Evidence map›Paper›PMID 25101079›Full record

ReviewFrontiers in immunology2014

Pattern-recognition receptors and gastric cancer.

Natalia Castaño-Rodríguez, Nadeem O Kaakoush, Hazel M Mitchell

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
84citing papers in PubMed, 2 pooled it
13.2field-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

84 citing papers in PubMed, 2 syntheses or guidelines pooled it, 143 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Role of Nod-like Receptors inMicroorganisms · 2026
    Review
  5. Review
  6. Update on the pathogenesis and clinical management ofWorld journal of gastrointestinal pathophysiology · 2025
    Review
  7. Article
  8. Review
  9. The role of TLRs (microbe recognition receptor) in gastric cancer: An update.Naunyn-Schmiedeberg's archives of pharmacology · 2025
    Review
  10. Role of Innate Immunity in Cancer.Advances in experimental medicine and biology · 2025
    Review
  11. Article
  12. Article
  13. Curcumin for gastric cancer: Mechanism predictionWorld journal of gastrointestinal oncology · 2024
    Article
  14. Review
  15. Review
  16. Article
  17. Pathogenomics of Helicobacter pylori.Current topics in microbiology and immunology · 2023
    Review
  18. Article
  19. Article
  20. Review

24 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

3 authors at 1 institution in 1 country.

Natalia Castaño-RodríguezSchool of Biotechnology and Biomolecular Sciences, The University of New South Wales , Sydney, NSW , Australia.
Nadeem O KaakoushSchool of Biotechnology and Biomolecular Sciences, The University of New South Wales , Sydney, NSW , Australia.
Hazel M MitchellSchool of Biotechnology and Biomolecular Sciences, The University of New South Wales , Sydney, NSW , Australia.
UNSW Sydney · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic inflammation has been associated with an increased risk of several human malignancies, a classic example being gastric adenocarcinoma (GC). Development of GC is known to result from infection of the gastric mucosa by Helicobacter pylori, which initially induces acute inflammation and, in a subset of patients, progresses over time to chronic inflammation, gastric atrophy, intestinal metaplasia, dysplasia, and finally intestinal-type GC. Germ-line encoded receptors known as pattern-recognition receptors (PRRs) are critical for generating mature pro-inflammatory cytokines that are crucial for both Th1 and Th2 responses. Given that H. pylori is initially targeted by PRRs, it is conceivable that dysfunction within genes of this arm of the immune system could modulate the host response against H. pylori infection, and subsequently influence the emergence of GC. Current evidence suggests that Toll-like receptors (TLRs) (TLR2, TLR3, TLR4, TLR5, and TLR9), nucleotide-binding oligomerization domain (NOD)-like receptors (NLRs) (NOD1, NOD2, and NLRP3), a C-type lectin receptor (DC-SIGN), and retinoic acid-inducible gene (RIG)-I-like receptors (RIG-I and MDA-5), are involved in both the recognition of H. pylori and gastric carcinogenesis. In addition, polymorphisms in genes involved in the TLR (TLR1, TLR2, TLR4, TLR5, TLR9, and CD14) and NLR (NOD1, NOD2, NLRP3, NLRP12, NLRX1, CASP1, ASC, and CARD8) signaling pathways have been shown to modulate the risk of H. pylori infection, gastric precancerous lesions, and/or GC. Further, the modulation of PRRs has been suggested to suppress H. pylori-induced inflammation and enhance GC cell apoptosis, highlighting their potential relevance in GC therapeutics. In this review, we present current advances in our understanding of the role of the TLR and NLR signaling pathways in the pathogenesis of GC, address the involvement of other recently identified PRRs in GC, and discuss the potential implications of PRRs in GC immunotherapy.

Indexed as

genetic polymorphismHelicobacter pyloriinflammationNOD-like receptorspattern-recognition receptorsstomach neoplasmtherapeuticsToll-like receptors

Identifiers

PMID25101079
PMCPMC4105827
OpenAlexW2043003819

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.