ArticleAdvanced healthcare materials2025
T Cells Spatially Regulate B Cell Receptor Signaling in Lymphomas through H3K9me3 Modifications.
Article in Advanced healthcare materials, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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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.
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.
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Who cites it
7 citing papers in PubMed.
- Ex vivo bone marrow subniches influence the fate of human antibody-secreting cells.Science advances · 2026Article
- Matrix Stiffness Regulates Diffuse Large B-Cell Lymphoma (DLBCL) Spheroid Formation in a Tunable 3D Chitosan Hydrogel Model.Gels (Basel, Switzerland) · 2026Article
- Microphysiological Systems of Lymphatics and Immune Organs.Advanced healthcare materials · 2026Review
- Rebuilding the MarrowOnco · 2025Article
- Review
- Organoids in Haematologic Research: Advances and Future Directions.Cell proliferation · 2025Review
- T Cells Spatially Regulate B Cell Receptor Signaling in Lymphomas through H3K9me3 Modifications.Advanced healthcare materials · 2025Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Activated B cell-like diffuse large B-cell lymphoma (ABC-DLBCL) is a subtype associated with poor survival outcomes. Despite identifying therapeutic targets through molecular characterization, targeted therapies have limited success. New strategies using immune-competent tissue models are needed to understand how DLBCL cells evade treatment. Here, synthetic hydrogel-based lymphoma organoids are used to demonstrate how signals in the lymphoid tumor microenvironment (Ly-TME) can alter B cell receptor (BCR) signaling and specific histone modifications, tri-methylation of histone 3 at lysine 9 (H3K9me3), dampening the effects of BCR pathway inhibition. Using imaging modalities, T cells increase DNA methyltransferase 3A expression and cytoskeleton formation in proximal ABC-DLBCL cells, regulated by H3K9me3. Expansion microscopy on lymphoma organoids reveals T cells increase the size and quantity of segregated H3K9me3 clusters in ABC-DLBCL cells. Findings suggest the re-organization of higher-order chromatin structures that may contribute to evasion or resistance to therapy via the emergence of novel transcriptional states. Treating ABC-DLBCL cells with a G9α histone methyltransferase inhibitor reverses T cell-mediated modulation of H3K9me3 and overcomes T cell-mediated attenuation of treatment response to BCR pathway inhibition. This study emphasizes the Ly-TME's role in altering DLBCL fate and suggests targeting aberrant signaling and microenvironmental cross-talk that can benefit high-risk patients.
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Registered trials
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.