Evidence map›Paper›PMID 9671767›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1998

Somatic mutations of the beta-catenin gene are frequent in mouse and human hepatocellular carcinomas.

A de La Coste, B Romagnolo, P Billuart, C A Renard, M A Buendia, O Soubrane, M Fabre, J Chelly, C Beldjord, A Kahn and 1 more

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 406 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
406citing papers in PubMed, 1 pooled it
17.5field-weighted citation impact, top 1% 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

406 citing papers in PubMed, 1 synthesis or guideline pooled it, 1,094 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Review
  6. Review
  7. Review
  8. Article
  9. Novel Therapeutics for Hepatocellular Carcinoma.Clinics in liver disease · 2025
    Review
  10. Review
  11. Hepatitis B virus integration and hepatocarcinogenesis.Liver research (Beijing, China) · 2025
    Review
  12. Article
  13. Review
  14. Review
  15. Article
  16. Review
  17. Review
  18. Article
  19. Article
  20. Article

346 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

11 authors at 5 institutions in 1 country.

A de La CosteInstitut National de la Santé et de la Recherche Médicale U129, Institut Cochin de Génétique Moléculaire, Université Paris V René Descartes, 24 rue du Faubourg Saint-Jacques, 75014 Paris, France.
B Romagnolo
P Billuart
C A Renard
M A Buendia
O Soubrane
M Fabre
J Chelly
C Beldjord
A Kahn
C Perret
Inserm · FRUniversité Paris Cité · FRHôpital Cochin · FRInstitut Cochin · FRInstitut Pasteur · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatocellular carcinoma (HCC) is the major primary malignant tumor in the human liver, but the molecular changes leading to liver cell transformation remain largely unknown. The Wnt-beta-catenin pathway is activated in colon cancers and some melanoma cell lines, but has not yet been investigated in HCC. We have examined the status of the beta-catenin gene in different transgenic mouse lines of HCC obtained with the oncogenes c-myc or H-ras. Fifty percent of the hepatic tumors in these transgenic mice had activating somatic mutations within the beta-catenin gene similar to those found in colon cancers and melanomas. These alterations in the beta-catenin gene (point mutations or deletions) lead to a disregulation of the signaling function of beta-catenin and thus to carcinogenesis. We then analyzed human HCCs and found similar mutations in eight of 31 (26%) human liver tumors tested and in HepG2 and HuH6 hepatoma cells. The mutations led to the accumulation of beta-catenin in the nucleus. Thus alterations in the beta-catenin gene frequently are selected for during liver tumorigenesis and suggest that disregulation of the Wnt-beta-catenin pathway is a major event in the development of HCC in humans and mice.

Indexed as

Point MutationTrans-ActivatorsAnimalsBase Sequencebeta CateninCalcium-Calmodulin-Dependent Protein KinasesCarcinoma, HepatocellularCytoskeletal ProteinsDNA PrimersGlycogen Synthase Kinase 3HumansLiver NeoplasmsMiceMice, TransgenicPhosphorylationTumor Cells, Culturedbeta CateninCalcium-Calmodulin-Dependent Protein KinasesCTNNB1 protein, humanCTNNB1 protein, mouseCytoskeletal ProteinsDNA PrimersGlycogen Synthase Kinase 3Trans-Activators

Identifiers

PMID9671767
PMCPMC21165
OpenAlexW1990563353

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.