Evidence map›Paper›PMID 27079437›Full record

ReviewCancer science2016

Inflammation in gastric cancer: Interplay of the COX-2/prostaglandin E2 and Toll-like receptor/MyD88 pathways.

Kanae Echizen, Osamu Hirose, Yusuke Maeda, Masanobu Oshima

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

Review in Cancer science, 2016. 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 129 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
129citing papers in PubMed, 1 pooled it
19.3field-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

129 citing papers in PubMed, 1 synthesis or guideline pooled it, 243 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. The role of NLRP3 inflammasome in 5-fluorouracil resistance of oral squamous cell carcinoma.Journal of experimental & clinical cancer research : CR · 2017
    Trial
  4. Review
  5. Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. Genetic architecture of gastric adenocarcinoma in West Asia.Clinical and translational medicine · 2025
    Article
  15. Review
  16. The role of TLRs (microbe recognition receptor) in gastric cancer: An update.Naunyn-Schmiedeberg's archives of pharmacology · 2025
    Review
  17. Article
  18. Article
  19. Article
  20. Review

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 3 institutions in 2 countries.

Kanae EchizenDivision of Genetics, Cancer Research Institute, Kanazawa University, Kanazawa, Japan.
Osamu HiroseFaculty of Electrical and Computer Engineering, Institute of Science and Engineering, Kanazawa University, Kanazawa, Japan.
Yusuke MaedaDivision of Genetics, Cancer Research Institute, Kanazawa University, Kanazawa, Japan.
Masanobu OshimaDivision of Genetics, Cancer Research Institute, Kanazawa University, Kanazawa, Japan.
Japan Agency for Medical Research and Development · JPInstitute for Advanced Medical Research · USKanazawa University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cyclooxygenase-2 (COX-2) and its downstream product prostaglandin E2 (PGE2 ) play a key role in generation of the inflammatory microenvironment in tumor tissues. Gastric cancer is closely associated with Helicobacter pylori infection, which stimulates innate immune responses through Toll-like receptors (TLRs), inducing COX-2/PGE2 pathway through nuclear factor-κB activation. A pathway analysis of human gastric cancer shows that both the COX-2 pathway and Wnt/β-catenin signaling are significantly activated in tubular-type gastric cancer, and basal levels of these pathways are also increased in other types of gastric cancer. Expression of interleukin-11, chemokine (C-X-C motif) ligand 1 (CXCL1), CXCL2, and CXCL5, which play tumor-promoting roles through a variety of mechanisms, is induced in a COX-2/PGE2 pathway-dependent manner in both human and mouse gastric tumors. Moreover, the COX-2/PGE2 pathway plays an important role in the maintenance of stemness with expression of stem cell markers, including CD44, Prom1, and Sox9, which are induced in both gastritis and gastric tumors through a COX-2/PGE2 -dependent mechanism. In contrast, disruption of Myd88 results in suppression of the inflammatory microenvironment in gastric tumors even when the COX-2/PGE2 pathway is activated, indicating that the interplay of the COX-2/PGE2 and TLR/MyD88 pathways is needed for inflammatory response in tumor tissues. Furthermore, TLR2/MyD88 signaling plays a role in maintenance of stemness in normal stem cells as well as gastric tumor cells. Accordingly, these results suggest that targeting the COX-2/PGE2 pathway together with TLR/MyD88 signaling, which would suppress the inflammatory microenvironment and maintenance of stemness, could be an effective preventive or therapeutic strategy for gastric cancer.

Indexed as

AnimalsCyclooxygenase 2DinoprostoneHumansInflammationMiceMyeloid Differentiation Factor 88Neoplasm ProteinsSignal TransductionStomach NeoplasmsToll-Like Receptor 2Tumor MicroenvironmentCyclooxygenase 2DinoprostoneMYD88 protein, humanMyeloid Differentiation Factor 88Neoplasm ProteinsPTGS2 protein, humanToll-Like Receptor 2Gastric cancerinflammationinnate immunitymicroenvironmentstemness

Identifiers

PMID27079437
PMCPMC4832872
OpenAlexW2315204759

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.