ReviewStem cell investigation2016
Bone marrow fibrosis in primary myelofibrosis: pathogenic mechanisms and the role of TGF-β.
Review in Stem cell investigation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
57 citing papers in PubMed, 69 citations in OpenAlex.
- Trial
- Evaluation of an alternative ruxolitinib dosing regimen in patients with myelofibrosis: an open-label phase 2 study.Journal of hematology & oncology · 2018Trial
- Overuse of thrombopoietin receptor agonists driven by suboptimal response is associated with myelofibrosis in pediatric immune thrombocytopenia.Haematologica · 2026Article
- Fibrocytes drive JAK2V617F-mutated myelofibrosis: pitavastatin reverses marrow fibrosis and anemia.Blood · 2026Article
- The Role of Single-Nucleotide Polymorphisms in Acquired Aplastic Anaemia.Scandinavian journal of immunology · 2026Review
- Inflammatory and Immune Microenvironment in Myeloproliferative Neoplasms: Pathogenic Mechanisms and Therapeutic Opportunities.Cancers · 2026Review
- When Platelet Stimulation Becomes Marrow Stress: Rethinking Thrombopoietin Receptor Agonist Intensification in Pediatric Immune Thrombocytopenia.Pediatric reports · 2026Article
- The Intricate Dance Between Inflammation and Myeloproliferative Neoplasms: From Origins to Outcomes.Current hematologic malignancy reports · 2026Review
- Quantitative assessment of innate myeloid cells in myelofibrosis: insights into myeloid and plasmacytoid dendritic cell depletion and disease progression.Annals of hematology · 2025Article
- High-selective HDAC6 inhibitor alleviates bone marrow fibrosis through inhibiting collagen formation and extracellular matrix deposition.Scientific reports · 2025Article
- Article
- The Ongoing Challenges of Managing Cytopenic Myelofibrosis in 2025: The Emergence of Non-JAK Inhibitor Therapies.Blood and lymphatic cancer : targets and therapy · 2025Review
- Investigational drugs in early phase trials for myelofibrosis.Expert opinion on investigational drugs · 2024Review
- SHP2 inhibition displays efficacy as a monotherapy and in combination with JAK2 inhibition in preclinical models of myeloproliferative neoplasms.American journal of hematology · 2024Article
- Fibrosis and bone marrow: understanding causation and pathobiology.Journal of translational medicine · 2023Review
- Article
- Whole bone subcutaneous transplantation as a strategy to study precisely the bone marrow niche.Stem cell reviews and reports · 2023Article
- Myelofibrosis progression grading based on type I and type III collagen and fibrillin 1 expression boosted by whole slide image analysis.Histopathology · 2023Article
- Brucellosis complicated by myelofibrosis: report of five cases and review of literature.International journal of clinical and experimental pathology · 2023Article
- Calreticulin in renal fibrosis: A short review.Journal of cellular and molecular medicine · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Primary myelofibrosis (PMF) is a Philadelphia chromosome negative myeloproliferative neoplasm (MPN) with adverse prognosis and is associated with bone marrow fibrosis and extramedullary hematopoiesis. Even though the discovery of the Janus kinase 2 (JAK2), thrombopoietin receptor (MPL) and calreticulin (CALR) mutations have brought new insights into the complex pathogenesis of MPNs, the etiology of fibrosis is not well understood. Furthermore, since JAK2 inhibitors do not lead to reversal of fibrosis further understanding of the biology of fibrotic process is needed for future therapeutic discovery. Transforming growth factor beta (TGF-β) is implicated as an important cytokine in pathogenesis of bone marrow fibrosis. Various mouse models have been developed and have established the role of TGF-β in the pathogenesis of fibrosis. Understanding the molecular alterations that lead to TGF-β mediated effects on bone marrow microenvironment can uncover newer therapeutic targets against myelofibrosis. Inhibition of the TGF-β pathway in conjunction with other therapies might prove useful in the reversal of bone marrow fibrosis in PMF.
Indexed as
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.