The DOI matches its Crossref record; 69 of the 69 references it cites were found in a registry or an index.
Myeloproliferative neoplasms and inflammation: whether to target the malignant clone or the inflammatory process or both
Abstract
The Philadelphia-negative myeloproliferative neoplasms (MPNs) are clonal disorders involving hematopoietic stem and progenitor cells and are associated with myeloproliferation, splenomegaly and constitutional symptoms. Similar signs and symptoms can also be found in patients with chronic inflammatory diseases, and inflammatory processes have been found to play an important role in the pathogenesis and progression of MPNs. Signal transduction pathways involving JAK1, JAK2, STAT3 and STAT5 are causally involved in driving both the malignant cells and the inflammatory process. Moreover, anti-inflammatory and immune-modulating drugs have been used successfully in the treatment of MPNs. However, to date, many unresoved issues remain. These include the role of somatic mutations that are present in addition to JAK2V617F, CALR and MPL W515 mutations, the interdependency of malignant and nonmalignant cells and the means to eradicate MPN-initiating and -maintaining cells. It is imperative for successful therapeutic approaches to define whether the malignant clone or the inflammatory cells or both should be targeted. The present review will cover three aspects of the role of inflammation in MPNs: inflammatory states as important differential diagnoses in cases of suspected MPN (that is, in the absence of a clonal marker), the role of inflammation in MPN pathogenesis and progression and the use of anti-inflammatory drugs for MPNs. The findings emphasize the need to separate the inflammat…
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“Given that emerging evidence suggests that inflammation very likely plays a causative role in the pathology of MPN (Fleischman, 2015; Koschmieder et al., 2016)”
From Inhibition of Inflammatory Signaling in Tet2 Mutant Preleukemic Cells Mitigates Stress-Induced Abnormalities and Clonal Hematopoiesis (2018) · cites this paper as Koschmieder et al., 2016
Citations
Cites
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Self-citationSomatic Mutations of Calreticulin in Myeloproliferative Neoplasms
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Self-citationSomatic CALR Mutations in Myeloproliferative Neoplasms with Nonmutated JAK2
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Cited by
The Continuum of Aging and Age-Related Diseases: Common Mechanisms but Different Rates
Franceschi, C., Garagnani, P., Morsiani, C., Conte, M., Santoro, A., Grignolio, A., Monti, D., Capri, M., & Salvioli, S. (2018) · Frontiers in Medicine · doi:10.3389/fmed.2018.00061 · Cited by 945
Cai, Z., Kotzin, J. J., Ramdas, B., Chen, S., Nelanuthala, S., Palam, L. R., Pandey, R., Mali, R. S., Liu, Y., Kelley, M. R., et al. (2018) · Cell Stem Cell · doi:10.1016/j.stem.2018.10.013 · Cited by 394
Inflammatory Pathophysiology as a Contributor to Myeloproliferative Neoplasms
Fisher, D. A. C., Fowles, J. S., Zhou, A., & Oh, S. T. (2021) · Frontiers in Immunology · doi:10.3389/fimmu.2021.683401 · Cited by 115
Philadelphia-negative myeloproliferative neoplasms as disorders marked by cytokine modulation
Cacemiro, M. D. C., Cominal, J. G., Tognon, R., Nunes, N. D. S., Simões, B. P., Figueiredo-Pontes, L. L. D., Catto, L. F. B., Traina, F., Souto, E. X., Zambuzi, F. A., et al. (2018) · Hematology, Transfusion and Cell Therapy · doi:10.1016/j.htct.2017.12.003 · Cited by 55
Metadata
- Authors
- Koschmieder, S., Mughal, T. I., Hasselbalch, H. C., Barosi, G., Valent, P., Kiladjian, J.-J., Jeryczynski, G., Gisslinger, H., Jutzi, J. S., Pahl, H. L., Hehlmann, R., Maria Vannucchi, A., Cervantes, F., Silver, R. T., & Barbui, T.
- Venue
- Leukemia
- Published
- 2016-02-08
- Volume
- 30
- Issue
- 5
- Pages
- 1018-1024
- ISSN
- 0887-6924
- 1476-5551
- Cited by
- 161
- References
- 69
- Language
- en
- Licence
- www.springer.com/tdm (tdm)
- www.springer.com/tdm (vor)
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- Koschmieder, S., Mughal, T. I., Hasselbalch, H. C., Barosi, G., Valent, P., Kiladjian, J.-J., Jeryczynski, G., Gisslinger, H., Jutzi, J. S., Pahl, H. L., Hehlmann, R., Maria Vannucchi, A., Cervantes, F., Silver, R. T., & Barbui, T. (2016). Myeloproliferative neoplasms and inflammation: whether to target the malignant clone or the inflammatory process or both. Leukemia. https://doi.org/10.1038/leu.2016.12
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
