Evidence map›Paper›PMID 30910700›Full record

ArticleCellular and molecular gastroenterology and hepatology2019

Deficiency of Stomach-Type Claudin-18 in Mice Induces Gastric Tumor Formation Independent of H pylori Infection.

Koya Suzuki, Kazuhiro Sentani, Hiroo Tanaka, Tomoki Yano, Kazuo Suzuki, Masanobu Oshima, Wataru Yasui, Atsushi Tamura, Sachiko Tsukita

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

Article in Cellular and molecular gastroenterology and hepatology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 10% 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

38 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. World journal of gastrointestinal oncology · 2024
    Article
  10. Review
  11. Claudin 18.2 as a novel therapeutic target.Nature reviews. Clinical oncology · 2024
    Review
  12. Review
  13. Article
  14. Article
  15. Research (Washington, D.C.) · 2024
    Article
  16. Review
  17. Review
  18. Review
  19. Review
  20. World journal of clinical cases · 2023
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 4 institutions in 1 country.

Koya SuzukiLaboratory of Biological Science, Graduate School of Frontier Biosciences, and Graduate School of Medicine, Osaka University, Osaka, Japan; Research Institute for Diseases of Old Age and Department of Clinical Laboratory Medicine, Graduate School of Medicine, Juntendo University, Tokyo, Japan. Electronic address: koya-suzuki@juntendo.ac.jp.
Kazuhiro SentaniDepartment of Molecular Pathology, Hiroshima University, Institute of Biomedical and Health Sciences, Hiroshima, Japan.
Hiroo TanakaLaboratory of Biological Science, Graduate School of Frontier Biosciences, and Graduate School of Medicine, Osaka University, Osaka, Japan.
Tomoki YanoLaboratory of Biological Science, Graduate School of Frontier Biosciences, and Graduate School of Medicine, Osaka University, Osaka, Japan.
Kazuo SuzukiDepartment of Health Protection, Graduate School of Medicine, Asia International Institute of Infectious Disease Control, Teikyo University, Tokyo, Japan.
Masanobu OshimaDivision of Genetics, Cancer Research Institute, and Nano Life Science Institute, Kanazawa University, Kanazawa, Japan.
Wataru YasuiDepartment of Molecular Pathology, Hiroshima University, Institute of Biomedical and Health Sciences, Hiroshima, Japan.
Atsushi TamuraLaboratory of Biological Science, Graduate School of Frontier Biosciences, and Graduate School of Medicine, Osaka University, Osaka, Japan. Electronic address: atamura@biosci.med.osaka-u.ac.jp.
Sachiko TsukitaLaboratory of Biological Science, Graduate School of Frontier Biosciences, and Graduate School of Medicine, Osaka University, Osaka, Japan. Electronic address: atsukita@biosci.med.osaka-u.ac.jp.
The University of Osaka · JPHiroshima University · JPJuntendo University · JPKanazawa University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND &

aimsEpithelial cells are joined by tight junctions (TJs) to form a cell sheet. In the stomach, epithelial cell sheet forms an essential barrier against gastric material, including gastric acid. Although the decreased expression of stomach-type claudin-18 (stCldn18), a TJ protein, is generally observed in human gastritis and gastric cancer, its pathological roles are not fully understood. We previously reported that mice lacking stCldn18 (stCldn18-/-) exhibit gastric acid leakage through TJs, which induces active gastritis at a young age. Here, we examined the gastric pathologies in mice after long-term stCldn18 deficiency.

methodsThe gastric pathologies in stCldn18-/- mice were sequentially analyzed from youth to old age, and compared to those in humans. To examine the relationship between stCldn18 deficiency-induced gastric pathologies and Wnt-dependent tumorigenesis, we generated Wnt1-overexpressing stCldn18-/- mice.

resultsStCldn18-/- mice developed chronic active gastritis at middle age, with expression of the chemoattractant CCL28. At old age, 20-30% of these mice developed gastric tumors with CXCL5 expression, indicative of EMT. In this process, spasmolytic polypeptide-expressing metaplasia (SPEM) cells appeared. Increased expressions of CD44-variants, TLR2, and CXCL5 indicated age-dependent changes in cell characteristics. Some features of the stCldn18-/- mouse gastric tumorigenesis resembled H pylori-infection-related human carcinogenesis. The gastric tumorigenesis was accelerated in Wnt1-overexpressing stCldn18-/- mice, indicating that Wnt is involved in the stCldn18-/- mouse gastric tumorigenesis.

conclusionsStCldn18 deficiency induced gastric tumorigenesis in mice without H pylori infection. Our findings revealed that several signaling networks, including the cytokine-, stemness-, and Wnt-signaling pathways, may be activated under the stCldn18-deficiency-induced chronic active gastritis to accelerate the gastric tumorigenesis.

Indexed as

AnimalsClaudinsCytokinesDisease Models, AnimalDisease ProgressionGastritisHumansMiceSignal TransductionStomach NeoplasmsWnt1 ProteinWnt Signaling PathwayClaudinsCldn18 protein, mouseCytokinesWnt1 ProteinWnt1 protein, mouseChronic Active GastritisEpithelial BarrierSPEMTight Junction

Identifiers

PMID30910700
PMCPMC6554658
OpenAlexW2926997922

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.