Evidence map›Paper›PMID 39753532›Full record

ArticleNature communications2025

Genomic and phenotypic stability of fusion-driven pediatric sarcoma cell lines.

Merve Kasan, Florian H Geyer, Jana Siebenlist, Martin Sill, Rupert Öllinger, Tobias Faehling, Enrique de Álava, Didier Surdez, Uta Dirksen, Ina Oehme and 7 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 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

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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

17 authors.

Merve KasanHopp Children's Cancer Center (KiTZ), Heidelberg, Germany.
Florian H GeyerHopp Children's Cancer Center (KiTZ), Heidelberg, Germany.
Jana SiebenlistHopp Children's Cancer Center (KiTZ), Heidelberg, Germany.
Martin SillHopp Children's Cancer Center (KiTZ), Heidelberg, Germany.
Rupert ÖllingerTranslaTUM, Center for Translational Cancer Research, Technical University of Munich, Munich, Germany.ORCID 0000-0002-2292-5982
Tobias FaehlingHopp Children's Cancer Center (KiTZ), Heidelberg, Germany.ORCID 0000-0002-5500-4987
Enrique de ÁlavaInstitute of Biomedicine of Sevilla (IBiS), Virgen del Rocio University Hospital/CSIC/University of Sevilla/CIBERONC, Seville, Spain.ORCID 0000-0001-8400-046X
Didier SurdezINSERM U830, Diversity and Plasticity of Childhood Tumors Lab, PSL Research University, SIREDO Oncology Center, Institut Curie Research Center, Paris, France.
Uta DirksenDepartment of Pediatrics, University Hospital Essen, Essen, Germany.ORCID 0000-0002-5435-7860
Ina OehmeHopp Children's Cancer Center (KiTZ), Heidelberg, Germany.ORCID 0000-0002-0827-2356
Katia ScotlandiExperimental Oncology Laboratory, IRCCS Istituto Ortopedico Rizzoli, Bologna, Italy.ORCID 0000-0001-6114-9499
Olivier DelattreINSERM U830, Diversity and Plasticity of Childhood Tumors Lab, PSL Research University, SIREDO Oncology Center, Institut Curie Research Center, Paris, France.ORCID 0000-0002-8730-2276
Martina Müller-NurasyidInstitute of Medical Biostatistics, Epidemiology and Informatics (IMBEI), University Medical Center, Johannes Gutenberg University, Mainz, Germany.
Roland RadTranslaTUM, Center for Translational Cancer Research, Technical University of Munich, Munich, Germany.
Konstantin StrauchInstitute of Medical Biostatistics, Epidemiology and Informatics (IMBEI), University Medical Center, Johannes Gutenberg University, Mainz, Germany.
Thomas G P GrünewaldHopp Children's Cancer Center (KiTZ), Heidelberg, Germany.
Florencia Cidre-AranazHopp Children's Cancer Center (KiTZ), Heidelberg, Germany. florencia.cidrearanaz@dkfz.de.ORCID 0000-0002-0246-7179

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Human cancer cell lines are the mainstay of cancer research. Recent reports showed that highly mutated adult carcinoma cell lines (mainly HeLa and MCF-7) present striking diversity across laboratories and that long-term continuous culturing results in genomic/transcriptomic heterogeneity with strong phenotypical implications. Here, we hypothesize that oligomutated pediatric sarcoma cell lines mainly driven by a fusion transcription factor, such as Ewing sarcoma (EwS), are genetically and phenotypically more stable than the previously investigated adult carcinoma cell lines. A comprehensive molecular and phenotypic characterization of multiple EwS cell line strains, together with a simultaneous analysis during 12 months of continuous cell culture show that fusion-driven pediatric sarcoma cell line strains are genomically more stable than adult carcinoma strains, display remarkably stable and homogenous transcriptomes, and exhibit uniform and stable drug response. Additionally, the analysis of multiple EwS cell lines subjected to long-term continuous culture reveals that variable degrees of genomic/transcriptomic/phenotypic changes among fusion-driven cell lines, further exemplifying that the potential for reproducibility of in vitro scientific results may be rather understood as a spectrum, even within the same tumor entity.

Indexed as

Oncogene Proteins, FusionPhenotypeSarcoma, EwingCell Line, TumorChildGene Expression Regulation, NeoplasticGenomic InstabilityGenomicsHumansMutationRNA-Binding Protein EWSSarcomaTranscriptomeOncogene Proteins, FusionRNA-Binding Protein EWS

Identifiers

PMID39753532
PMCPMC11699042

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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.