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Cited by 161

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

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·Leukemia
DOI 10.1038/leu.2016.12
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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…

Overview

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Crossref · 10.1038/leu.2016.12

Cites

69 of 69 references verified0 citation errors · 0 not checkable

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Citations

Cites

1 retracted

Research works printed but not linked: 2

  1. Jaffe ES, Harris NL, Vardiman J, Campo E, Arber DM . Hematopathology. Elsevier Health Sciences 2010.
  2. Mascarenhas J, Talpaz M, Gupta V, Savona M, Coughlin P, Winton E et al. An open-label, phase II study of the JAK1 inhibitor INCB039110 in patients with myelofibrosis. Blood 2013; 122: 663–663.

Cited by

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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
Publisher
Springer Science and Business Media LLC
Published
2016-02-08
Volume
30
Issue
5
Pages
1018-1024
ISSN
  • 0887-6924
  • 1476-5551
DOI
10.1038/leu.2016.12
Cited by
161
References
69
Language
en
Licence

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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

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.