ArticleScience advances2023
Highly connected 3D chromatin networks established by an oncogenic fusion protein shape tumor cell identity.
Article in Science advances, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed.
- Origins and consequences of oncogenic 3D chromatin remodelling.Nature reviews. Cancer · 2026Review
- Lineage master regulator and cancer-selective partner transcription factors rewire 3D genome topology for tumor-specific gene control.Science advances · 2026Article
- Decoding 3D chromatin architecture reveals distinct enhancer classes underlying hierarchical gene regulation in prostate cancer.Genome biology · 2026Article
- A conserved hormonal signalling-H2A.Z axis rapidly reorganizes 3D chromatin interactions in adipocyte thermogenesis.Nature metabolism · 2026Article
- STAG2 loss amplifies EWS-FLI1-driven microsatellite enhancer activity promoting Ewing sarcoma aggressiveness.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- KLF5 controls subtype-independent highly interactive enhancers in pancreatic cancer to regulate cell survival.Science advances · 2026Article
- Genome-wide association study meta-analysis identifies susceptibility loci informing Ewing sarcoma etiology and potential mechanisms of risk.medRxiv : the preprint server for health sciences · 2026Article
- Fusion oncoproteins orchestrate tumorigenesis and sustain malignant progression via a positive feedback mechanism.Cell & bioscience · 2026Review
- The hegemonic EWSR1::ETS oncoprotein overrules core regulatory circuitry principles in Ewing sarcoma.NPJ precision oncology · 2025Article
- Rewiring the Fusion Oncoprotein EWSR1::FLI1 in Ewing Sarcoma with Bivalent Small Molecules.Journal of the American Chemical Society · 2025Article
- Transcriptional pause release at enhancers mediates cell identity.NAR cancer · 2025Review
- Precision theranostics in cervical Cancer: Harnessing stimuli-responsive hydrogels for tumor microenvironment-targeted therapy and diagnosis.Materials today. Bio · 2025Review
- EWS::FLI1 expression in human embryonic mesenchymal stem cells leads to transcriptional reprograming, defective DNA damage repair and Ewing sarcoma.Nature communications · 2025Article
- Subversion of mRNA degradation pathways by EWSR1::FLI1 represents a therapeutic vulnerability in Ewing sarcoma.Nature communications · 2025Article
- CREPT is required for the metastasis of triple-negative breast cancer through a co-operational-chromatin loop-based gene regulation.Molecular cancer · 2025Article
- Biomolecular condensates in immune cell fate.Nature reviews. Immunology · 2025Review
- Rewiring cancer: 3D genome determinants of cancer hallmarks.Current opinion in genetics & development · 2025Review
- Pioneer factor GATA6 promotes colorectal cancer through 3D genome regulation.Science advances · 2025Article
- The Role of Chronic Inflammation in Pediatric Cancer.Cancers · 2025Review
- STAG2 loss in Ewing sarcoma alters enhancer-promoter contacts dependent and independent of EWS::FLI1.EMBO reports · 2024Article
Corrections and comments
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Authors and funding
20 authors.
Funding
Abstract
Cell fate transitions observed in embryonic development involve changes in three-dimensional genomic organization that provide proper lineage specification. Whether similar events occur within tumor cells and contribute to cancer evolution remains largely unexplored. We modeled this process in the pediatric cancer Ewing sarcoma and investigated high-resolution looping and large-scale nuclear conformation changes associated with the oncogenic fusion protein EWS-FLI1. We show that chromatin interactions in tumor cells are dominated by highly connected looping hubs centered on EWS-FLI1 binding sites, which directly control the activity of linked enhancers and promoters to establish oncogenic expression programs. Conversely, EWS-FLI1 depletion led to the disassembly of these looping networks and a widespread nuclear reorganization through the establishment of new looping patterns and large-scale compartment configuration matching those observed in mesenchymal stem cells, a candidate Ewing sarcoma progenitor. Our data demonstrate that major architectural features of nuclear organization in cancer cells can depend on single oncogenes and are readily reversed to reestablish latent differentiation programs.
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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.