Evidence map›Paper›PMID 24901306›Full record

ArticlePloS one2014

The NOD-like receptor signalling pathway in Helicobacter pylori infection and related gastric cancer: a case-control study and gene expression analyses.

Natalia Castaño-Rodríguez, Nadeem O Kaakoush, Khean-Lee Goh, Kwong Ming Fock, Hazel M Mitchell

Erratum issuedOpen access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 72 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed, 1 pooled it
7.0field-weighted citation impact, top 3% 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

72 citing papers in PubMed, 1 synthesis or guideline pooled it, 115 citations in OpenAlex.

  1. Pooled it
  2. [Molecular mechanisms of chronic gastric mucosal inflammation induced byZhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2026
    Review
  3. Review
  4. Role of Nod-like Receptors inMicroorganisms · 2026
    Review
  5. Review
  6. Review
  7. Research and development prospects of TRIM65.Journal of cancer research and clinical oncology · 2025
    Review
  8. Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Review
  14. Article
  15. NLRP inflammasomes in health and disease.Molecular biomedicine · 2024
    Review
  16. Article
  17. Review
  18. Article
  19. Review
  20. Article

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 3 institutions in 3 countries.

Natalia Castaño-RodríguezSchool of Biotechnology and Biomolecular Sciences, The University of New South Wales, Sydney, New South Wales, Australia.
Nadeem O KaakoushSchool of Biotechnology and Biomolecular Sciences, The University of New South Wales, Sydney, New South Wales, Australia.
Khean-Lee GohDepartment of Medicine, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia.
Kwong Ming FockDivision of Gastroenterology, Department of Medicine, Changi General Hospital, Singapore, Singapore.
Hazel M MitchellSchool of Biotechnology and Biomolecular Sciences, The University of New South Wales, Sydney, New South Wales, Australia.
UNSW Sydney · AUChangi General Hospital · SGUniversity of Malaya · MY

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCurrently, it is well established that cancer arises in chronically inflamed tissue. A number of NOD-like receptors (NLRs) form inflammasomes, intracellular multiprotein complexes critical for generating mature pro-inflammatory cytokines (IL-1β and IL-18). As chronic inflammation of the gastric mucosa is a consequence of Helicobacter pylori infection, we investigated the role of genetic polymorphisms and expression of genes involved in the NLR signalling pathway in H. pylori infection and related gastric cancer (GC). MATERIALS AND

methodsFifty-one genetic polymorphisms were genotyped in 310 ethnic Chinese (87 non-cardia GC cases and 223 controls with functional dyspepsia). In addition, gene expression of 84 molecules involved in the NLR signalling pathway was assessed in THP-1 cells challenged with two H. pylori strains, GC026 (GC) and 26695 (gastritis).

resultsCARD8-rs11672725, NLRP3-rs10754558, NLRP3-rs4612666, NLRP12-rs199475867 and NLRX1-rs10790286 showed significant associations with GC. On multivariate analysis, CARD8-rs11672725 remained a risk factor (OR: 4.80, 95% CI: 1.39-16.58). Further, NLRP12-rs2866112 increased the risk of H. pylori infection (OR: 2.13, 95% CI: 1.22-3.71). Statistical analyses assessing the joint effect of H. pylori infection and the selected polymorphisms revealed strong associations with GC (CARD8, NLRP3, CASP1 and NLRP12 polymorphisms). In gene expression analyses, five genes encoding NLRs were significantly regulated in H. pylori-challenged cells (NLRC4, NLRC5, NLRP9, NLRP12 and NLRX1). Interestingly, persistent up-regulation of NFKB1 with simultaneous down-regulation of NLRP12 and NLRX1 was observed in H. pylori GC026-challenged cells. Further, NF-κB target genes encoding pro-inflammatory cytokines, chemokines and molecules involved in carcinogenesis were markedly up-regulated in H. pylori GC026-challenged cells.

conclusionsNovel associations between polymorphisms in the NLR signalling pathway (CARD8, NLRP3, NLRP12, NLRX1, and CASP1) and GC were identified in Chinese individuals. Our genetic polymorphisms and gene expression results highlight the relevance of the NLR signalling pathway in gastric carcinogenesis and its close interaction with NF-κB.

Indexed as

Helicobacter pyloriSignal TransductionAdultAgedAged, 80 and overAllelesAsian PeopleCase-Control StudiesCell LineChinaCytokinesFemaleGene Expression ProfilingGene Expression RegulationGenetic Predisposition to DiseaseGenotypeCytokinesReceptors, Pattern Recognition

Identifiers

PMID24901306
PMCPMC4047072
OpenAlexW1983412451

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.