Evidence map›Paper›PMID 26814181›Full record

ReviewmBio2016

Helicobacter pylori Diversity and Gastric Cancer Risk.

Timothy L Cover

Open access · goldAbstract readReview
In one paragraph

Review in mBio, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 123 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
123citing papers in PubMed, 2 pooled it
25.4field-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

123 citing papers in PubMed, 2 syntheses or guidelines pooled it, 215 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Microbiology and molecular biology reviews : MMBR · 2026
    Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Global diversity of integrating conjugative elements (ICEs) inbioRxiv : the preprint server for biology · 2025
    Article
  10. Species-specific components of theInfection and immunity · 2025
    Article
  11. Infection and immunity · 2025
    Article
  12. The influence ofFrontiers in immunology · 2025
    Article
  13. Review
  14. Article
  15. Subdomains of theLife science alliance · 2024
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. The immunopathogenesis ofFrontiers in microbiology · 2024
    Review

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

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

1 author at 1 institution in 1 country.

Timothy L CoverDepartment of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee, USA Department of Pathology, Microbiology and Immunology, Vanderbilt University School of Medicine, Nashville, Tennessee, USA Veterans Affairs Tennessee Valley Healthcare System, Nashville, Tennessee, USA timothy.l.cover@vanderbilt.edu.ORCID http://orcid.org/0000-0001-8503-002X
Vanderbilt University · US

Funding

Translational Analysis CoreP30DK058404 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI RICHARD M. PEEK · 2002 to 2026
$29.9M
Role of Iron and B-Catenin Activation in Gastric CarcinogenesisP01CA116087 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI RICHARD M. PEEK · 2009 to 2026
$27.5M
Structure-function analysis of H. pylori VacAR01AI039657 · NIAID · VANDERBILT UNIVERSITY MEDICAL CENTER · PI TIMOTHY L COVER · 1996 to 2026
$8.3M
Pathogenesis of Helicobacter pylori infectionI01BX000627 · VA · VETERANS HEALTH ADMINISTRATION · PI COVER, TIMOTHY L · 2011 to 2018
–
BLRD VA I01 BX000627NCI NIH HHS CA116087NCI NIH HHS P01 CA116087NIAID NIH HHS AI039657NIAID NIH HHS R01 AI039657NIDDK NIH HHS P30 DK058404
6 · The paper itself

Abstract

Gastric cancer is a leading cause of cancer-related death worldwide. Helicobacter pylori infection is the strongest known risk factor for this malignancy. An important goal is to identify H. pylori-infected persons at high risk for gastric cancer, so that these individuals can be targeted for therapeutic intervention. H. pylori exhibits a high level of intraspecies genetic diversity, and over the past two decades, many studies have endeavored to identify strain-specific features of H. pylori that are linked to development of gastric cancer. One of the most prominent differences among H. pylori strains is the presence or absence of a 40-kb chromosomal region known as the cag pathogenicity island (PAI). Current evidence suggests that the risk of gastric cancer is very low among persons harboring H. pylori strains that lack the cag PAI. Among persons harboring strains that contain the cag PAI, the risk of gastric cancer is shaped by a complex interplay among multiple strain-specific bacterial factors as well as host factors. This review discusses the strain-specific properties of H. pylori that correlate with increased gastric cancer risk, focusing in particular on secreted proteins and surface-exposed proteins, and describes evidence from cell culture and animal models linking these factors to gastric cancer pathogenesis. Strain-specific features of H. pylori that may account for geographic variation in gastric cancer incidence are also discussed.

Indexed as

Genetic VariationAnimalsDisease Models, AnimalGenomic IslandsHelicobacter InfectionsHelicobacter pyloriHost-Pathogen InteractionsHumansRisk AssessmentStomach NeoplasmsVirulence FactorsVirulence Factors

Identifiers

PMID26814181
PMCPMC4742704
OpenAlexW2287302929

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.