Evidence map›Paper›PMID 29396430›Full record

ArticleScientific reports2018

Functional loss of p53 cooperates with the in vivo microenvironment to promote malignant progression of gastric cancers.

Junko Ohtsuka, Hiroko Oshima, Issei Ezawa, Ryo Abe, Masanobu Oshima, Rieko Ohki

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 13% 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

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 40 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Molecular characteristics andFrontiers in oncology · 2026
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  10. Review
  11. Combined loss of CDH1 and downstream regulatory sequences drive early-onset diffuse gastric cancer and increase penetrance of hereditary diffuse gastric cancer.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2023
    Article
  12. Article
  13. Journal of thoracic disease · 2022
    Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Viruses join the circular RNA world.The FEBS journal · 2021
    Review
  19. Review
  20. Review
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

6 authors at 3 institutions in 1 country.

Junko OhtsukaLaboratory of Fundamental Oncology, National Cancer Center Research Institute, Tsukiji 5-1-1, Chuo-ku, Tokyo, 104-0045, Japan.
Hiroko OshimaDivision of Genetics, Cancer Research Institute, Kanazawa University, Kanazawa, 920-1192, Japan.
Issei EzawaLaboratory of Fundamental Oncology, National Cancer Center Research Institute, Tsukiji 5-1-1, Chuo-ku, Tokyo, 104-0045, Japan.
Ryo AbeDivision of Immunobiology, Research Institute for Biomedical Sciences, Tokyo University of Science, 2669 Yamazaki, Noda City, Chiba, 278-0022, Japan.
Masanobu OshimaDivision of Genetics, Cancer Research Institute, Kanazawa University, Kanazawa, 920-1192, Japan.
Rieko OhkiLaboratory of Fundamental Oncology, National Cancer Center Research Institute, Tsukiji 5-1-1, Chuo-ku, Tokyo, 104-0045, Japan. rohki@ncc.go.jp.
Kanazawa University · JPTokyo University of Science · JPWaseda University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

p53 mutations are frequently detected in malignant gastric cancers. However, the molecular mechanisms by which loss of p53 function promotes gastric cancer are not clear. We utilized Gan mice (K19-Wnt1/C2mE), which have functional p53 and develop intestinal-type gastric tumors, to investigate the role of p53 in gastric cancer progression by knocking out p53. We found that gastric epithelial cells acquire tumorigenicity in the subcutis of C57BL/6 mice as a result of Wnt activation, COX-2 activation and p53 deficiency. With repeated allograft transfers, these gastric epithelial cells gradually acquired the properties of malignant gastric cancer. Loss of p53 conferred cell stemness and induced epithelial to mesenchymal transition (EMT) in gastric epithelial cells, and these properties were further enhanced by the in vivo microenvironment, ultimately leading to gastric cancer formation and metastasis. We also found that the in vivo microenvironment enhanced activation of the COX-2 pathway, which further contributed to cancer progression. With this system, we have succeeded in recapitulating the development of malignant gastric cancer from gastric epithelial cells in a normal immune environment.

Indexed as

CarcinogenesisAnimalsCells, CulturedCyclooxygenase 2Disease Models, AnimalEpithelial CellsEpithelial-Mesenchymal TransitionMice, Inbred C57BLMice, KnockoutStomach NeoplasmsTumor MicroenvironmentTumor Suppressor Protein p53Wnt Signaling PathwayCyclooxygenase 2Ptgs2 protein, mouseTrp53 protein, mouseTumor Suppressor Protein p53

Identifiers

PMID29396430
PMCPMC5797237
OpenAlexW2803552020

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.