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http://dx.doi.org/10.1016/j.thromres.2016.06.019 | DOI Listing |
Ann Hematol
August 2025
U.O.C. di Ematologia, Ospedale di Ravenna e Università di Bologna, Ravenna, Italy.
The prevalence of paroxysmal nocturnal hemoglobinuria (PNH) clones is little investigated in myeloproliferative neoplasms (MPN) patients. The aim of this multicenter study was to evaluate the prevalence of PNH clones (glycosyl-phosphatidyl-inositol lacking) in 119 Ph- negative MPN patients having anemia, LDH elevation, asthenia and history of thrombosis. All the participating centers performed the standardized diagnostic test by using a single lyophilized template for granulocytes, monocytes, and erythrocytes.
View Article and Find Full Text PDFLeukemia
August 2025
Laboratory of Cell and Developmental Biology, Institute of Molecular Genetics of the Czech Academy of Sciences, Prague, Czech Republic.
The acquired JAK2-V617F mutation plays a causal role in myeloproliferative neoplasms (MPN). Weakly activating JAK2 germline variants have been associated with MPN risk, but the underlying mechanisms remain unclear. We previously identified the JAK2-R1063H germline variant, which contributes to hereditary MPN and increased disease severity in essential thrombocythemia.
View Article and Find Full Text PDFJ Biol Chem
August 2025
Toronto General Hospital Research Institute, University Health Network, Toronto, Ontario, M5G 2C4, Canada; Department of Immunology, University of Toronto, Toronto, Ontario, M5G 2M9, Canada; Institute of Medical Science and Department of Pharmacology and Toxicology, University of Toronto, Toronto, O
Cardiovascular disease (CVD) is the leading cause of mortality worldwide, of which atherosclerosis is the major pathology. Chronic inflammation underlies atherosclerosis, and Janus kinase 2 (Jak2) is a critical signaling node that mediates this process. Jak2 activating mutation has recently been implicated in clonal hematopoiesis of indeterminate potential as an emerging major CVD risk factor.
View Article and Find Full Text PDFCancer
August 2025
Division of Hematology-Oncology, Chang Gung Memorial Hospital at Linkou, Taoyuan, Taiwan.
Background: Clonal evolution drives progression of myeloproliferative neoplasms (MPN) from chronic phase (CP) to blastic phase (BP).
Methods: Targeted next-generation sequencing of 46 paired MPN-CP/BP samples was performed to assess clonal evolution through variant allele frequency changes.
Results: The median time from MPN-CP to BP was 6.
Cell Commun Signal
August 2025
Healthcampus Immunology, Inflammation and Infectiology (GC-I3), Medical Faculty, Otto-von-Guericke University, Magdeburg, Germany.
Background: The JAK2-V617F mutation is the most frequent driver mutation in a group of malignant hematopoietic disorders called myeloproliferative neoplasms (MPN). JAK2-V617F is a somatic mutation originating in a hematopoietic stem cell and results in constitutively activated JAK-STAT signaling. High levels of pro-inflammatory cytokines in the blood are a hallmark of MPN patients and are a key factor in the severe clinical symptoms seen in these patients.
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