Evidence map›Paper›PMID 10698519›Full record

ArticleOncogene2000

Activation of beta-catenin in epithelial and mesenchymal hepatoblastomas.

Y Wei, M Fabre, S Branchereau, F Gauthier, G Perilongo, M A Buendia

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
4.2field-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

43 citing papers in PubMed, 169 citations in OpenAlex.

  1. HGF/c-Met related activation of β-catenin in hepatoblastoma.Journal of experimental & clinical cancer research : CR · 2011
    Trial
  2. Article
  3. Review
  4. Review
  5. DLK1/DIO3 locus upregulation by a β-catenin-dependent enhancer drives cell proliferation and liver tumorigenesis.Molecular therapy : the journal of the American Society of Gene Therapy · 2024
    Article
  6. Article
  7. Genes · 2022
    Article
  8. Article
  9. Article
  10. A MicroRNA Cluster in theFrontiers in oncology · 2020
    Article
  11. Article
  12. Review
  13. Wnt-β-catenin signalling in liver development, health and disease.Nature reviews. Gastroenterology & hepatology · 2019
    Review
  14. Article
  15. Observational
  16. Article
  17. Article
  18. Review
  19. Activated macrophages promote Wnt/β-catenin signaling in cholangiocarcinoma cells.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
    Article
  20. Article
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 2 countries.

Y WeiUnité de Recombinasion et Expression Génétique INSERM U163, Institut Pasteur, Paris, France.
M Fabre
S Branchereau
F Gauthier
G Perilongo
M A Buendia
Bicêtre Hospital · FRInserm · FRUniversity of Padua · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Wnt/beta-catenin signaling is frequently activated in cancer cells by stabilizing mutations of beta-catenin or loss-of-function mutations of the APC tumor suppressor gene. We have analysed the role of beta-catenin in the pathogenesis of hepatoblastoma (HB), an embryonic liver tumor occurring mainly in children under 2 years of age. Sequence analysis of the beta-catenin NH2-terminal domain in 18 epithelial and mixed HBs revealed missense mutations in the GSK3beta phosphorylation motif or interstitial deletions in 12 tumors (67%). In the remaining cases, no truncating mutation of APC could be evidenced. Immunohistochemical analysis of beta-catenin in 11 HBs demonstrated nuclear/cytoplasmic accumulation of the protein in all tumors analysed, with predominant nuclear beta-catenin immunostaining in undifferentiated cells. Membranous beta-catenin localization was preserved only in fetal-type tumoral hepatocytes and was associated with E-cadherin expression. Moreover, we show that beta-catenin is aberrantly overexpressed in a large spectrum of tumor components, including hepatocyte-like cells at various differentiation stages and heterologous elements such as squamous, osteoid and chrondroid tissues, and in occasional other mesenchymally-derived cells. These data strongly suggest that activation of beta-catenin signaling is an obligatory step in HB pathogenesis, and raise the possibility that it interferes with developmental signals that specify different tissue types at early stages of hepatic differentiation.

Indexed as

MutationTrans-Activatorsbeta CateninBiological TransportCadherinsCalcium-Calmodulin-Dependent Protein KinasesCell DifferentiationCell LineCell LineageChild, PreschoolCodonCytoskeletal ProteinsDNA Mutational AnalysisDNA, NeoplasmEpithelial CellsFemalebeta CateninCadherinsCalcium-Calmodulin-Dependent Protein KinasesCodonCTNNB1 protein, humanCytoskeletal ProteinsDNA, NeoplasmGlycogen Synthase Kinase 3Neoplasm ProteinsTrans-Activators

Identifiers

PMID10698519
OpenAlexW1984927780

What OpenQuestion holds

Textmetadata
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.