Inflammation and myeloproliferative neoplasms
Abstract
Myeloproliferative neoplasms (MPN) include three main entities: Polycythemia Vera (PV), Essential Thrombocythemia (ET), and Myelofibrosis (MF). MPN represent a unique model of the relationship between the clonal development of a hematologic malignancy and chronic inflammation. The neoplastic clone is the main driver of this inflammatory reaction as demonstrated by the curative effect of allogeneic stem cell transplantation which leads not only to a complete restore of the hematopoiesis, but also to regression of bone marrow fibrosis. The neoplastic clone and its differentiated progeny are also the main source of an indirect paracrine secretion of inflammatory cytokines released by different normal cells present within the tumor microenvironment. In the end, the cytokine storm within the bone marrow niche leads to fibrosis. In addition, chronic inflammation is responsible of the constitutional symptoms which negatively affect the quality of life of MPN patients and represents a major driver for the development of premature atherosclerosis and disease progression. Here we describe the available data about the link between MPN and chronic inflammation in animal models as well as in clinical studies. We also review the practical value of including acute phase inflammatory proteins such as high sensitivity C-reactive protein (hs-CRP) and pentraxin 3 (PTX-3) in prognostic stratification of MPN patients. Interestingly, the plasma levels of these proteins is often increase in MPN pat…
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
A myriad of inflammatory mediators are overexpressed in MPN.
“with a myriad of inflammatory mediators overexpressed in MPN50.”
From Single-cell multi-omics identifies chronic inflammation as a driver of TP53-mutant leukemic evolution (2023) · cites this paper as [50]
Cites
Danesh, J., Wheeler, J. G., Hirschfield, G. M., Eda, S., Eiriksdottir, G., Rumley, A., Lowe, G. D. O., Pepys, M. B., & Gudnason, V. (2004) · New England Journal of Medicine · doi:10.1056/nejmoa032804 · Cited by 2,953 · see citing works
Somatic Mutations of Calreticulin in Myeloproliferative Neoplasms
Klampfl, T., Gisslinger, H., Harutyunyan, A. S., Nivarthi, H., Rumi, E., Milosevic, J. D., Them, N. C. C., Berg, T., Gisslinger, B., Pietra, D., et al. (2013) · New England Journal of Medicine · doi:10.1056/nejmoa1311347 · Cited by 2,003 · see citing works
Somatic <i>CALR</i> Mutations in Myeloproliferative Neoplasms with Nonmutated <i>JAK2</i>
Nangalia, J., Massie, C. E., Baxter, E. J., Nice, F. L., Gundem, G., Wedge, D. C., Avezov, E., Li, J., Kollmann, K., Kent, D. G., et al. (2013) · New England Journal of Medicine · doi:10.1056/nejmoa1312542 · Cited by 1,756 · see citing works
Flagged first, then by citations
Cited by
Sorted by citations
Rodriguez-Meira, A., Norfo, R., Wen, S., Chédeville, A. L., Rahman, H., O’Sullivan, J., Wang, G., Louka, E., Kretzschmar, W. W., Paterson, A., et al. (2023) · Nature Genetics · doi:10.1038/s41588-023-01480-1 · Cited by 158 · see citing works
The Nlrp3 inflammasome as a “rising star” in studies of normal and malignant hematopoiesis
Ratajczak, M. Z., Bujko, K., Cymer, M., Thapa, A., Adamiak, M., Ratajczak, J., Abdel-Latif, A. K., & Kucia, M. (2020) · Leukemia · doi:10.1038/s41375-020-0827-8 · Cited by 102 · see citing works
Verstovsek, S., Al-Ali, H. K., Mascarenhas, J., Perkins, A., Vannucchi, A. M., Mohan, S. R., Scott, B. L., Woszczyk, D., Koschmieder, S., García-Delgado, R., et al. (2022) · Future Oncology · doi:10.2217/fon-2022-0901 · Cited by 41 · see citing works
- Authors
- Lussana, F., & Rambaldi, A.
- Affiliations
- Ospedale Papa Giovanni XXIII (IT)
- University of Milan (IT)
- Corresponding author
- Rambaldi, Alessandro
- Venue
- Journal of Autoimmunity
- Publisher
- Elsevier BV
- Published
- 2017-12
- Volume
- 85
- Pages
- 58-63
- ISSN
- 0896-8411 (ISSN-L)
- OpenAlex
- W2732945346
- Cited by
- 136
- References
- 3
- Citations by year
- 2026: 5 · 2025: 13 · 2024: 16 · 2023: 13 · 2022: 18 · 2021: 29 · 2020: 25 · 2019: 8 · 2018: 8 · 2017: 1
- FWCI
- 1.62
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Autoimmunity (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Genetics › Myeloproliferative Neoplasms: Diagnosis and Treatment
- Health Sciences › Medicine › Hematology › Platelet Disorders and Treatments
- Health Sciences › Medicine › Emergency Medicine › Hematological disorders and diagnostics
- Keywords
- myeloproliferative neoplasms, chronic inflammation, polycythemia vera, essential thrombocythemia, myelofibrosis, bone marrow fibrosis, tumor microenvironment, acute phase proteins, C-reactive protein, pentraxin 3, thrombosis risk, atherosclerosis, ruxolitinib, allogeneic stem cell transplantation, prognostic stratification, constitutional symptoms
- MeSH terms
- Animals, Humans, Inflammation, Myeloproliferative Disorders, Neoplasms, Polycythemia Vera, Prognosis, Thrombocythemia, Essential, Primary Myelofibrosis
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review