which H. pylori eradication has led to the prevention of at least part of the gastric cancers. Experimental studies have highlighted the role of bone marrow-derived cells (BMDCs) and particularly mesenchymal stem cells, in the neoplastic process in about a quarter of the cases and possibly an epithelial-mesenchymal transition (EMT) in the other cases. Different studies have confirmed that chronic infection with H. pylori induces a chronic inflammation and subsequent damage of the gastric epithelial mucosa, leading to BMDC recruitment. Once recruited, these cells home and differentiate by cell-cell fusion with local gastric epithelial cells, bearing local stem cell failure and participating in tissue regeneration. The context of chronic infection and inflammation leads to an EMT and altered tissue regeneration and differentiation from both local epithelial stem cells and BMDC. EMT induces the emergence of CD44+ cells possessing mesenchymal and stem cell properties, resulting in metaplastic and dysplastic lesions to give rise, after additional epigenetic and mutational events, to the emergence of cancer stem cells (CSCs) and adenocarcinoma.

Indexed as

AdenocarcinomaAnimalsCell Transformation, NeoplasticChronic DiseaseEpithelial-Mesenchymal TransitionHelicobacter InfectionsHelicobacter pyloriHumansInflammationMesenchymal Stem CellsNeoplastic Stem CellsStomach Neoplasms

Identifiers

PMID25043305
OpenAlexW2039782798

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.