ArticleMolecular cell2022
EBF1 nuclear repositioning instructs chromatin refolding to promote therapy resistance in T leukemic cells.
Article in Molecular cell, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 30 citations in OpenAlex.
- Transcription factors as drivers of 3D enhancer-promoter interactions.Current opinion in structural biology · 2026Review
- Igh nuclear speckle association promotes V(D)J recombination.Nature communications · 2026Article
- Lineage-determining transcription factors EBF1 and TCF1 shape chromatin fibre folding.Nature cell biology · 2026Article
- Lineage-determining transcription factors constrain cohesin to drive multi-enhancer oncogene regulation.Nature cell biology · 2026Article
- OLIVE provides rapid visualization and analysis of chromatin tracing experiments.Cell reports methods · 2025Article
- Targeting the 3D genome by anthracyclines for chemotherapeutic effects.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Advances in Research on the B-Lineage Transcription Factor EBF1 in Solid Tumors.International journal of molecular sciences · 2025Review
- An era of immunological discoveries heralded by molecular biology.Trends in immunology · 2025Article
- Cis-Regulatory Element and Transcription Factor Circuitry Required for Cell-Type Specific Expression of FOXP3.bioRxiv : the preprint server for biology · 2025Article
- Splenic fibroblasts control marginal zone B cell movement and function via two distinct Notch2-dependent regulatory programs.Immunity · 2025Article
- A multiomic atlas identifies a treatment-resistant, bone marrow progenitor-like cell population in T cell acute lymphoblastic leukemia.Nature cancer · 2025Article
- Enhancer-promoter hubs organize transcriptional networks promoting oncogenesis and drug resistance.Nature communications · 2024Article
- Oncogenic transcription factors instruct promoter-enhancer hubs in individual triple negative breast cancer cells.Science advances · 2024Article
- Spatial promoter-enhancer hubs in cancer: organization, regulation, and function.Trends in cancer · 2023Review
- Identifying quantitatively differential chromosomal compartmentalization changes and their biological significance from Hi-C data using DARIC.BMC genomics · 2023Article
- Cancer Metabolism Historical Perspectives: A Chronicle of Controversies and Consensus.Cold Spring Harbor perspectives in medicine · 2023Article
- Three-dimensional genome organization in immune cell fate and function.Nature reviews. Immunology · 2023Review
- AP-2δ Is the Most Relevant Target of AP-2 Family-Focused Cancer Therapy and Affects Genome Organization.Cells · 2022Article
- The Interplay of Transcription and Genome Topology Programs T Cell Development and Differentiation.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- Tnpo3 enables EBF1 function in conditions of antagonistic Notch signaling.Genes & development · 2022Article
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9 authors at 2 institutions in 1 country.
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Abstract
Chromatin misfolding has been implicated in cancer pathogenesis; yet, its role in therapy resistance remains unclear. Here, we systematically integrated sequencing and imaging data to examine the spatial and linear chromatin structures in targeted therapy-sensitive and -resistant human T cell acute lymphoblastic leukemia (T-ALL). We found widespread alterations in successive layers of chromatin organization including spatial compartments, contact domain boundaries, and enhancer positioning upon the emergence of targeted therapy resistance. The reorganization of genome folding structures closely coincides with the restructuring of chromatin activity and redistribution of architectural proteins. Mechanistically, the derepression and repositioning of the B-lineage-determining transcription factor EBF1 from the heterochromatic nuclear envelope to the euchromatic interior instructs widespread genome refolding and promotes therapy resistance in leukemic T cells. Together, our findings suggest that lineage-determining transcription factors can instruct changes in genome topology as a driving force for epigenetic adaptations in targeted therapy resistance.
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