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Mediators of Inflammation
Volume 2015, Article ID 606819, 6 pages
Review Article

Inflammation as a Driver of Clonal Evolution in Myeloproliferative Neoplasm

University of California, Irvine, CA 92697, USA

Received 1 July 2015; Accepted 2 August 2015

Academic Editor: Sylvie Hermouet

Copyright © 2015 Angela G. Fleischman. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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.