Evidence map›Paper›PMID 21992464›Full record

Trial reportJournal of experimental & clinical cancer research : CR2011

HGF/c-Met related activation of β-catenin in hepatoblastoma.

Rachel Purcell, Margaret Childs, Rudolf Maibach, Carina Miles, Clinton Turner, Arthur Zimmermann, Michael Sullivan

Open access · goldAbstract readMulticenter StudyRandomized Controlled Trial
In one paragraph

Trial report in Journal of experimental & clinical cancer research : CR, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 2 pooled it
3.1field-weighted citation impact, top 8% 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, 2 syntheses or guidelines pooled it, 72 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Article
  5. Article
  6. Review
  7. Wnt/β-Catenin Signaling in Liver Pathobiology.Annual review of pathology · 2025
    Review
  8. Review
  9. Article
  10. Wnt/β-catenin signaling pathway in liver biology and tumorigenesis.In vitro cellular & developmental biology. Animal · 2024
    Review
  11. Article
  12. Review
  13. Review
  14. Molecular Mechanisms of Hepatoblastoma.Seminars in liver disease · 2021
    Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. 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

7 authors at 4 institutions in 3 countries.

Rachel PurcellChildren's Cancer Research Group, University of Otago, Christchurch, Christchurch, New Zealand. rachel.purcell@otago.ac.nz
Margaret Childs
Rudolf Maibach
Carina Miles
Clinton Turner
Arthur Zimmermann
Michael Sullivan
Canterbury Health Laboratories · NZUniversity of Otago · NZUniversity of Bern · CHUniversity of Leicester · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundActivation of beta-catenin is a hallmark of hepatoblastoma (HB) and appears to play a crucial role in its pathogenesis. While aberrant accumulation of the beta-catenin is a common event in HB, mutations or deletions in CTNNB1 (beta-catenin gene) do not always account for the high frequency of protein expression. In this study we have investigated alternative activation of beta-catenin by HGF/c-Met signaling in a large cohort of 98 HB patients enrolled in the SIOPEL-3 clinical trial.

methodsWe performed immunohistochemistry, using antibodies to total beta-catenin and tyrosine654-phosphorylated beta-catenin, which is a good surrogate marker of HGF/c-Met activation. CTNNB1 mutation analysis was also carried out on all samples. We also investigated beta-catenin pathway activation in two liver cancer cell lines, HuH-6 and HuH-7.

resultsAberrant beta-catenin expression was seen in the cytoplasm and/or nucleus of 87% of tumour samples. Our results also revealed a large subset of HB, 83%, with cytoplasmic expression of tyrosine654-phosphorylated beta-catenin and 30% showing additional nuclear accumulation. Sequence analysis revealed mutations in 15% of our cohort. Statistical analysis showed an association between nuclear expression of c-Met-activated beta-catenin and wild type CTNNB1 (P-value = 0.015). Analysis of total beta-catenin and Y654-beta-catenin in response to HGF activation in the cell lines, mirrors that observed in our HB tumour cohort.

resultsWe identified a significant subset of hepatoblastoma patients for whom targeting of the c-Met pathway may be a treatment option and also demonstrate distinct mechanisms of beta-catenin activation in HB.

Indexed as

Antineoplastic Combined Chemotherapy Protocolsbeta CateninCarboplatinCell NucleusCisplatinCohort StudiesCytoplasmDNA, NeoplasmDoxorubicinFollow-Up StudiesHepatoblastomaHepatocyte Growth FactorHumansImmunoenzyme TechniquesInternational AgenciesLiver Neoplasmsbeta CateninCarboplatinCisplatinCTNNB1 protein, humanDNA, NeoplasmDoxorubicinHepatocyte Growth FactorProto-Oncogene Proteins c-metRNA, MessengerRNA, NeoplasmTyrosine

Identifiers

PMID21992464
PMCPMC3207961
OpenAlexW1992214889

What OpenQuestion holds

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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.