Evidence map›Paper›PMID 12663641›Full record

ArticleJournal of clinical pathology2003

Helicobacter pylori babA2, cagA, and s1 vacA genes work synergistically in causing intestinal metaplasia.

C-F Zambon, F Navaglia, D Basso, M Rugge, M Plebani

Open access · bronzeAbstract read
In one paragraph

Article in Journal of clinical pathology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed, 3 pooled it
10.1field-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

51 citing papers in PubMed, 3 syntheses or guidelines pooled it, 163 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Article
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  10. Toxins · 2021
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  11. Increased Risk of Severe Gastric Symptoms by Virulence FactorsJournal of microbiology and biotechnology · 2021
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  12. Cells · 2020
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  13. Evolutionarily-RelatedMicroorganisms · 2020
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  14. Prevalence of theThe Canadian journal of infectious diseases & medical microbiology = Journal canadien des maladies infectieuses et de la microbiologie medicale · 2020
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  15. World journal of gastroenterology · 2019
    Review
  16. Article
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  18. Activation of CD3Cancer biology & therapy · 2019
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  19. Article
  20. Host pathogen interactions inWorld journal of gastroenterology · 2017
    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

5 authors at 1 institution in 1 country.

C-F ZambonDepartment of Medical and Surgical Sciences, University-Hospital of Padova, Via Giustiniani 2, 35128 Padova, Italy.
F Navaglia
D Basso
M Rugge
M Plebani
University of Padua · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsTo determine any associations between the Helicobacter pylori genes babA2, oipA, cagA and the s and m alleles of vacA. In addition, to verify whether these genes work synergistically or independently in causing gastritis, peptic ulcer, and intestinal metaplasia.

methodsOne hundred and sixty seven H pylori positive patients were studied (52 antral gastritis, 41 diffuse gastritis, 41 peptic ulcer, and 33 duodenitis). Helicobacter pylori virulence genes were amplified by means of the polymerase chain reaction.

resultsSignificant associations were found between babA2 and the other H pylori genes studied. When considered singly, all the genes were associated with disease diagnosis, inflammation, and intestinal metaplasia. Four H pylori groups were defined. Group A: cagA-, s2m2, babA2-; group B: cagA+, s1m1, babA2+; group C: cagA+, s1m2, babA2+; group D: cagA+, s1m2, babA2-. Group A infecting strains were associated with less severe endoscopic and inflammatory conditions, whereas group B strains were associated with the worst endoscopic and inflammatory findings. Intestinal metaplasia was a rare finding in group A infected patients (< 10%), whereas it was frequent in those infected with group B strains (48%).

conclusionsThe H pylori genes cagA, oipA "on", s1 and m1 vacA, and babA2 are associated with each other, possibly as a result of shared selective pressure. When coexpressed by the same H pylori strain, cagA, s1 and m1 vacA, and babA2 work synergistically in worsening inflammation. Infections caused by strains coexpressing cagA, s1m1 vacA, and babA2 are those at higher risk for intestinal metaplasia.

Indexed as

Adhesins, BacterialGenes, BacterialAdolescentAdultAgedAged, 80 and overAntigens, BacterialBacterial ProteinsCarrier ProteinsDuodenitisFemaleGastric MucosaGastritisHelicobacter InfectionsHelicobacter pyloriHumansAdhesins, BacterialAntigens, BacterialBabA protein, Helicobacter pyloriBacterial ProteinscagA protein, Helicobacter pyloriCarrier ProteinsVacA protein, Helicobacter pylori

Identifiers

PMID12663641
PMCPMC1769933
OpenAlexW2118387596

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.