Resolution of thrombocytopenia, but not polycythemia after ruxolitinib for polycythemia vera with detectable mutation in the exon 12 of the JAK2 gene

Helbig, Grzegorz; Wichary, Ryszard; Torba, Karolina; Kyrcz‐Krzemień, Sławomira

doi:10.1007/s12032-017-0891-8

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“…Ruxolitinib, a drug approved a few years ago by the FDA, is also considered an excellent pharmacological choice in patients resistant to HU in PV [ 108 ]. However, murine models demonstrated that its pharmacological action does not present anti-leukemic activity in vivo in the bone marrow [ 109 ], which is a finding that could suggest a possible contribution from other deregulated cellular signaling, and is a target that would also be interesting in the prognosis of these patients.…”

Section: Summary and Perspectivesmentioning

confidence: 99%

JAK2 Variant Signaling: Genetic, Hematologic and Immune Implication in Chronic Myeloproliferative Neoplasms

et al. 2022

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The JAK2V617F variant constitutes a genetic alteration of higher frequency in BCR/ABL1 negative chronic myeloproliferative neoplasms, which is caused by a substitution of a G ˃ T at position 1849 and results in the substitution of valine with phenylalanine at codon 617 of the polypeptide chain. Clinical, morphological and molecular genetic features define the diagnosis criteria of polycythemia vera, essential thrombocythemia and primary myelofibrosis. Currently, JAK2V617F is associated with clonal hematopoiesis, genomic instability, dysregulations in hemostasis and immune response. JAK2V617F clones induce an inflammatory immune response and lead to a process of immunothrombosis. Recent research has shown great interest in trying to understand the mechanisms associated with JAK2V617F signaling and activation of cellular and molecular responses that progressively contribute to the development of inflammatory and vascular conditions in association with chronic myeloproliferative neoplasms. Thus, the aim of this review is to describe the main genetic, hematological and immunological findings that are linked to JAK2 variant signaling in chronic myeloproliferative neoplasms.

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Section: Summary and Perspectivesmentioning

confidence: 99%