ArticleBlood2023
CXCL8/CXCR2 signaling mediates bone marrow fibrosis and is a therapeutic target in myelofibrosis.
Article in Blood, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 35 citations in OpenAlex.
- Pelabresib plus ruxolitinib for JAK inhibitor-naive myelofibrosis: a randomized phase 3 trial.Nature medicine · 2025Trial
- Megakaryocytes in myelofibrosis: mechanisms of fibrotic niche remodeling and therapeutic implications.Biomarker research · 2026Review
- Single-cell long-read genotyping of transcripts reveals discrete mechanisms of clonal evolution in post-MPN AML.Blood advances · 2026Article
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- Physiological MplW514L expression in hematopoietic stem cell causes an essential thrombocythemia and progressive myelofibrosis.The Journal of clinical investigation · 2026Article
- Prospects of Chimeric Antigen Receptor T-Cell Therapy in Myelofibrosis: From Immunopathogenesis to Therapeutic Strategies.Cancers · 2026Review
- Platelets Outperform Leukocytes in Transcriptomic Liquid Biopsy Profiling of Myeloproliferative Neoplasms.bioRxiv : the preprint server for biology · 2026Article
- Cxcr2 is Required for Osteoclast Regulation, Bone Structure, and Hematological Response During Bone (Re)modeling.Calcified tissue international · 2026Article
- Immune and cytokine landscape differs between cytopenic and proliferative phenotypes in primary myelofibrosis.Therapeutic advances in hematology · 2026Article
- Preclinical efficacy of tasquinimod-based combinations in advanced myeloproliferative neoplasms in blastic phase.Blood advances · 2025Article
- Transforming cancer immunotherapy: integration of distinct immune-based approaches as redefined dual immunotherapy with potential third-sensitizer.Experimental hematology & oncology · 2025Review
- Genetic deletion of P-selectin prevents fibrosis development by inhibiting the neutrophil megakaryocyte emperipolesis in the Gata1European journal of histochemistry : EJH · 2025Article
- Bidirectional Interaction Between PGEProteomes · 2025Article
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- Review
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- Suppressed activation of the IRF7 and TLR9 by JAK2V617F gold nanoparticles.Immunogenetics · 2025Article
- Review
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- Perivascular cells function as key mediators of mechanical and structural changes in vascular capillaries.Science advances · 2025Article
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Authors and funding
39 authors at 9 institutions in 3 countries.
Funding
Abstract
Proinflammatory signaling is a hallmark feature of human cancer, including in myeloproliferative neoplasms (MPNs), most notably myelofibrosis (MF). Dysregulated inflammatory signaling contributes to fibrotic progression in MF; however, the individual cytokine mediators elicited by malignant MPN cells to promote collagen-producing fibrosis and disease evolution are yet to be fully elucidated. Previously, we identified a critical role for combined constitutive JAK/STAT and aberrant NF-κB proinflammatory signaling in MF development. Using single-cell transcriptional and cytokine-secretion studies of primary cells from patients with MF and the human MPLW515L (hMPLW515L) murine model of MF, we extend our previous work and delineate the role of CXCL8/CXCR2 signaling in MF pathogenesis and bone marrow fibrosis progression. Hematopoietic stem/progenitor cells from patients with MF are enriched for a CXCL8/CXCR2 gene signature and display enhanced proliferation and fitness in response to an exogenous CXCL8 ligand in vitro. Genetic deletion of Cxcr2 in the hMPLW515L-adoptive transfer model abrogates fibrosis and extends overall survival, and pharmacologic inhibition of the CXCR1/2 pathway improves hematologic parameters, attenuates bone marrow fibrosis, and synergizes with JAK inhibitor therapy. Our mechanistic insights provide a rationale for therapeutic targeting of the CXCL8/CXCR2 pathway among patients with MF.
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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.