Article in Science advances, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
0numbers the graph read from it
0cells of the map it votes in
2citing 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.
Emma D WrennBen Towne Center for Childhood Cancer & Blood Disorders Research, Seattle Children's Research Institute, Seattle, WA, USA.ORCID 0000-0002-9643-457X
Jacob C HarrisBen Towne Center for Childhood Cancer & Blood Disorders Research, Seattle Children's Research Institute, Seattle, WA, USA.ORCID 0009-0005-4345-762X
April A ApfelbaumDepartment of Pediatric Oncology, Dana-Farber Cancer/Boston Children's Cancer and Blood Disorders Center, Boston, MA, USA.
Jonah R ValentiBen Towne Center for Childhood Cancer & Blood Disorders Research, Seattle Children's Research Institute, Seattle, WA, USA.
Patricia A LipsonBen Towne Center for Childhood Cancer & Blood Disorders Research, Seattle Children's Research Institute, Seattle, WA, USA.ORCID 0000-0002-6398-5068
Stephanie I WalterBen Towne Center for Childhood Cancer & Blood Disorders Research, Seattle Children's Research Institute, Seattle, WA, USA.
Nicolas M GarciaBen Towne Center for Childhood Cancer & Blood Disorders Research, Seattle Children's Research Institute, Seattle, WA, USA.ORCID 0000-0002-3717-5520
Aya MiyakiBen Towne Center for Childhood Cancer & Blood Disorders Research, Seattle Children's Research Institute, Seattle, WA, USA.ORCID 0009-0008-6748-4595
Steven C ChenBen Towne Center for Childhood Cancer & Blood Disorders Research, Seattle Children's Research Institute, Seattle, WA, USA.ORCID 0009-0002-5269-7383
Jim M OlsonBen Towne Center for Childhood Cancer & Blood Disorders Research, Seattle Children's Research Institute, Seattle, WA, USA.ORCID 0000-0001-5990-6534
Jason P PriceBen Towne Center for Childhood Cancer & Blood Disorders Research, Seattle Children's Research Institute, Seattle, WA, USA.
Kelly M BaileyDepartment of Pediatrics, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.ORCID 0000-0003-3925-3243
Elizabeth R LawlorBen Towne Center for Childhood Cancer & Blood Disorders Research, Seattle Children's Research Institute, Seattle, WA, USA.ORCID 0000-0002-2350-1540
Funding
Regulation and function of HOX genes in Ewing sarcoma pathogenesisR01CA215981 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI LAWLOR, ELIZABETH R · 2018 to 2022
$2.0M
DNA Damage and Immunogenicity in Ewing SarcomaK08CA252178 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI BAILEY, KELLY · 2021 to 2025
$765k
The role of HOXD13 in controlling Ewing sarcoma cell plasticity and metastasisF31CA247104 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI APFELBAUM, APRIL · 2021 to 2022
Subpopulations of cancer-associated fibroblast (CAF)-like tumor cells deposit extracellular matrix (ECM) proteins that support Ewing sarcoma (EwS) progression and metastasis. We previously showed a hallmark of CAF-like EwS cells is their hybrid transcriptional state wherein the driver fusion oncogene, EWS::FLI1, maintains activation of proliferative programs but loses capacity to repress mesenchymal genes. Here, we studied primary patient tumors and cell line models to identify molecular drivers of this hybrid state. Our data reveal that hybrid EwS cells are induced and maintained by a transforming growth factor-β (TGFβ) signaling positive feedback loop. Hybrid cells derepress
Indexed as
Autocrine CommunicationSarcoma, EwingTranscription, GeneticTransforming Growth Factor beta2Cell Line, TumorCell ProliferationExtracellular MatrixGene Expression Regulation, NeoplasticHumansOncogene Proteins, FusionProto-Oncogene Protein c-fli-1Receptor, Transforming Growth Factor-beta Type IIRNA-Binding Protein EWSSignal TransductionTransforming Growth Factor beta1EWS-FLI fusion proteinOncogene Proteins, FusionProto-Oncogene Protein c-fli-1Receptor, Transforming Growth Factor-beta Type IIRNA-Binding Protein EWSTGFBR2 protein, humanTransforming Growth Factor beta1Transforming Growth Factor beta2
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.
Autocrine TGFβ2 enforces a transcriptionally hybrid cell state in Ewing sarcoma. · full record | OpenQuestion