Evidence map›Paper›PMID 10597266›Full record

ArticleOncogene1999

Predominance of beta-catenin mutations and beta-catenin dysregulation in sporadic aggressive fibromatosis (desmoid tumor).

S Tejpar, F Nollet, C Li, J S Wunder, G Michils, P dal Cin, E Van Cutsem, B Bapat, F van Roy, J J Cassiman and 1 more

Abstract read
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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 102 papers.

0numbers the graph read from it
0cells of the map it votes in
102citing papers in PubMed
6.8field-weighted citation impact, top 2% 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

102 citing papers in PubMed, 345 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. An intra-abdominal desmoid tumour: Case report.International journal of surgery case reports · 2025
    Article
  7. Article
  8. Article
  9. Molecular testing of soft tissue tumors.Diagnostic cytopathology · 2023
    Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. CRISPR-SID: Identifying EZH2 as a druggable target for desmoid tumors via in vivo dependency mapping.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article

42 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 2 countries.

S TejparProgramme in Development Biology, Hospital for Sick Children, Toronto Ontario, Canada.
F Nollet
C Li
J S Wunder
G Michils
P dal Cin
E Van Cutsem
B Bapat
F van Roy
J J Cassiman
B A Alman
KU Leuven · BEGhent University · BEHospital for Sick Children · CAMount Sinai Hospital · CAUniversity of Toronto · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aggressive fibromatosis (also called desmoid tumor) occurs as a sporadic lesion or as part of Familial Adenomatous Polyposis, which is caused by germ line mutations in the Adenomatous polyposis Coli (APC) gene. APC is involved in the regulation of the cellular level of beta-catenin, which is a mediator in Wnt signaling. Mutational analysis of the beta-catenin and APC genes was performed in 42 sporadic aggressive fibromatoses. Nine tumors had mutations in APC, and 22 had a point mutation in beta-catenin at either codon 45 or codon 41 (producing a stabilized beta-catenin protein product). Immunohistochemistry showed an elevated beta-catenin protein level in all tumors, regardless of mutational status. Beta-catenin localized to the nucleus, and was not tyrosine phosphorylated in the six tumors in which this was tested. The demonstration of mutations in two mediators in the Wnt-APC-beta-catenin pathway implicates beta-catenin stabilization as the key factor in the pathogenesis of aggressive fibromatosis. This is the first demonstration of somatic beta-catenin mutations in a locally invasive, but non metastatic lesion composed of spindle cells, illustrating the importance of beta-catenin stabilization in a variety of cell types and neoplastic processes. Moreover, this tumor has one of the highest reported frequencies of beta-catenin mutations of any tumor type.

Indexed as

Gene Expression RegulationGenes, APCMutationTrans-ActivatorsBase Sequencebeta CateninCytoskeletal ProteinsDNAFibromaHumansPhosphorylationTyrosinebeta CateninCTNNB1 protein, humanCytoskeletal ProteinsDNATrans-ActivatorsTyrosine

Identifiers

PMID10597266
OpenAlexW1982804269

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.