ArticleHaematologica2023
Article in Haematologica, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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
22 citing papers in PubMed, 10 citations in OpenAlex.
- Reversible Eltrombopag-Associated Bone Marrow Fibrosis With Hematologic Recovery After Drug Withdrawal inEJHaem · 2026Article
- Megakaryocytes in myelofibrosis: mechanisms of fibrotic niche remodeling and therapeutic implications.Biomarker research · 2026Review
- Molecular Abnormalities and Associated Clinical Features in Polycythemia Vera.Medical sciences (Basel, Switzerland) · 2026Review
- What Explains the Pattern of Fibrosis in Chronic Graft-Versus-Host Disease?Clinical transplantation · 2026Review
- Glycolytic-inflammatory crosstalk mediated by Glyco-PMF-Rux hub genes drives PMF progression and ruxolitinib resistance.Genes & genomics · 2026Article
- Unleashed condensation by recurrent mutations of an epigenetic regulator promotes cancer.bioRxiv : the preprint server for biology · 2026Article
- The Role and Impact of Non-driver Gene Mutations in Myelofibrosis.Current hematologic malignancy reports · 2026Review
- Setd2 ensures the establishment of a precise basal inflammatory state within murine hematopoietic stem/progenitor cells.Cell death & disease · 2025Article
- Monocyte Involvement in the Pathogenesis of Myeloproliferative Neoplasms.International journal of molecular sciences · 2025Review
- A correlation of ineffective erythropoiesis and dysregulated signaling pathways in myelodysplastic syndromes/neoplasms.Experimental hematology & oncology · 2025Article
- Article
- DNA Methylation in Ph-Negative Myeloproliferative Neoplasms: Prognostic Role and Therapeutic Implications.Current issues in molecular biology · 2025Review
- Comprehensive biomarker profiles in hematological malignancies: improving diagnosis, prognosis, and treatment.Biomarkers in medicine · 2025Review
- The Role of Signalling Pathways in Myocardial Fibrosis in Hypertrophic Cardiomyopathy.Reviews in cardiovascular medicine · 2025Review
- The Role of Somatic Mutations in Ischemic Stroke: CHIP's Impact on Vascular Health.Neurology international · 2025Review
- Chronic Inflammation in Primary Myelofibrosis: In-Depth Insights Into Pathogenesis and Promising Anti-Inflammatory Therapeutic Strategies.Mediators of inflammation · 2025Review
- Clonal hematopoiesis in LGI1-antibody encephalitis.Annals of clinical and translational neurology · 2024Article
- TNF-α is a predictive marker in distinguishing myeloproliferative neoplasm and idiopathic erythrocytosis/thrombocytosis: development and validation of a non-invasive diagnostic model.Frontiers in oncology · 2024Article
- Micheliolide exerts effects in myeloproliferative neoplasms through inhibiting STAT3/5 phosphorylation via covalent binding to STAT3/5 proteins.Blood science (Baltimore, Md.) · 2023Article
- Association of Myelofibrosis Phenotypes with Clinical Manifestations, Molecular Profiles, and Treatments.Cancers · 2023Review
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Authors and funding
20 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Apart from the central role of the activated JAK/STAT signaling pathway, ASXL1 mutations are the most recurrent additional mutations in myeloproliferative neoplasms and occur much more commonly in myelofibrosis than in essential thrombocythemia and polycythemia vera. However, the mechanism of the association with ASXL1 mutations and bone marrow fibrosis remains unknown. Here, integrating our own data from patients with myeloproliferative neoplasms and a hematopoietic-specific Asxl1 deletion/Jak2V617F mouse model, we show that ASXL1 mutations are associated with advanced myeloproliferative neoplasm phenotypes and onset of myelofibrosis. ASXL1 mutations induce skewed monocyte/macrophage and neoplastic monocyte-derived fibrocyte differentiation, consequently they enhance inflammation and bone marrow fibrosis. Consistently, the loss of ASXL1 and JAK2V617F mutations in hematopoietic stem and progenitor cells leads to enhanced activation of polycomb group target genes, such as EGR1. The upregulation of EGR1, in turn, accounts for increased hematopoietic stem and progenitor cell commitment to the monocyte/macrophage lineage. Moreover, EGR1 induces the activation of TNFA and thereby further drives the differentiation of monocytes to fibrocytes. Accordingly, combined treatment with a TNFR antagonist and ruxolitinib significantly reduces fibrocyte production in vitro. Altogether, these findings demonstrate that ASXL1 mutations accelerate fibrocyte production and inflammation in myeloproliferative neoplasms via the EGR1-TNFA axis, explaining the cellular and molecular basis for bone marrow fibrosis and the proof-ofconcept for anti-fibrosis treatment.
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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.