Imatinib therapy of chronic myeloid leukemia restores the expression levels of key genes for DNA damage and cell cycle progression

ABSTRACT: 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 (IM) is the standard therapy for newly diagnosed CML patients. IM targets the oncogenic kinase activity of BCR-ABL. Objective: To study the gene expression profile of BM hematopoietic cells in the same patients with CML before and one 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

ORGANISM(S): Homo sapiens

SUBMITTER: ROCIO BENITO 

PROVIDER: E-GEOD-33075 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress