Evidence map›Paper›PMID 24133496›Full record

ReviewFrontiers in immunology2013

Helicobacter pylori CagA: From Pathogenic Mechanisms to Its Use as an Anti-Cancer Vaccine.

Markus Stein, Paolo Ruggiero, Rino Rappuoli, Fabio Bagnoli

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
9.6field-weighted citation impact, top 2% 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

41 citing papers in PubMed, 85 citations in OpenAlex.

  1. Review
  2. Article
  3. Frontiers in cell and developmental biology · 2025
    Article
  4. Article
  5. Developing a potent vaccine againstExpert reviews in molecular medicine · 2024
    Review
  6. Article
  7. Article
  8. Review
  9. Influence ofWorld journal of clinical oncology · 2022
    Review
  10. Review
  11. Transient recombinant expression of highly immunogenicBiotechnology reports (Amsterdam, Netherlands) · 2022
    Article
  12. Article
  13. Article
  14. World journal of gastroenterology · 2021
    Review
  15. Article
  16. Review
  17. Immune Response inGastroenterology research and practice · 2020
    Review
  18. Article
  19. Review
  20. 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 2 countries.

Markus SteinAlbany College of Pharmacy and Health Sciences , Albany, NY , USA.
Paolo Ruggiero
Rino Rappuoli
Fabio Bagnoli
Novartis (Italy) · ITAlbany College of Pharmacy and Health Sciences · US

Funding

Par1-substrates responsible for CagA-mediated pathogenesis of Helicobacter pyloriR01CA160790 · NCI · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI MUESCH, ANNE · 2012 to 2016
$2.6M
NCI NIH HHS R01 CA160790
6 · The paper itself

Abstract

Helicobacter pylori colonizes the gastric mucosa of more than 50% of the human population, causing chronic inflammation, which however is largely asymptomatic. Nevertheless, H. pylori-infected subjects can develop chronic gastritis, peptic ulcer, gastric mucosa-associated lymphoid tissue lymphoma, and gastric cancer. Chronic exposure to the pathogen and its ability to induce epithelial to mesenchymal transition (EMT) through the injection of cytotoxin-associated gene A into gastric epithelial cells may be key triggers of carcinogenesis. By deregulating cell-cell and cell-matrix interactions as well as DNA methylation, histone modifications, expression of micro RNAs, and resistance to apoptosis, EMT can actively contribute to early stages of the cancer formation. Host response to the infection significantly contributes to disease development and the concomitance of particular genotypes of both pathogen and host may turn into the most severe outcomes. T regulatory cells (Treg) have been recently demonstrated to play an important role in H. pylori-related disease development and at the same time the Treg-induced tolerance has been proposed as a possible mechanism that leads to less severe disease. Efficacy of antibiotic therapies of H. pylori infection has significantly dropped. Unfortunately, no vaccine against H. pylori is currently licensed, and protective immunity mechanisms against H. pylori are only partially understood. In spite of promising results obtained in animal models of infection with a number of vaccine candidates, few clinical trials have been conducted so far and with no satisfactory outcomes. However, prophylactic vaccination may be the only means to efficiently prevent H. pylori-associated cancers.

Indexed as

CagAcancerepithelial to mesenchymal transitionHelicobacter pylorijunctionstype IV secretion systemvaccine

Identifiers

PMID24133496
PMCPMC3796731
OpenAlexW1984027402

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.