ArticleBlood advances2025
Lymphoma B cells remodel bone marrow stromal cells into extracellular matrix-producing cancer-associated fibroblasts.
Article in Blood advances, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Targeting cancer-associated fibroblasts: therapeutic strategies, translational challenges, and future perspectives.Journal of hematology & oncology · 2026Review
- Extracellular Matrix Remodeling in Tumors: Forces Beyond Fibroblasts.Cancer research · 2026Article
- Clinical pathological features and prognosis of diffuse large B-cell lymphoma initially diagnosed by bone marrow biopsy in patients presenting with peripheral blood cytopenia.Virchows Archiv : an international journal of pathology · 2026Article
- Cytokines and cancer-associated fibroblasts.Journal of hematology & oncology · 2026Review
- Metabolic reprogramming in tumor-associated cells of hematologic malignancies: mechanisms, crosstalk networks, and therapeutic implications in the tumor microenvironment.Frontiers in immunology · 2026Review
- Lymphoid stroma in all its states.Frontiers in immunology · 2025Review
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Authors and funding
18 authors.
Funding
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Abstract
abstractBone marrow (BM) involvement is a common feature of germinal center-derived B-cell lymphomas and is associated with a poor prognosis. In particular, follicular lymphoma (FL) infiltrates the BM in 70% of cases, and analysis of in vitro-expanded FL BM mesenchymal stromal cells (MSCs) has revealed an extensive alteration of BM stromal cell phenotypic, transcriptomic, and functional profiles. However, the mechanisms underlying the direct interplay between lymphoma B cells and their permissive stromal niche in situ have not yet been identified. In this study, we identified a significant remodeling of extracellular matrix (ECM) composition and organization in the BM of patients with FL and in a murine model of lymphoma B-cell BM xenograft. In particular, murine leptin receptor (LepR+) MSCs were identified by single-cell RNA sequencing as engaged in a bidirectional cross talk with malignant B cells, triggering their specific and progressive reprogramming and commitment toward a phenotype resembling that of human ECM/transforming growth factor β (TGFβ) myofibroblastic cancer-associated fibroblasts (CAFs) and FL-CAFs. Kinetic analysis of FL BM samples showed that ECM and TGFβ deregulation persisted after treatment, suggesting it may contribute to disease persistence and relapse. Overall, this work sheds new light on the kinetics and mechanisms of BM stromal niche reshaping in B-cell lymphomas.
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