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Cited by 53

The DOI matches its Crossref record; 62 of the 62 references it cites were found in a registry or an index.

Inflammation as a Driver of Clonal Evolution in Myeloproliferative Neoplasm

Fleischman, Angela G.·2015·Mediators of Inflammation

Abstract

Our understanding of inflammation’s role in the pathogenesis of myeloproliferative neoplasm (MPN) is evolving. The impact of chronic inflammation, a characteristic feature of MPN, likely goes far beyond its role as a driver of constitutional symptoms. An inflammatory response to the neoplastic clone may be responsible for some pathologic aspects of MPN. Moreover, JAK2V617F mutated hematopoietic stem and progenitor cells are resistant to inflammation, and this gives the neoplastic clone a selective advantage allowing for its clonal expansion. Because inflammation plays a central role in MPN inflammation is a logical therapeutic target in MPN.

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Crossref · 10.1155/2015/606819

Cites

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Statistics

Figures

Figure 1 Putative role of inflammation in shaping MPN disease phenotype.
Figure 1 Putative role of inflammation in shaping MPN disease phenotype.CC BY · PubMed Central
Figure 2 Model of inflammation as a driver of expansion of the JAK2V617F clone in MPN. JAK2V617F-mutated hematopoietic stem cells (HSC) are resistant to inflammation giving them a selective advantage in environments with high inflammation.
Figure 2 Model of inflammation as a driver of expansion of the JAK2V617F clone in MPN. JAK2V617F-mutated hematopoietic stem cells (HSC) are resistant to inflammation giving them a selective advantage in environments with high inflammation.CC BY · PubMed Central

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Metadata

Authors
Fleischman, A. G.
Venue
Mediators of Inflammation
Publisher
Wiley
Published
2015-01
Volume
2015
Issue
1
ISSN
  • 0962-9351
  • 1466-1861
Cited by
53
References
62
Language
en

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