Evidence map›Paper›PMID 11120777›Full record

ArticleThe Journal of experimental medicine2000

Impaired preneoplastic changes and liver tumor formation in tumor necrosis factor receptor type 1 knockout mice.

B Knight, G C Yeoh, K L Husk, T Ly, L J Abraham, C Yu, J A Rhim, N Fausto

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers.

0numbers the graph read from it
0cells of the map it votes in
91citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

91 citing papers in PubMed, 295 citations in OpenAlex.

  1. Article
  2. Review
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  4. Article
  5. ATXN2-mediated translation of TNFR1 promotes esophageal squamous cell carcinoma via mMolecular therapy : the journal of the American Society of Gene Therapy · 2022
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  7. Article
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  9. Review
  10. Heparanase and the hallmarks of cancer.Journal of translational medicine · 2020
    Review
  11. Liver progenitor cell-driven liver regeneration.Experimental & molecular medicine · 2020
    Review
  12. Review
  13. Redox Control of the Immune Response in the Hepatic Progenitor Cell Niche.Frontiers in cell and developmental biology · 2020
    Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Review

31 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

8 authors at 3 institutions in 2 countries.

B KnightUniversity of Western Australia, Department of Biochemistry, Nedlands WA 6907, Australia.
G C Yeoh
K L Husk
T Ly
L J Abraham
C Yu
J A Rhim
N Fausto
University of Washington · USUniversity of Western Australia · AUHarry Perkins Institute of Medical Research · AU

Funding

Pathogenesis of Hepatocellular CarcinomasR01CA074131 · NCI · UNIVERSITY OF WASHINGTON · PI FAUSTO, NELSON · 1997 to 2010
$3.1M
NCI NIH HHS CA74131NCI NIH HHS R01 CA074131
6 · The paper itself

Abstract

Hepatic stem cells (oval cells) proliferate within the liver after exposure to a variety of hepatic carcinogens and can generate both hepatocytes and bile duct cells. Oval cell proliferation is commonly seen in the preneoplastic stages of liver carcinogenesis, often accompanied by an inflammatory response. Tumor necrosis factor (TNF), an inflammatory cytokine, is also important in liver regeneration and hepatocellular growth. The experiments reported here explore the relationship among the TNF inflammatory pathway, liver stem cell activation, and tumorigenesis. We demonstrate that TNF is upregulated during oval cell proliferation induced by a choline-deficient, ethionine-supplemented diet and that it is expressed by oval cells. In TNF receptor type 1 knockout mice, oval cell proliferation is substantially impaired and tumorigenesis is reduced. Oval cell proliferation is impaired to a lesser extent in interleukin 6 knockout mice and is unchanged in TNF receptor type 2 knockout mice. These findings demonstrate that TNF signaling participates in the proliferation of oval cells during the preneoplastic phase of liver carcinogenesis and that loss of signaling through the TNF receptor type 1 reduces the incidence of tumor formation. The TNF inflammatory pathway may be a target for therapeutic intervention during the early stages of liver carcinogenesis.

Indexed as

Gene DeletionAnimalsCarcinogensCell CountCell DivisionCells, CulturedDietEthionineGene Expression RegulationHistocytochemistryInterleukin-6LiverLiver NeoplasmsMiceMice, KnockoutPrecancerous ConditionsCarcinogensEthionineInterleukin-6Receptors, Tumor Necrosis FactorRNA, MessengerTumor Necrosis Factor-alpha

Identifiers

PMID11120777
PMCPMC2213505
OpenAlexW2163478957

What OpenQuestion holds

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LicenceCC BY-NC-SA
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.