SF3B1+ cases were enriched in primary myelofibrosis in both prefibrotic and fibrotic stage, but mutations of SF3B1 seem to occur only as a late event in the fibrotic phase of essential thrombocythemia and polycythemia vera.
These results indicated that PV dominantly expressed β-catenin and proliferation marker Ki67 in bone marrow, while PMF is linked preferentially to PPAR-γ immunopositive megakaryocytes characterized by abnormal maturation.
LIG3 as an essential part of the SSB was significantly lower expressed compared to controls in all three entities (essential thrombocythemia (ET), polycythemia vera (PV), and myelofibrosis (MF)).
Finally, by using knockout mice, we demonstrated that TLR2 and IFN type I play crucial roles in modulating the early neuroinflammatory response and clinical outcome of PRV infection in mice.
Our results indicate that the JAK2V617F<sup>+</sup> PV progenitors utilize DUSP1 activity as a protection mechanism against DNA damage accumulation, promoting their proliferation and survival in the inflammatory microenvironment, identifying DUSP1 as a potential therapeutic target in PV.
We identify mutational cooperation between Jak2V617F expression and Dnmt3a loss that drives progression from early-stage polycythemia vera to advanced myelofibrosis.
We assessed SPP1 and LGALS3 protein levels in 115 PMF, 47 ET and 24 PV patients plasma samples and we found that SPP1 plasma levels are significantly higher in PMF compared with ET and PV patients.
We show that the peripheral CD3<sup>+</sup>CD8<sup>+</sup> T cell pool in PV patients is clearly divided into two discrete populations, a more granular CD3<sup>+</sup>CD8<sup>high</sup> T cell population enriched in effector-memory CD45RA<sup>+</sup> T cells (CD8<sup>+</sup> TEMRA) when compared to CTR (P < 0.001), and a less granular CD3<sup>+</sup>CD8<sup>int</sup> T cell population that is completely absent in the CTR group (78 vs. 0%, P < 0.001) and is a mixture of naïve (CD8<sup>+</sup> T<sub>N</sub>) and CD8<sup>+</sup> TEMRA cells expressing intermediate levels of CD28, i.e., CD3<sup>+</sup>CD8<sup>int</sup>CD28<sup>int</sup>.
Both decreased circulating iron and increased erythroferrone levels, which occur as a consequence of erythroid hyperplasia in PV, are anticipated to suppress hepcidin and enable recovery from iron deficiency.
JMJD1C binding to the <i>NFE2</i> promoter is increased in PV patients, decreasing both H3K9me2 levels and binding of the repressive heterochromatin protein-1α (HP1α).
Investigation of the molecular mechanisms of ENPP1 during PRV infection showed that ENPP1 hydrolyzed cGAMP in PRV-infected or cGAMP-transfected cells and inhibited IRF3 phosphorylation, reducing IFN-β secretion.
Finally, we report that PV patients' lymphocytes and monocytes display lower levels of closed (W6/32<sup>+</sup>) MHC-I conformers at the cell surface while exhibiting increased amounts of open (HC-10<sup>+</sup>) MHC-I conformers.
The results suggested that plasma Dkk-1 levels could differentiate ET from pre-PMF, in JAK2 V617F-positive as well as in CALR-positive patients, and also ET from PV in JAK2 V617F-positive patients.
Mutations in the ENG, ACVRL1, and SMAD4 genes and clinical manifestations of hereditary haemorrhagic telangiectasia: experience from the Center for Osler's Disease, Uppsala University Hospital.
The S100A8 plasma levels were found to be increased in MPN, the S100A9 plasma levels in PMF and essential thrombocythemia (ET), and the S100A12 plasma levels in polycythemia vera (PV).
The S100A8 plasma levels were found to be increased in MPN, the S100A9 plasma levels in PMF and essential thrombocythemia (ET), and the S100A12 plasma levels in polycythemia vera (PV).
These results, combined with those for porcine cGAS, demonstrate that ENPP1 acts coordinately with cGAS to maintain the reservoir of cGAMP and participates in PRV infection.
Cellular responses of an established cell line from human intestinal epithelial cells (INT-407 cells) against poliovirus (PV) infections were investigated in order to find cellular genetic markers for infectious PV detection.
The S100A8 plasma levels were found to be increased in MPN, the S100A9 plasma levels in PMF and essential thrombocythemia (ET), and the S100A12 plasma levels in polycythemia vera (PV).