ArticleFibrogenesis & tissue repair2012
Primary myelofibrosis and the "bad seeds in bad soil" concept.
Article in Fibrogenesis & tissue repair, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
27 citing papers in PubMed, 45 citations in OpenAlex.
- Does Double Mean Trouble? Coexistence of Myeloproliferative and Lymphoproliferative Neoplasms.Journal of clinical medicine · 2024Article
- Revisiting Circulating Extracellular Matrix Fragments as Disease Markers in Myelofibrosis and Related Neoplasms.Cancers · 2023Review
- Tracking fibrosis in myeloproliferative neoplasms by CCR2 expression on CD34Frontiers in oncology · 2022Article
- New Markers of Disease Progression in Myelofibrosis.Cancers · 2021Review
- Increased Plasma Levels of lncRNAsCancers · 2021Article
- The Dynamic Interface Between the Bone Marrow Vascular Niche and Hematopoietic Stem Cells in Myeloid Malignancy.Frontiers in cell and developmental biology · 2021Review
- Deciphering Tumor Niches: Lessons From Solid and Hematological Malignancies.Frontiers in immunology · 2021Review
- Heterogeneity of the bone marrow niche in patients with myeloproliferative neoplasms: ActivinA secretion by mesenchymal stromal cells correlates with the degree of marrow fibrosis.Annals of hematology · 2021Article
- EXPAND, a dose-finding study of ruxolitinib in patients with myelofibrosis and low platelet counts: 48-week follow-up analysis.Haematologica · 2019Article
- Coexistence of Myeloid and Lymphoid Neoplasms: A Single-Center Experience.Advances in hematology · 2019Article
- Understanding deregulated cellular and molecular dynamics in the haematopoietic stem cell niche to develop novel therapeutics for bone marrow fibrosis.The Journal of pathology · 2018Review
- Role of the microenvironment in myeloid malignancies.Cellular and molecular life sciences : CMLS · 2018Review
- Long-term effects of ruxolitinib versus best available therapy on bone marrow fibrosis in patients with myelofibrosis.Journal of hematology & oncology · 2018Article
- Involvement of MAF/SPP1 axis in the development of bone marrow fibrosis in PMF patients.Leukemia · 2018Article
- The spleen microenvironment influences disease transformation in a mouse model of KITScientific reports · 2017Article
- Role of miR-34a-5p in Hematopoietic Progenitor Cells Proliferation and Fate Decision: Novel Insights into the Pathogenesis of Primary Myelofibrosis.International journal of molecular sciences · 2017Article
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- In vivo magnetic resonance imaging of a mouse model of myelofibrosis.Blood cancer journal · 2016Article
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Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Primary Myelofibrosis (PMF) is a chronic myeloproliferative neoplasm characterized by a clonal myeloproliferation and a myelofibrosis. The concomitant presence of neoangiogenesis and osteosclerosis suggests a deregulation of medullar stem cell niches in which hematopoietic stem cells are engaged in a constant crosstalk with their stromal environment. Despite the recently discovered mutations including the JAK2(Val617F) mutation, the primitive molecular event responsible for the clonal hematopoietic proliferation is still unknown. We propose that the "specificity" of the pathological process that caracterizes PMF results from alterations in the cross talk between hematopoietic and stromal cells. These alterations contribute in creating a abnormal microenvironment that participates in the maintenance of the neoplasic clone leading to a misbalance disfavouring normal hematopoiesis; in return or simultaneously, stromal cells constituting the niches are modulated by hematopoietic cells resulting in stroma dysfunctions. Therefore, PMF is a remarkable "model" in which deregulation of the stem cell niche is of utmost importance for the disease development. A better understanding of the crosstalk between stem cells and their niches should imply new therapeutic strategies targeting not only intrinsic defects in stem cells but also regulatory niche-derived signals and, consequently, hematopoietic cell proliferation.
Identifiers
What OpenQuestion holds
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.