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Analysis of 5-Azacytidine Resistance Models Reveals a Set of Targetable Pathways

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    SYSNO ASEP0557510
    Document TypeJ - Journal Article
    R&D Document TypeJournal Article
    Subsidiary JČlánek ve WOS
    TitleAnalysis of 5-Azacytidine Resistance Models Reveals a Set of Targetable Pathways
    Author(s) Minařík, L. (CZ)
    Pimková, K. (CZ)
    Kokavec, J. (CZ)
    Schaffartzikova, A. (CZ)
    Vellieux, F. (CZ)
    Kulvait, V. (CZ)
    Daumová, L. (CZ)
    Dusilkova, N. (CZ)
    Jonasova, A. (CZ)
    Vargova, K. (CZ)
    Králová Viziová, Petra (UMG-J)
    Sedláček, Radislav (UMG-J) RID
    Zemanová, Z. (CZ)
    Stopka, T. (CZ)
    Number of authors14
    Article number223
    Source TitleCells. - : MDPI
    Roč. 11, č. 2 (2022)
    Number of pages13 s.
    Publication formOnline - E
    Languageeng - English
    CountryCH - Switzerland
    Keywordsmyelodysplastic syndrome ; Azacytidine ; resistance ; CDX mice ; pi3k ; AKT signaling
    Subject RIVEB - Genetics ; Molecular Biology
    OECD categoryCell biology
    R&D ProjectsLM2018126 GA MŠMT - Ministry of Education, Youth and Sports (MEYS)
    GA19-03586S GA ČR - Czech Science Foundation (CSF)
    Method of publishingOpen access
    Institutional supportUMG-J - RVO:68378050
    UT WOS000757973600001
    DOI10.3390/cells11020223
    AnnotationThe mechanisms by which myelodysplastic syndrome (MDS) cells resist the effects of hypomethylating agents (HMA) are currently the subject of intensive research. A better understanding of mechanisms by which the MDS cell becomes to tolerate HMA and progresses to acute myeloid leukemia (AML) requires the development of new cellular models. From MDS/AML cell lines we developed a model of 5-azacytidine (AZA) resistance whose stability was validated by a transplantation approach into immunocompromised mice. When investigating mRNA expression and DNA variants of the AZA resistant phenotype we observed deregulation of several cancer-related pathways including the phosphatidylinosito-3 kinase signaling. We have further shown that these pathways can be modulated by specific inhibitors that, while blocking the proliferation of AZA resistant cells, are unable to increase their sensitivity to AZA. Our data reveal a set of molecular mechanisms that can be targeted to expand therapeutic options during progression on AZA therapy.
    WorkplaceInstitute of Molecular Genetics
    ContactNikol Škňouřilová, nikol.sknourilova@img.cas.cz, Tel.: 241 063 217
    Year of Publishing2023
    Electronic addresshttps://www.mdpi.com/2073-4409/11/2/223
Number of the records: 1  

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