Evidence map›Paper›PMID 19138977›Full record

SynthesisCancer prevention research (Philadelphia, Pa.)2008

Helicobacter pylori and esophageal cancer risk: a meta-analysis.

Farhad Islami, Farin Kamangar

Abstract readMeta-Analysis
PubMed Full text at PMC Publisher
In one paragraph

Synthesis in Cancer prevention research (Philadelphia, Pa.), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 156 papers, 8 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
156citing papers in PubMed, 8 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.

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

156 citing papers in PubMed, 8 syntheses or guidelines pooled it.

  1. Should we pay more attention to the potential link betweenWorld journal of gastroenterology · 2024
    Pooled it
  2. Pooled it
  3. Non-invasive diagnostic tests for Helicobacter pylori infection.The Cochrane database of systematic reviews · 2018
    Pooled it
  4. Pooled it
  5. Pooled it
  6. Pooled it
  7. Pooled it
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  9. Trial
  10. Trial
  11. Review
  12. Article
  13. Review
  14. Virulence · 2025
    Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. Article

96 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors.

Farhad IslamiDigestive Disease Research Center, Medical Sciences/University of Tehran, Tehran, Iran.
Farin Kamangar

Funding

Upper Gastrointestinal Cancer StudiesZIACP000185 · NCI · DIVISION OF CANCER EPIDEMIOLOGY AND GENETICS · PI ABNET, CHRISTIAN · 2009 to 2025
$25.6M
Intramural NIH HHS Z99 CA999999NCI NIH HHS Y99 CA999999
6 · The paper itself

Abstract

We conducted this meta-analysis to examine the association between Helicobacter pylori and esophageal adenocarcinoma (EAC) and esophageal squamous cell carcinoma. We searched the PubMed database, the ISI database, and the references of the selected articles. Case-control or nested case-control studies were selected if they used serology or endoscopic methods to detect H. pylori in the stomach and if control subjects were not restricted to upper gastrointestinal tract cancer or peptic ulcer disease patients. A total of 19 studies were used for this analysis. Summary odds ratios (OR) and 95% confidence intervals (95% CI) were calculated using the DerSimonian-Laird method. Q statistics and I(2) statistics were calculated to examine heterogeneity. Subgroup analyses were conducted by CagA status. For EAC, the summary OR (95% CI) was 0.56 (0.46-0.68). There was little heterogeneity among studies (I(2) = 15%). Further analysis showed that colonization with CagA-positive strains was inversely associated with EAC risk (OR, 0.41; 95% CI, 0.28-0.62) but colonization with CagA-negative strains was not (OR, 1.08; 95% CI, 0.76-1.53). For esophageal squamous cell carcinoma, the summary OR (95% CI) was 1.10 (0.78-1.55). However, there was substantial heterogeneity among studies (I(2) = 73%), with statistically significant associations in both directions. Our results suggest an inverse association between CagA-positive H. pylori colonization and risk of EAC. The prominent decline of H. pylori colonization in the past few decades may be partly responsible for the recent increase in EAC incidence in Western countries.

Indexed as

AdenocarcinomaAntigens, BacterialBacterial ProteinsCarcinoma, Squamous CellCase-Control StudiesCohort StudiesEsophageal NeoplasmsHelicobacter InfectionsHelicobacter pyloriHumansOdds RatioRisk FactorsAntigens, BacterialBacterial ProteinscagA protein, Helicobacter pylori

Identifiers

PMID19138977
PMCPMC3501739

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.