Evidence map›Paper›PMID 41136396›Full record

ArticleNature communications2025

EWS::FLI1 expression in human embryonic mesenchymal stem cells leads to transcriptional reprograming, defective DNA damage repair and Ewing sarcoma.

Inmaculada Hernández-Muñoz, Irene Cuervas, Estela Prada, Julian Pulecio, Ramón Gimeno, Evelyn Andrades, Soledad Gómez-González, Pau Berenguer-Molins, Ariadna Acedo-Terrades, Júlia Perera-Bel and 14 more

Abstract read
In one paragraph

Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Review
  3. 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

24 authors.

Inmaculada Hernández-MuñozGroup of Inflammatory and Neoplastic Dermatological Diseases, Hospital del Mar Research Institute, Barcelona, Spain. mhernandez@researchmar.net.ORCID http://orcid.org/0000-0003-3436-9634
Irene Cuervas *Group of Inflammatory and Neoplastic Dermatological Diseases, Hospital del Mar Research Institute, Barcelona, Spain.ORCID http://orcid.org/0009-0008-2355-2082
Estela Prada *Developmental Tumor Biology Laboratory, Institut de Recerca Sant Joan de Déu, Barcelona, Spain.
Julian PulecioRegenerative Medicine Program, Bellvitge Biomedical Research Institute (IDIBELL), L'Hospitalet de Llobregat, Spain.ORCID http://orcid.org/0000-0002-4455-8095
Ramón GimenoLaboratory of Immunology, Department of Pathology, Hospital del Mar, Barcelona, Spain.
Evelyn AndradesGroup of Inflammatory and Neoplastic Dermatological Diseases, Hospital del Mar Research Institute, Barcelona, Spain.
Soledad Gómez-GonzálezDevelopmental Tumor Biology Laboratory, Institut de Recerca Sant Joan de Déu, Barcelona, Spain.
Pau Berenguer-MolinsHospital del Mar Research Institute (HMRIB), Barcelona, Spain.ORCID http://orcid.org/0000-0002-0170-2931
Ariadna Acedo-TerradesHospital del Mar Research Institute (HMRIB), Barcelona, Spain.
Júlia Perera-BelHospital del Mar Research Institute (HMRIB), Barcelona, Spain.ORCID http://orcid.org/0000-0002-6809-132X
Marta Bódalo-TorruellaHospital del Mar Research Institute (HMRIB), Barcelona, Spain.
Lara NonellVall d'Hebron Institute of Oncology (VHIO), Barcelona, Spain.
Elena PérezJosep Carreras Leukaemia Research Institute (IJC), Badalona, Spain.
Daniela GrasesJosep Carreras Leukaemia Research Institute (IJC), Badalona, Spain.
Caterina MataJosep Carreras Leukaemia Research Institute (IJC), Badalona, Spain.
José YélamosLaboratory of Immunology, Department of Pathology, Hospital del Mar, Barcelona, Spain.
Yvonne Richaud-PatinRegenerative Medicine Program, Bellvitge Biomedical Research Institute (IDIBELL), L'Hospitalet de Llobregat, Spain.
Enrique VidalGene Regulation, Stem Cells and Cancer Program, Center for Genomic Regulation (CRG), The Barcelona Institute of Science and Technology, Barcelona, Spain.
Yasmina CuarteroGene Regulation, Stem Cells and Cancer Program, Center for Genomic Regulation (CRG), The Barcelona Institute of Science and Technology, Barcelona, Spain.
François Le DilyGene Regulation, Stem Cells and Cancer Program, Center for Genomic Regulation (CRG), The Barcelona Institute of Science and Technology, Barcelona, Spain.ORCID http://orcid.org/0000-0002-8324-7927
Mariona SuñolDepartment of Pathology, Hospital Sant Joan de Déu, Barcelona, Spain.
Alejandro ManzanaresDevelopmental Tumor Biology Laboratory, Institut de Recerca Sant Joan de Déu, Barcelona, Spain.ORCID http://orcid.org/0000-0001-9268-8188
Angel RayaRegenerative Medicine Program, Bellvitge Biomedical Research Institute (IDIBELL), L'Hospitalet de Llobregat, Spain.
Jaume MoraDevelopmental Tumor Biology Laboratory, Institut de Recerca Sant Joan de Déu, Barcelona, Spain. jaume.mora@sjd.es.ORCID http://orcid.org/0000-0002-9386-5980

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI SELWYN M VICKERS · 1985 to 2026
$347.4M
Fundació la Marató de TV3 (TV3 Marathon Foundation) 201928Fundació la Marató de TV3 (TV3 Marathon Foundation) 202331Ministry of Economy and Competitiveness | Instituto de Salud Carlos III (Institute of Health Carlos III) PI22/00364NCI NIH HHS P30 CA008748
6 · The paper itself

Abstract

Ewing sarcoma (ES) is an aggressive bone and soft tissue neoplasm characterized by EWSR::ETS rearrangements whose cellular origin remains unclear. EWS::FLI1 expression in human pediatric mesenchymal stem cells (MSCs) induces a transcriptional response distinct from that of human adult MSCs, but fails to form tumors. Here we show that EWS::FLI1 expression in human embryonic mesenchymal stem cells (heMSCs) results in the acquisition of an ES transcriptome, with the oncogene not preferentially binding to gene promoters, but to intronic and intergenic microsatellites. In heMSCs, EWS::FLI1 directly regulates the expression of the DNA repair protein BRCA1, although cells expressing EWS::FLI1 show DNA damage. Xenografting of EWS::FLI1-transduced heMSCs results in the formation of tumors expressing characteristic ES markers. In summary, we show that EWS::FLI1 enforces an aberrant transcriptome and solely is able to endow transforming capacity when expressed in undifferentiated, early heMSCs.

Indexed as

Bone NeoplasmsCellular ReprogrammingDNA RepairMesenchymal Stem CellsOncogene Proteins, FusionProto-Oncogene Protein c-fli-1RNA-Binding Protein EWSSarcoma, EwingAnimalsBRCA1 ProteinDNA DamageGene Expression Regulation, NeoplasticHumansMiceTranscriptomeBRCA1 ProteinBRCA1 protein, humanEWS-FLI fusion proteinFLI1 protein, humanOncogene Proteins, FusionProto-Oncogene Protein c-fli-1RNA-Binding Protein EWS

Identifiers

PMID41136396
PMCPMC12552549

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.