Evidence map›Paper›PMID 25732381›Full record

ArticleCancer research2015

Modification of Helicobacter pylori Peptidoglycan Enhances NOD1 Activation and Promotes Cancer of the Stomach.

Giovanni Suarez, Judith Romero-Gallo, M Blanca Piazuelo, Ge Wang, Robert J Maier, Lennart S Forsberg, Parastoo Azadi, Martin A Gomez, Pelayo Correa, Richard M Peek

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed, 1 pooled it
9.1field-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

54 citing papers in PubMed, 1 synthesis or guideline pooled it, 82 citations in OpenAlex.

  1. Pooled it
  2. Microbiology and molecular biology reviews : MMBR · 2026
    Review
  3. Review
  4. Article
  5. Role of Nod-like Receptors inMicroorganisms · 2026
    Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Programmed cell death inFrontiers in cellular and infection microbiology · 2024
    Review
  11. Review
  12. Article
  13. Microorganisms · 2023
    Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. 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

10 authors at 3 institutions in 2 countries.

Giovanni SuarezDepartments of Cancer Biology and Medicine, Vanderbilt University, Nashville, Tennessee.
Judith Romero-GalloDepartments of Cancer Biology and Medicine, Vanderbilt University, Nashville, Tennessee.
M Blanca PiazueloDepartments of Cancer Biology and Medicine, Vanderbilt University, Nashville, Tennessee.
Ge WangDepartment of Microbiology, University of Georgia, Athens, Georgia.
Robert J MaierDepartment of Microbiology, University of Georgia, Athens, Georgia.
Lennart S ForsbergComplex Carbohydrate Research Center, University of Georgia, Athens, Georgia.
Parastoo AzadiComplex Carbohydrate Research Center, University of Georgia, Athens, Georgia.
Martin A GomezDepartment of Medicine, National University of Colombia, Bogota, Colombia. Hospital El Tunal Unit of Gastroenterology, Bogota, Colombia.
Pelayo CorreaDepartments of Cancer Biology and Medicine, Vanderbilt University, Nashville, Tennessee.
Richard M PeekDepartments of Cancer Biology and Medicine, Vanderbilt University, Nashville, Tennessee. richard.peek@vanderbilt.edu.
Vanderbilt University · USUniversity of Georgia · USUniversidad Nacional de Colombia · CO

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
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
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 BX001453NCI NIH HHS P01 CA028842NCI NIH HHS P01-CA028842NCI NIH HHS P01 CA116087NCI NIH HHS P01-CA116087NCI NIH HHS R01 CA077955NCI NIH HHS R01-CA77955NIDDK NIH HHS P30 DK058404NIDDK NIH HHS P30-DK058404NIDDK NIH HHS R01 DK053620NIDDK NIH HHS R01 DK058587NIDDK NIH HHS R01-DK58587
6 · The paper itself

Abstract

Helicobacter pylori (H. pylori) is the strongest known risk factor for gastric carcinogenesis. One cancer-linked locus is the cag pathogenicity island, which translocates components of peptidoglycan into host cells. NOD1 is an intracellular immune receptor that senses peptidoglycan from Gram-negative bacteria and responds by inducing autophagy and activating NF-κB, leading to inflammation-mediated bacterial clearance; however chronic pathogens can evade NOD1-mediated clearance by altering peptidoglycan structure. We previously demonstrated that the H. pylori cag(+) strain 7.13 rapidly induces gastric cancer in Mongolian gerbils. Using 2D-DIGE and mass spectrometry, we identified a novel mutation within the gene encoding the peptidoglycan deacetylase PgdA; therefore, we sought to define the role of H. pylori PgdA in NOD1-dependent activation of NF-κB, inflammation, and cancer. Coculture of H. pylori strain 7.13 or its pgdA(-) isogenic mutant with AGS gastric epithelial cells or HEK293 epithelial cells expressing a NF-κB reporter revealed that pgdA inactivation significantly decreased NOD1-dependent NF-κB activation and autophagy. Infection of Mongolian gerbils with an H. pylori pgdA(-) mutant strain led to significantly decreased levels of inflammation and malignant lesions in the stomach; however, preactivation of NOD1 before bacterial challenge reciprocally suppressed inflammation and cancer in response to wild-type H. pylori. Expression of NOD1 differs in human gastric cancer specimens compared with noncancer samples harvested from the same patients. These results indicate that peptidoglycan deacetylation plays an important role in modulating host inflammatory responses to H. pylori, allowing the bacteria to persist and induce carcinogenic consequences in the gastric niche.

Indexed as

AcetylationAcetyltransferasesAdenocarcinomaAgedAmidohydrolasesAnimalsBacterial ProteinsCells, CulturedCell Transformation, NeoplasticFemaleGastritisGene SilencingGerbillinaeHEK293 CellsHelicobacter pyloriHost-Pathogen InteractionsAcetyltransferasesAmidohydrolasesBacterial ProteinsNOD1 protein, humanNod1 Signaling Adaptor ProteinPeptidoglycan

Identifiers

PMID25732381
PMCPMC4401661
OpenAlexW2047184114

What OpenQuestion holds

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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.