Evidence map›Paper›PMID 41606383›Full record

ArticleVirchows Archiv : an international journal of pathology2026

CTNNB1 mutation represents a recurrent driver molecular alteration in a subset of endometrial stromal tumors.

Pavel Dundr, Eliška Radová, Jan Hojný, Nikola Kudrnová, Michaela Kendall Bártů, Kristýna Němejcová, Marta Kalousová, Filip Frühauf, David Cibula, Radoslav Matěj and 2 more

Abstract readCase Reports
In one paragraph

Article in Virchows Archiv : an international journal of pathology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. 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

12 authors.

Pavel DundrDepartment of Pathology, First Faculty of Medicine, Charles University and General University Hospital in Prague, Studničkova 2, 12800, Prague 2, Czech Republic. pavel.dundr@vfn.cz.ORCID http://orcid.org/0000-0002-8940-6124
Eliška RadováDepartment of Pathology, First Faculty of Medicine, Charles University and General University Hospital in Prague, Studničkova 2, 12800, Prague 2, Czech Republic.
Jan HojnýDepartment of Pathology, First Faculty of Medicine, Charles University and General University Hospital in Prague, Studničkova 2, 12800, Prague 2, Czech Republic.
Nikola KudrnováDepartment of Pathology, First Faculty of Medicine, Charles University and General University Hospital in Prague, Studničkova 2, 12800, Prague 2, Czech Republic.
Michaela Kendall BártůDepartment of Pathology, First Faculty of Medicine, Charles University and General University Hospital in Prague, Studničkova 2, 12800, Prague 2, Czech Republic.
Kristýna NěmejcováDepartment of Pathology, First Faculty of Medicine, Charles University and General University Hospital in Prague, Studničkova 2, 12800, Prague 2, Czech Republic.
Marta KalousováInstitute of Medical Biochemistry and Laboratory Diagnostics, First Faculty of Medicine, Charles University and General University Hospital in Prague, Prague, Czech Republic.
Filip FrühaufGynecologic Oncology Centre, Department of Gynaecology, Obstetrics and Neonatology, First Faculty of Medicine, Charles University and General University Hospital in Prague, Prague, Czech Republic.
David CibulaGynecologic Oncology Centre, Department of Gynaecology, Obstetrics and Neonatology, First Faculty of Medicine, Charles University and General University Hospital in Prague, Prague, Czech Republic.
Radoslav MatějDepartment of Pathology, First Faculty of Medicine, Charles University and General University Hospital in Prague, Studničkova 2, 12800, Prague 2, Czech Republic.
W Glenn McCluggageDepartment of Pathology, Belfast Health and Social Care Trust, Belfast, UK.
Ivana StružinskáDepartment of Pathology, First Faculty of Medicine, Charles University and General University Hospital in Prague, Studničkova 2, 12800, Prague 2, Czech Republic.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Low-grade endometrial stromal sarcomas (LGESS) and endometrial stromal nodules represent a distinct entity with characteristic morphology, immunohistochemical profile, and molecular features. It has been suggested that the activation of the Wnt signaling pathway is a potential driver in some of these tumors. Approximately 70-75% of LGESS are characterized by non-random recurrent fusions mostly involving JAZF1 and PHF1 genes. Although the exact mechanism remains unclear, activation of the Wnt signaling pathway appears to be related to the functional deregulation of chromatin remodeling complexes caused by these fusion proteins. However, knowledge about other possible mechanisms and recurrent molecular alterations occurring at the DNA level in LGESS remains limited. We report three cases of LGESS in patients aged 39, 49, and 50, lacking recurrent fusions but harboring CTNNB1 mutations in exon 3 as the sole detectable molecular alteration. One case had morphological features of typical LGESS (in some areas with perivascular whorling, which was not a dominant feature), the second case showed features of the fibroblastic variant of LGESS, and the third case comprised a LGESS with a peculiar morphology with diffuse whorling morphologically identical to the recently described entity endometrial stromal tumor with GREB1::CTNNB1 fusion. RNA-Seq-based clustering analysis of the three cases and a set of 193 uterine tumors showed that the CTNNB1-mutated cases clustered near LGESS cases. This study adds to the growing body of evidence that CTNNB1 mutations represent a driver molecular event in a small subset of endometrial stromal tumors. Moreover, the results of our study suggest that tumors with CTNNB1 mutation and GREB1::CTNNB1 fusion may exhibit identical morphology and potentially represent the same category of tumor. Characterization and reporting of additional cases are needed to determine whether these are part of the spectrum of low-grade endometrial stromal tumors (either endometrial stromal nodule or LGESS) or represent a separate category of tumors characterized by CTNNB1 alteration as a driver event.

Indexed as

beta CateninBiomarkers, TumorEndometrial NeoplasmsEndometrial Stromal TumorsMutationSarcoma, Endometrial StromalAdultDNA Mutational AnalysisFemaleHumansMiddle Agedbeta CateninBiomarkers, TumorCTNNB1 protein, humanCTNNB1 gene mutationEndometrial stromal tumor with whorlingLow-grade endometrial stromal sarcomaUterine tumor

Identifiers

PMID41606383
PMCPMC12963160

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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.