Evidence map›Paper›PMID 10597262›Full record

ArticleOncogene1999

Close correlation between beta-catenin gene alterations and nuclear accumulation of the protein in human hepatocellular carcinomas.

B Terris, P Pineau, L Bregeaud, D Valla, J Belghiti, P Tiollais, C Degott, A Dejean

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

36 citing papers in PubMed, 120 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. Correlation of exon 3 β-catenin mutations with glutamine synthetase staining patterns in hepatocellular adenoma and hepatocellular carcinoma.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2016
    Article
  12. DNA markers in molecular diagnostics for hepatocellular carcinoma.Expert review of molecular diagnostics · 2014
    Review
  13. Expression of RUNX3 and β-catenin in the carcinogenesis of sporadic colorectal tubular adenoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
    Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Article
  20. Molecular genetics of hepatocellular neoplasia.American journal of translational research · 2010
    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

8 authors at 3 institutions in 1 country.

B TerrisService d'Anatomie Pathologique, Hôpital Beaujon, Clichy, France.
P Pineau
L Bregeaud
D Valla
J Belghiti
P Tiollais
C Degott
A Dejean
Hôpital Beaujon · FRInserm · FRInstitut Pasteur · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Several lines of evidence indicate that beta-catenin acquires oncogenic activity when its intracellular concentration increases as a result of either mutation in the beta-catenin gene itself or inactivation of the adenomatous polyposis coli (APC) gene. In an attempt to elucidate the molecular mechanisms underlying hepatocellular carcinogenesis, we have studied the frequency of beta-catenin gene alterations in exon 3, a region known to represent a mutation hot spot, and its inappropriate protein expression by immunohistochemistry in 73 hepatocellular carcinomas (HCCs). The results were correlated with different clinical and pathological data, particularly with the presence or not of an associated cirrhosis. Fourteen (19%) HCCs showed beta-catenin gene alterations with missense mutations in nine cases and interstitial deletions in five cases. These genetic alterations were present in both cirrhotic and non-cirrhotic groups. By contrast, we did not find any beta-catenin gene alterations in the nine fibromellar carcinomas we examined. Nuclear accumulation of the protein was observed in 18 of them (25%). Remarkably, these included ten of the 14 tumors harboring somatic mutations in the beta-catenin gene (P < 0.001). Our results indicate that accumulation of beta-catenin resulting from genetic mutations is a frequent event in non-fibrolamellar type hepatocellular carcinoma. The close association between increased beta-catenin protein stability and mutation indicates that immunohistochemistry may be a powerful method for the detection of the mutated protein in future clinical practice.

Indexed as

MutationTrans-Activatorsbeta CateninCarcinoma, HepatocellularCell NucleusCytoskeletal ProteinsHumansImmunohistochemistryLiver Neoplasmsbeta CateninCTNNB1 protein, humanCytoskeletal ProteinsTrans-Activators

Identifiers

PMID10597262
OpenAlexW2316712853

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.