Person:
Buño Borde, Ismael

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First Name
Ismael
Last Name
Buño Borde
Affiliation
Universidad Complutense de Madrid
Faculty / Institute
Medicina
Department
Biología Celular
Area
Biología Celular
Identifiers
UCM identifierORCIDScopus Author IDWeb of Science ResearcherIDDialnet ID

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Now showing 1 - 2 of 2
  • Item
    Project number: 443
    El formato vídeo como herramienta para el aprendizaje de la Histología. Implementación de “HistoApp” para la autoevaluación individual y asistida del alumno como refuerzo para el aprendizaje
    (2023) Buño Borde, Ismael; Sacedón Ayuso, Rosa; Novillo Villajos, Apolonia; Jiménez Pérez, Eva; Zuluaga Arias, María Del Pilar; Escribano Martínez, Catalina; Orera Clemente, María Asunción; Ortega Salmerón, Lucía; Buño Borde, Ismael
  • Item
    Role of Intracellular Drug Disposition in the Response of Acute Myeloid Leukemia to Cytarabine and Idarubicin Induction Chemotherapy
    (Cancers, 2023) Rodríguez-Macías, Gabriela; Briz, Oscar; Cives-Losada, Candela; Chillón, María; Martínez-Laperche, Carolina; Martínez-Arranz, Ibon; González-Díaz, Marcos; Marin, Jose; Macias, Rocio; Buño Borde, Ismael; Díez Martín, José Luis
    Despite its often low efficacy and high toxicity, the standard treatment for acute myeloid leukemia (AML) is induction chemotherapy with cytarabine and idarubicin. Here, we have investigated the role of transporters and drug-metabolizing enzymes in this poor outcome. The expression levels (RT-qPCR) of potentially responsible genes in blasts collected at diagnosis were related to the subsequent response to two-cycle induction chemotherapy. The high expression of uptake carriers (ENT2), export ATP-binding cassette (ABC) pumps (MDR1), and enzymes (DCK, 5-NT, and CDA) in the blasts was associated with a lower response. Moreover, the sensitivity to cytarabine in AML cell lines was associated with ENT2 expression, whereas the expression of ABC pumps and enzymes was reduced. No ability of any AML cell line to export idarubicin through the ABC pumps, MDR1 and MRP, was found. The exposure of AML cells to cytarabine or idarubicin upregulated the detoxifying enzymes (5-NT and DCK). In AML patients, 5-NT and DCK expression was associated with the lack of response to induction chemotherapy (high sensitivity and specificity). In conclusion, in the blasts of AML patients, the reduction of the intracellular concentration of the active metabolite of cytarabine, mainly due to the increased expression of inactivating enzymes, can determine the response to induction chemotherapy.