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Novel germline JAK SUP R715T SUP mutation causing PV-like erythrocytosis in 3 generations. Amelioration by Ropeg-Interferon

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F68378050%3A_____%2F24%3A00586895" target="_blank" >RIV/68378050:_____/24:00586895 - isvavai.cz</a>

  • Result on the web

    <a href="https://onlinelibrary.wiley.com/doi/10.1002/ajh.27311" target="_blank" >https://onlinelibrary.wiley.com/doi/10.1002/ajh.27311</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.1002/ajh.27311" target="_blank" >10.1002/ajh.27311</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

    Novel germline JAK SUP R715T SUP mutation causing PV-like erythrocytosis in 3 generations. Amelioration by Ropeg-Interferon

  • Original language description

    Polycythemia vera (PV) is a clonal disorder arising from the acquired somatic mutations of the JAK2 gene, including JAK2(V617F) or several others in exon 12. A 38-year-old female had a stroke at age 32 and found to have elevated hemoglobin, normal leukocytes, normal platelets, and tested negative for JAK2(V617F) and exon 12 mutations. Next generation sequencing revealed a novel mutation: JAK2(R715T) in the pseudokinase domain (JH2) at 47.5%. Its presence in her nail DNA confirmed a germline origin. Her mother and her son similarly had erythrocytosis and a JAK2(R715T) mutation. Computer modeling indicated gain-of-function JAK2 activity. The propositus and her mother had polyclonal myelopoiesis, ruling out another somatic mutation-derived clonal hematopoiesis. Some erythroid progenitors of all three generations grew without erythropoietin, a hallmark of PV. The in vitro reporter assay confirmed increased activity of the JAK2(R715T) kinase. Similar to PV, the JAK2(R715T) native cells have increased STAT5 phosphorylation, augmented transcripts of prothrombotic and inflammatory genes, and decreased KLF2 transcripts. The propositus was not controlled by hydroxyurea, and JAK2 inhibitors were not tolerated, however, Ropeginterferon-alfa-2b (Ropeg-IFN-alpha) induced a remission. Ropeg-IFN-alpha treatment also reduced JAK2 activity in the propositus, her mother and JAK2(V617F) PV subjects. We report dominantly inherited erythrocytosis secondary to a novel germline JAK2(R715T) gain-of-function mutation with many but not all comparable molecular features to JAK2(V617F) PV. We also document a previously unreported inhibitory mechanism of JAK2 signaling by Ropeg-IFN-alpha.

  • Czech name

  • Czech description

Classification

  • Type

    J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database

  • CEP classification

  • OECD FORD branch

    10601 - Cell biology

Result continuities

  • Project

    Result was created during the realization of more than one project. More information in the Projects tab.

  • Continuities

    P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Others

  • Publication year

    2024

  • Confidentiality

    S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Data specific for result type

  • Name of the periodical

    American Journal of Hematology

  • ISSN

    0361-8609

  • e-ISSN

    1096-8652

  • Volume of the periodical

    99

  • Issue of the periodical within the volume

    7

  • Country of publishing house

    US - UNITED STATES

  • Number of pages

    10

  • Pages from-to

    1220-1229

  • UT code for WoS article

    001204101600001

  • EID of the result in the Scopus database

    2-s2.0-85190944349