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. 2020 Apr 7;12(4):903. doi: 10.3390/cancers12040903

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© 2020 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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Schematic model of PV disease evolution, showing the central role of JAK2 V617F-dependent protection mechanisms (upregulation of DUSP1, RECQL5, and oxidative buffering system activity) in the overall long-term maintenance of low DNA damage and genomic stability during the chronic proliferation phase of the disease. Upon exhaustion of protection mechanism capacity, the disease progresses mostly towards post-PV myelofibrosis. In a minor subset of cases, selection of pre-leukemia mutations inhibiting DDR and subclonal evolution towards leukemia stem cell (LSC) marks the onset of secondary acute myeloid leukemias (AML). DDR, DNA damage response; HSC, hematopoietic stem cell; Pre-LSC, pre-leukemia stem cell; LSC, leukemia stem cell.