ReviewMediators of inflammation2015
Inflammation as a Keystone of Bone Marrow Stroma Alterations in Primary Myelofibrosis.
Review in Mediators of inflammation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 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
40 citing papers in PubMed, 63 citations in OpenAlex.
- Association of frailty with clinical outcomes in myelofibrosis: a retrospective cohort study.British journal of haematology · 2021Trial
- Spleen-derived circulating intercellular adhesion molecule 2 promotes osteosclerosis in chronic myelofibrosis.Bone research · 2026Article
- DNA methylation in primary myelofibrosis is partly associated with driver mutations and distinct from other myeloid malignancies.Clinical epigenetics · 2025Article
- STK405759 targets microtubules, modulates STAT1, and enhances ruxolitinib efficacy in myeloproliferative neoplasms.American journal of cancer research · 2025Article
- Investigational drugs in early phase trials for myelofibrosis.Expert opinion on investigational drugs · 2024Review
- Engagement of Mesenchymal Stromal Cells in the Remodeling of the Bone Marrow Microenvironment in Hematological Cancers.Biomolecules · 2023Review
- Revisiting Circulating Extracellular Matrix Fragments as Disease Markers in Myelofibrosis and Related Neoplasms.Cancers · 2023Review
- Mesenchymal stromal cells in tumor microenvironment remodeling of BCR-ABL negative myeloproliferative diseases.Frontiers in oncology · 2023Review
- Philadelphia-negative myeloproliferative neoplasms display alterations in monocyte subpopulations frequency and immunophenotype.Medical oncology (Northwood, London, England) · 2022Article
- Article
- Megakaryocytes Are Regulators of the Tumor Microenvironment and Malignant Hematopoietic Progenitor Cells in Myelofibrosis.Frontiers in oncology · 2022Review
- New Markers of Disease Progression in Myelofibrosis.Cancers · 2021Review
- Potential of Immunotherapies in Treating Hematological Cancer-Infection Comorbidities-A Mathematical Modelling Approach.Cancers · 2021Article
- Pro-fibrotic phenotype of bone marrow stromal cells in Modic type 1 changes.European cells & materials · 2021Article
- Inflammatory Microenvironment and Specific T Cells in Myeloproliferative Neoplasms: Immunopathogenesis and Novel Immunotherapies.International journal of molecular sciences · 2021Review
- Distinct profile of CD34Journal of experimental & clinical cancer research : CR · 2021Article
- Focus on Osteosclerotic Progression in Primary Myelofibrosis.Biomolecules · 2021Review
- Deciphering Tumor Niches: Lessons From Solid and Hematological Malignancies.Frontiers in immunology · 2021Review
- Could cytokine release syndrome induce acute myelofibrosis in CD19 chimeric antigen receptor T cells therapy?Bioengineered · 2020Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Primary myelofibrosis (PMF) is a clonal myeloproliferative neoplasm where severity as well as treatment complexity is mainly attributed to a long lasting disease and presence of bone marrow stroma alterations as evidenced by myelofibrosis, neoangiogenesis, and osteosclerosis. While recent understanding of mutations role in hematopoietic cells provides an explanation for pathological myeloproliferation, functional involvement of stromal cells in the disease pathogenesis remains poorly understood. The current dogma is that stromal changes are secondary to the cytokine "storm" produced by the hematopoietic clone cells. However, despite therapies targeting the myeloproliferation-sustaining clones, PMF is still regarded as an incurable disease except for patients, who are successful recipients of allogeneic stem cell transplantation. Although the clinical benefits of these inhibitors have been correlated with a marked reduction in serum proinflammatory cytokines produced by the hematopoietic clones, further demonstrating the importance of inflammation in the pathological process, these treatments do not address the role of the altered bone marrow stroma in the pathological process. In this review, we propose hypotheses suggesting that the stroma is inflammatory-imprinted by clonal hematopoietic cells up to a point where it becomes "independent" of hematopoietic cell stimulation, resulting in an inflammatory vicious circle requiring combined stroma targeted therapies.
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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.