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Review
. 2015:2015:606819.
doi: 10.1155/2015/606819. Epub 2015 Oct 11.

Inflammation as a Driver of Clonal Evolution in Myeloproliferative Neoplasm

Angela G Fleischman  1
Affiliations
Review

Inflammation as a Driver of Clonal Evolution in Myeloproliferative Neoplasm

Angela G Fleischman. Mediators Inflamm. 2015.

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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Figures

Figure 1
Figure 1
Putative role of inflammation in shaping MPN disease phenotype.
Figure 2
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.
See this image and copyright information in PMC

References

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