Inflammatory Pathophysiology as a Contributor to Myeloproliferative Neoplasms
Open accessAbstract
Myeloid neoplasms, including acute myeloid leukemia (AML), myeloproliferative neoplasms (MPNs), and myelodysplastic syndromes (MDS), feature clonal dominance and remodeling of the bone marrow niche in a manner that promotes malignant over non-malignant hematopoiesis. This take-over of hematopoiesis by the malignant clone is hypothesized to include hyperactivation of inflammatory signaling and overproduction of inflammatory cytokines. In the Ph-negative MPNs, inflammatory cytokines are considered to be responsible for a highly deleterious pathophysiologic process: the phenotypic transformation of polycythemia vera (PV) or essential thrombocythemia (ET) to secondary myelofibrosis (MF), and the equivalent emergence of primary myelofibrosis (PMF). Bone marrow fibrosis itself is thought to be mediated heavily by the cytokine TGF-β, and possibly other cytokines produced as a result of hyperactivated JAK2 kinase in the malignant clone. MF also features extramedullary hematopoiesis and progression to bone marrow failure, both of which may be mediated in part by responses to cytokines. In MF, elevated levels of individual cytokines in plasma are adverse prognostic indicators: elevated IL-8/CXCL8, in particular, predicts risk of transformation of MF to secondary AML (sAML). Tumor necrosis factor (TNF, also known as TNFα), may underlie malignant clonal dominance, based on results from mouse models. Human PV and ET, as well as MF, harbor overproduction of multiple cytokines, above what is observed in normal aging, which can lead to cellular signaling abnormalities separate from those directly mediated by hyperactivated JAK2 or MPL kinases. Evidence that NFκB pathway signaling is frequently hyperactivated in a pan-hematopoietic pattern in MPNs, including in cells outside the malignant clone, emphasizes that MPNs are pan-hematopoietic diseases, which remodel the bone marrow milieu to favor persistence of the malignancy. Clinical evidence that JAK2 inhibition by ruxolitinib in MF neither reliably reduces malignant clonal burden nor eliminates cytokine elevations, suggests targeting cytokine mediated signaling as a therapeutic strategy, which is being pursued in new clinical trials. Greater knowledge of inflammatory pathophysiology in MPNs can therefore contribute to the development of more effective therapy.
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Within the MkPs, the proliferative effects of IFNa were modest in the mutated cells compared to those at baseline.
“However, in contrast to the other myeloid progenitors, within the MkPs (wherein the CALR mutation exerts the greatest phenotypic effects due to the activation of the thrombopoietin receptor 21,54-57 ), the proliferative effects of IFNa were modest in the mutated cells compared to those at baseline ( Fig. 3e ), suggesting that the rate of cell cycle entry of the mutated cells was already near or at”
From Type 1 interferon perturbates clonal competition by reshaping human blood development (2026) · cites this paper as [21]
The citation is attached to the parenthetical explanation about CALR, not to the IFNα proliferation result, which the citing sentence attributes to its own Fig. 3e. In “Hyperactivation of JAK2 or MPL Causes Myeloproliferation, Cytokine Production, and Myelofibrosis” (page unavailable), the source says mutant CALR activates the thrombopoietin receptor MPL and that MPL is expressed in the megakaryocytic lineage. It does not establish that CALR has its greatest phenotypic effects specifically in MkPs. (LLM, conf=0.82)
Experimental — accuracy not yet measuredThe rate of cell cycle entry of the mutated cells was already near or at the point of saturation due to the CALR mutation.
“However, in contrast to the other myeloid progenitors, within the MkPs (wherein the CALR mutation exerts the greatest phenotypic effects due to the activation of the thrombopoietin receptor 21,54-57 ), the proliferative effects of IFNa were modest in the mutated cells compared to those at baseline ( Fig. 3e ), suggesting that the rate of cell cycle entry of the mutated cells was already near or at”
From Type 1 interferon perturbates clonal competition by reshaping human blood development (2026) · cites this paper as [21]
The section “Hyperactivation of JAK2 or MPL Causes Myeloproliferation, Cytokine Production, and Myelofibrosis” explains that mutant CALR activates the thrombopoietin receptor MPL, but does not address whether cell-cycle entry is near saturation. Searches for CALR-mutant progenitor cell-cycle entry and IFNα response found no passage supporting that inference. In the citing sentence, the saturation statement appears to be the citing authors’ interpretation, not the point attached to the citation. (LLM, conf=0.76)
Experimental — accuracy not yet measured
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- Authors
- Fisher, D. A. C., Fowles, J. S., Zhou, A., & Oh, S. T.
- Affiliations
- Washington University in St. Louis (US)
- Corresponding author
- Oh, Stephen Tracy
- Venue
- Frontiers in Immunology
- Publisher
- Frontiers Media SA
- Published
- 2021-06-01
- Volume
- 12
- Pages
- 683401-683401
- ISSN
- 1664-3224 (ISSN-L)
- PMC
- PMC8204249
- OpenAlex
- W3167008187
- Cited by
- 115
- References
- 196
- Citations by year
- 2026: 21 · 2025: 20 · 2024: 23 · 2023: 19 · 2022: 27 · 2021: 4 · 2012: 1
- FWCI
- 2.60
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Frontiers in Immunology (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Digital Commons@Becker (Washington University School of Medicine) (submittedVersion, cc-by)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (P30AR073752)
- Topics
- Health Sciences › Medicine › Genetics › Myeloproliferative Neoplasms: Diagnosis and Treatment
- Health Sciences › Medicine › Hematology › Acute Myeloid Leukemia Research
- Health Sciences › Medicine › Hematology › Platelet Disorders and Treatments
- Keywords
- myeloproliferative neoplasms, inflammatory cytokines, bone marrow microenvironment, clonal dominance, secondary myelofibrosis, polycythemia vera, essential thrombocythemia, primary myelofibrosis, TGF-beta, JAK2, NF-κB signaling, IL-8/CXCL8, TNF-α, ruxolitinib, cytokine-targeted therapy, extramedullary hematopoiesis, bone marrow failure, myeloid neoplasms
- MeSH terms
- Age Factors, Cell Transformation, Neoplastic, Disease Susceptibility, Humans, Models, Biological, Myeloproliferative Disorders, Signal Transduction, Biomarkers, Cytokines, Inflammation Mediators, Primary Myelofibrosis
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