ReviewCytokine: X2019
Cytokines frequently implicated in myeloproliferative neoplasms.
Review in Cytokine: X, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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
28 citing papers in PubMed, 32 citations in OpenAlex.
- Targeting nuclear export and Janus Kinase/Signal Transducer and Activator of Transcription (JAK/STAT) signalling in myelofibrosis: A novel combinatorial strategy that impacts intrinsic and microenvironment-related pathways.British journal of haematology · 2026Article
- The inflammatory/fibrotic axis across organs: myelofibrosis as a model of reversibility.JCI insight · 2026Review
- Promises and Pitfalls of Whole Exome Sequencing in Therapy-Resistant Chronic Thrombocytopenia in Childhood: A Case Report.Journal of personalized medicine · 2026Article
- PD-1/PD-L1-CXCR3 Coexpression and CXCR3 on Intermediate Monocytes Predict Fibrosis, Leukemic Transformation, and Survival in Egyptian Philadelphia-Negative Myeloproliferative Neoplasms.Clinical Medicine Insights. Oncology · 2026Article
- Parallel Evolution of Leukemic Clones in Myeloproliferative Neoplasms.Research square · 2025Article
- Preclinical efficacy of tasquinimod-based combinations in advanced myeloproliferative neoplasms in blastic phase.Blood advances · 2025Article
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- Suppressed activation of the IRF7 and TLR9 by JAK2V617F gold nanoparticles.Immunogenetics · 2025Article
- Low Renalase Levels in Newly Diagnosed CML: Dysregulation Sensitive to Modulation by Tyrosine Kinase Inhibitors.Pathophysiology : the official journal of the International Society for Pathophysiology · 2024Article
- Unraveling the impact of lysosomal dysfunction on myeloproliferative neoplasm.Cancer medicine · 2024Article
- MAPK-negative feedback regulation confers dependence to JAK2Leukemia · 2023Article
- Clonal hematopoiesis and bone marrow inflammation.Translational research : the journal of laboratory and clinical medicine · 2023Review
- The Role of NLRP3, a Star of Excellence in Myeloproliferative Neoplasms.International journal of molecular sciences · 2023Review
- Increase in Frequency of Myeloid-Derived Suppressor Cells in the Bone Marrow of Myeloproliferative Neoplasm: Potential Implications in Myelofibrosis.Advances in experimental medicine and biology · 2023Article
- The role of JAK inhibitors in hematopoietic cell transplantation.Bone marrow transplantation · 2022Review
- Myeloproliferative disorders and their effects on bone homeostasis: the role of megakaryocytes.Blood · 2022Review
- Thromboinflammation in Myeloproliferative Neoplasms (MPN)-A Puzzle Still to Be Solved.International journal of molecular sciences · 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
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Classical myeloproliferative neoplasms (MPN) include polycythemia vera (PV), essential thrombocythemia (ET) and primary myelofibrosis (PMF). MPN has been defined as a chronic inflammation-driven tumor model. It is clear that there is a close link between chronic inflammation and MPN pathogenesis. Several studies have demonstrated cytokine profiles in MPN patients. Other studies have used cell lines or animal models aiming to clarify the underlying mechanism of cytokines in the pathogenesis of MPN. However, important questions remain: (1) among all these cytokines, which are more predictive? and (2) which are more critical? In this review, we summarize cytokines that have been investigated in MPN and highlight several cytokines that may be more significant in MPN. We suggest that cytokines are more critical in PMF than PV or ET. These cytokines include IL-1β, TNF-α, IL-6, IL-8, VEGF, PDGF, IFNs and TGF-β, all of which should be more closely investigated in MPN. Based on our extensive literature search, several key factors have emerged in our understanding of MPN: first, TNF-α could correlate with MPN progression including PMF, PV and ET. IL-1β plays a role in PMF progression, while it showed no relation with PV or ET. Second, IL-8 could be a prognostic factor for PMF, and IL-6 could be important for MPN progression. Third, VEGF and PDGF play an indirect role in MPN development and their inhibitors could be effective. Fourth, different subtypes of IFNs could have different effects in MPN. Finally, TGF-β is closely linked to MF, although the data are inconsistent. Agents that have targeted these cytokines described above are already in clinical trials, and some of them have even been used to treat MPN patients. Taken together, it will be critical to continue to investigate the precise role of these cytokines in the pathogenesis and progression of MPN.
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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.