Evidence map›Paper›PMID 38231214›Full record

ArticleCurrent topics in microbiology and immunology2023

Clinical Pathogenesis, Molecular Mechanisms of Gastric Cancer Development.

Lydia E Wroblewski, Richard M Peek

Open access · greenAbstract read
In one paragraph

Article in Current topics in microbiology and immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
23.9field-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

6 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Article
  3. Update on molecular pathogenesis ofWorld journal of gastrointestinal pathophysiology · 2025
    Review
  4. Distribution and Clinical Impact ofAntibiotics (Basel, Switzerland) · 2025
    Article
  5. Article
  6. 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

2 authors at 1 institution in 1 country.

Lydia E WroblewskiDivision of Gastroenterology, Hepatology, and Nutrition, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN, USA.
Richard M PeekDivision of Gastroenterology, Hepatology, and Nutrition, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN, USA. richard.peek@vumc.org.
Vanderbilt University Medical Center · US

Funding

Translational Analysis CoreP30DK058404 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI MARY Kay WASHINGTON · 2002 to 2026
$29.9M
Role of Iron and B-Catenin Activation in Gastric CarcinogenesisP01CA116087 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI Maria Blanca Piazuelo · 2009 to 2026
$27.5M
H.Pylori Relationship to Digestive Diseases and CancerR01CA077955 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI RICHARD M. PEEK · 2003 to 2026
$9.7M
Helicobacter Pylori and Gastrointestinal BiologyR01DK058587 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI PEEK, RICHARD M. · 2001 to 2024
$7.8M
Interactions Between the Microbiota and Helicobacter pylori in Gastric CarcinogenesisR01CA281732 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI JAMES G FOX, RICHARD M. PEEK · 2023 to 2026
$2.7M
Mechanism that regulate Helicobacter pylori-induced beta-caterin activationR01DK073902 · NIDDK · VANDERBILT UNIVERSITY · PI PEEK, RICHARD M. · 2006 to 2009
$1.2M
NCI NIH HHS P01 CA116087NCI NIH HHS R01 CA077955NCI NIH HHS R01 CA281732NIDDK NIH HHS P30 DK058404NIDDK NIH HHS R01 DK058587NIDDK NIH HHS R01 DK073902
6 · The paper itself

Abstract

The human pathogen Helicobacter pylori is the strongest known risk factor for gastric disease and cancer, and gastric cancer remains a leading cause of cancer-related death across the globe. Carcinogenic mechanisms associated with H. pylori are multifactorial and are driven by bacterial virulence constituents, host immune responses, environmental factors such as iron and salt, and the microbiota. Infection with strains that harbor the cytotoxin-associated genes (cag) pathogenicity island, which encodes a type IV secretion system (T4SS) confer increased risk for developing more severe gastric diseases. Other important H. pylori virulence factors that augment disease progression include vacuolating cytotoxin A (VacA), specifically type s1m1 vacA alleles, serine protease HtrA, and the outer-membrane adhesins HopQ, BabA, SabA and OipA. Additional risk factors for gastric cancer include dietary factors such as diets that are high in salt or low in iron, H. pylori-induced perturbations of the gastric microbiome, host genetic polymorphisms, and infection with Epstein-Barr virus. This chapter discusses in detail host factors and how H. pylori virulence factors augment the risk of developing gastric cancer in human patients as well as how the Mongolian gerbil model has been used to define mechanisms of H. pylori-induced inflammation and cancer.

Indexed as

Epstein-Barr Virus InfectionsHelicobacter pyloriStomach NeoplasmsCytotoxinsHerpesvirus 4, HumanHumansIronVirulence FactorsCytotoxinsIronVirulence FactorsGastric cancerGastric inflammationHelicobacter pyloriMongolian gerbilVirulence factors

Identifiers

PMID38231214
PMCPMC10924282
OpenAlexW4390940856

What OpenQuestion holds

Textmetadata
LicenceTDM
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.