Evidence map›Paper›PMID 24868089›Full record

ReviewJournal of leukocyte biology2014

At the Bench: Helicobacter pylori, dysregulated host responses, DNA damage, and gastric cancer.

Dana M Hardbower, Richard M Peek, Keith T Wilson

Abstract readReview
In one paragraph

Review in Journal of leukocyte biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
–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

55 citing papers in PubMed.

  1. Trial
  2. From gut to mouth: salivary signatures of carcinogenic microbiota.Frontiers in cellular and infection microbiology · 2026
    Review
  3. Article
  4. Update on molecular pathogenesis ofWorld journal of gastrointestinal pathophysiology · 2025
    Review
  5. Article
  6. Review
  7. Article
  8. Hyperoside AlleviatesPolish journal of microbiology · 2025
    Article
  9. Review
  10. Review
  11. Effects of RAD50 SNP, sodium intake, and H. pylori infection on gastric cancer survival in Korea.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2024
    Review
  12. Article
  13. Review
  14. Mucin Glycans: A Target for Cancer Therapy.Molecules (Basel, Switzerland) · 2023
    Review
  15. Review
  16. Review
  17. Article
  18. Global Trend on Machine Learning inGlobal health, epidemiology and genomics · 2023
    Article
  19. Review
  20. 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

3 authors.

Dana M HardbowerDepartments of Pathology, Microbiology, and Immunology and Division of Gastroenterology, Hepatology, and Nutrition, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA; and.
Richard M PeekDivision of Gastroenterology, Hepatology, and Nutrition, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA; and Cancer Biology, and.
Keith T WilsonDepartments of Pathology, Microbiology, and Immunology and Division of Gastroenterology, Hepatology, and Nutrition, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA; and Cancer Biology, and Veterans Affairs, Tennessee Valley Healthcare System, Nashville, Tennessee, USA keith.wilson@vanderbilt.edu.

Funding

VANDERBILT UNIVERSITY CTSA FOR PEDIATRIC RESEARCHUL1RR024975 · NCRR · VANDERBILT UNIVERSITY · PI BERNARD, GORDON RAPHAEL · 2007 to 2011
$45.7M
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
Project 3 - Molecular Signatures of Gastric Carcinogenesis in the Host Response to H. pyloriP01CA028842 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI WILSON, KEITH T. · 1985 to 2019
$15.8M
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
TRAINING PROGRAM IN CELLULAR, BIOCHEMICAL, &MOLECULAR ST32GM008554 · NIGMS · VANDERBILT UNIVERSITY · PI PATTON, JAMES G. · 1995 to 2020
$7.4M
Immunomodulatory effects of arginine supplementation in colitis and colon cancerR01AT004821 · NCCIH · VANDERBILT UNIVERSITY MEDICAL CENTER · PI WILSON, KEITH T. · 2008 to 2017
$4.0M
HPYLORI INDUCED DNA DAMAGE AND IMMUNE DYSREGULATIONR01DK053620 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI WILSON, KEITH T. · 1997 to 2014
$3.4M
Arginine Availability and Metabolism in the Immune Evasion of H. pyloriI01BX001453 · VA · VETERANS HEALTH ADMINISTRATION · PI WILSON, KEITH T. · 2012 to 2019
–
BLRD VA I01 BX001453NCCIH NIH HHS R01 AT004821NCCIH NIH HHS R01AT004821NCI NIH HHS P01 CA028842NCI NIH HHS P01CA028842NCI NIH HHS P01 CA116087NCI NIH HHS P01CA116087NCI NIH HHS R01 CA077955NCI NIH HHS R01CA77955NCRR NIH HHS UL1 RR024975NCRR NIH HHS UL1RR024975NIDDK NIH HHS P30 DK058404NIDDK NIH HHS P30DK058404NIDDK NIH HHS R01 DK053620NIDDK NIH HHS R01DK053620NIDDK NIH HHS R01 DK058587NIDDK NIH HHS R01DK58587NIGMS NIH HHS 5T32GM008554NIGMS NIH HHS T32 GM008554
6 · The paper itself

Abstract

Helicobacter pylori infection is the strongest known risk factor for the development of gastric cancer. Given that ∼50% of the global population is infected with this pathogen, there is great impetus to elucidate underlying causes that mediate progression from infection to cancer. Recent evidence suggests that H. pylori-induced chronic inflammation and oxidative stress create an environment conducive to DNA damage and tissue injury. DNA damage leads to genetic instability and eventually, neoplastic transformation. Pathogen-encoded virulence factors induce a robust but futile immune response and alter host pathways that lower the threshold for carcinogenesis, including DNA damage repair, polyamine synthesis and catabolism, antioxidant responses, and cytokine production. Collectively, such dysregulation creates a protumorigenic microenvironment within the stomach. This review seeks to address each of these aspects of H. pylori infection and to call attention to areas of particular interest within this field of research. This review also seeks to prioritize areas of translational research related to H. pylori-induced gastric cancer based on insights garnered from basic research in this field. See related review by Dalal and Moss, At the Bedside: H. pylori, dysregulated host responses, DNA damage, and gastric cancer.

Indexed as

DNA DamageGenetic Predisposition to DiseaseHelicobacter InfectionsHelicobacter pyloriHumansInflammationStomach NeoplasmscarcinogenesisDFMOoxidative stress

Identifiers

PMID24868089
PMCPMC4101087

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.