Identificador persistente para citar o vincular este elemento: http://hdl.handle.net/10553/113937
Título: Can the Gene Expression Profile of Patients with Acute Myeloid Leukemia Predict Complete Remission Following Induction Therapy?
Autores/as: Sánchez Sosa, José Santiago 
Rodriguez-Medina, C
Stuckey, R
Florido, Y
Santana, G
Martin, JMG
Cruz-Cruz, N
Torres-Ochando, M
Fernandez, R
Sanchez-Farias, N
Cionfrini, A
Molero Labarta, María Teresa 
Gómez Casares, María Teresa 
Bilbao Sieyro, Cristina 
Clasificación UNESCO: 32 Ciencias médicas
320101 Oncología
320504 Hematología
Palabras clave: Acute myeloid leukemia
Biomarkers
Patient outcome
Induction therapy
Molecular diagnostics
Fecha de publicación: 2022
Publicación seriada: Journal of Cancer 
Resumen: Recent advances in sequencing technologies and genomics have led to the development of several targeted therapies such as BCL2 and Bromodomain and extra-terminal (BET) protein inhibitors for a more personalized treatment of patients with acute myeloid leukemia (AML), yet the majority of patients still receive standard induction chemotherapy. The molecular profiles of patients who are likely to respond to induction therapy and novel directed therapies remain to be determined. The expression of AML-related genes that are targeted by novel therapies such as BCL2 and BRD4, as well as functionally related genes and associated epigenetic modulators (TET2, EZH2, ASXL1, MYC) were analyzed in a series of 176 consecutive AML patients at multiple points during the disease course - diagnosis (Dx), post-induction (PI), complete remission (CR) and relapse (RL) - and their relationship with clinical variables and outcome investigated. Higher TET2 expression was observed PI and at CR compared to Dx, with significantly superior TET2 expression after induction therapy in the group of patients who reached CR compared to those who did not. Thus, the upregulation of TET2 at PI may be a marker of CR in AML patients. On the other hand, cells with high levels of MYC and BCL2 may be vulnerable to BRD4 inhibition.
URI: http://hdl.handle.net/10553/113937
ISSN: 1837-9664
DOI: 10.7150/jca.57457
Fuente: Journal of Cancer [ISSN 1837-9664], v. 13 (4), p. 1356-1362 (Enero 2022)
Colección:Artículos
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