In summary, we find the transcriptional consequences of JAK2 exon 12 mutations in clonal erythroblasts from PV patients to be indistinguishable from those of het- erozygous JAK2V617F in ET. In contrast to JAK2V617F- positive PV, patients with exon 12 mutations show no evidence of attenuated STAT1 activation, demonstrating that this impairment is not necessary for an erythrocytosis. […]STAT1 activation has been associated with enhanced megakaryopoiesis and may contribute to the thrombocytosis observed in 20% of patients with exon 12 mutations, whilst absence of thrombocytosis in others may reflect STAT1-independent mechanisms such as accelerated platelet destruction. Taken together our data support the concept that the development of a PV or ET phe- notype reflects combinations of mechanisms that operate differently between individuals, and that, furthermore, these mechanisms differ between classes of JAK2 mutation.
MicroRNA-101 expression is associated with JAK2V617F activity and regulates JAK2/STAT5 signaling / Pagano, Francesca; Comoglio, Federico; Grinfeld, Jacob; Li, Juan; Godfrey, Anna; Baxter, Joanna; Silber, Yvonne; Green, Anthony R. - In: LEUKEMIA. - ISSN 0887-6924. - ELETTRONICO. - 32:8(2018), pp. 1826-1830. [10.1038/s41375-018-0053-9]
MicroRNA-101 expression is associated with JAK2V617F activity and regulates JAK2/STAT5 signaling
Pagano, FrancescaWriting – Original Draft Preparation
;
2018
Abstract
In summary, we find the transcriptional consequences of JAK2 exon 12 mutations in clonal erythroblasts from PV patients to be indistinguishable from those of het- erozygous JAK2V617F in ET. In contrast to JAK2V617F- positive PV, patients with exon 12 mutations show no evidence of attenuated STAT1 activation, demonstrating that this impairment is not necessary for an erythrocytosis. […]STAT1 activation has been associated with enhanced megakaryopoiesis and may contribute to the thrombocytosis observed in 20% of patients with exon 12 mutations, whilst absence of thrombocytosis in others may reflect STAT1-independent mechanisms such as accelerated platelet destruction. Taken together our data support the concept that the development of a PV or ET phe- notype reflects combinations of mechanisms that operate differently between individuals, and that, furthermore, these mechanisms differ between classes of JAK2 mutation.File | Dimensione | Formato | |
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