Compartir
Título
Imatinib therapy of chronic myeloid leukemia restores the expression levels of key genes for DNA damage and cell-cycle progression
Autor(es)
Materia
chronic myeloid leukemia
DNA repair
gene expression
imatinib mesylate
Clasificación UNESCO
3109.01 Anatomía
6310.03 Enfermedad
Fecha de publicación
2012
Editor
Board
Citación
Benito, R., Lumbreras, E., Abáigar, M., Gutiérrez, N. C., Delgado, M., Robledo, C., García, J.L., Rodríguez-Vicente, A.E., Cañizo, M.C., Hernández Rivas, J.M. (2012). Imatinib therapy of chronic myeloid leukemia restores the expression levels of key genes for DNA damage and cell-cycle progression. Pharmacogenetics and Genomics, 22 (5) pp 381-388. 10.1097/FPC.0b013e328351f3e9
Resumen
[EN] Background
Chronic myeloid leukemia (CML) is a malignant clonal disorder of the hematopoietic system caused by the expression of the BCR/ABL fusion oncogene. It is well known that CML cells are genetically unstable. However, the mechanisms by which these cells acquire genetic alterations are poorly understood. Imatinib mesylate is the standard therapy for newly diagnosed CML patients. Imatinib mesylate targets the oncogenic kinase activity of BCR-ABL.
Objective
To study the gene expression profile of bone marrow hematopoietic cells in the same patients with CML before and 1 month after imatinib therapy.
Methods
Samples from patients with CML were analyzed using Affymetrix GeneChip Expression Arrays.
Results
A total of 594 differentially expressed genes, most of which (393 genes) were downregulated, as a result of imatinib therapy were observed.
Conclusion
The blockade of oncoprotein Bcr-Abl by imatinib could cause a decrease in the expression of key DNA repair genes and substantially modify the expression profile of the bone marrow cells in the first days of therapy.
URI
ISSN
1744-6872
DOI
10.1097/FPC.0b013e328351f3e9
Versión del editor
Colecciones
Ficheros en el ítem
Nombre:
imatinib_therapy_of_chronic_myeloid_leukemia.7.pdfEmbargado hasta: 2099-09-09
Tamaño:
487.7Kb
Formato:
Adobe PDF