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    Por favor, use este identificador para citar o enlazar este ítem: https://hdl.handle.net/10259/12198

    Título
    Role of Pharmacogenetics in the Treatment of Acute Myeloid Leukemia: Systematic Review and Future Perspectives
    Autor
    Pinto Merino, Álvaro
    Labrador, Jorge
    Zubiaur, Pablo
    Alcaraz, Raquel
    Herrero, María José
    Montesinos, Pau
    Abad Santos, Francisco
    Saiz Rodríguez, MiriamAutoridad UBU Orcid
    Editorial
    MDPI
    Fecha de publicación
    2022-03
    DOI
    10.3390/PHARMACEUTICS14030559
    Zusammenfassung
    Acute myeloid leukemia (AML) is a heterogeneous disease characterized by remarkable toxicity and great variability in response to treatment. Plenteous pharmacogenetic studies have already been published for classical therapies, such as cytarabine or anthracyclines, but such studies remain scarce for newer drugs. There is evidence of the relevance of polymorphisms in response to treatment, although most studies have limitations in terms of cohort size or standardization of results. The different responses associated with genetic variability include both increased drug efficacy and toxicity and decreased response or resistance to treatment. A broad pharmacogenetic understanding may be useful in the design of dosing strategies and treatment guidelines. The aim of this study is to perform a review of the available publications and evidence related to the pharmacogenetics of AML, compiling those studies that may be useful in optimizing drug administration.
    Palabras clave
    Acute myeloid leukemia
    Pharmacogenetics
    Cytarabine
    Anthracyclines
    FLT3 inhibitors
    IDH inhibitors
    CD33 inhibitors
    Hypomethylating agents
    BCL2 inhibitors
    Materia
    Leucemia mieloide aguda
    Acute myeloid leukemia
    URI
    https://hdl.handle.net/10259/12198
    Versión del editor
    https://doi.org/10.3390/ pharmaceutics14030559
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    Documento(s) sujeto(s) a una licencia Creative Commons Atribución 4.0 Internacional
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    Pinto-pharmaceutics_2022.pdf
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