Pharmacogenetics and genomics, 2012-05, Vol.22 (5), p.381-388
2012
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- Autor(en) / Beteiligte
- Titel
- Imatinib therapy of chronic myeloid leukemia restores the expression levels of key genes for DNA damage and cell-cycle progression
- Ist Teil von
- Pharmacogenetics and genomics, 2012-05, Vol.22 (5), p.381-388
- Ort / Verlag
- Hagerstown, MD: Lippincott Williams & Wilkins, Inc
- Erscheinungsjahr
- 2012
- Quelle
- MEDLINE
- Beschreibungen/Notizen
- BACKGROUNDChronic 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. OBJECTIVETo study the gene expression profile of bone marrow hematopoietic cells in the same patients with CML before and 1 month after imatinib therapy. METHODSSamples from patients with CML were analyzed using Affymetrix GeneChip Expression Arrays. RESULTSA total of 594 differentially expressed genes, most of which (393 genes) were downregulated, as a result of imatinib therapy were observed. CONCLUSIONThe 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.
- Sprache
- Englisch
- Identifikatoren
- ISSN: 1744-6872eISSN: 1744-6880DOI: 10.1097/FPC.0b013e328351f3e9Titel-ID: cdi_proquest_miscellaneous_1000402514
- Format
- –
- Schlagworte
- Adolescent, Adult, Benzamides, Biological and medical sciences, Bone Marrow Cells - metabolism, Cell Cycle Proteins - genetics, Cell cycle, cell proliferation, Cell physiology, DNA Damage - genetics, DNA Repair - genetics, Drug Resistance, Neoplasm - genetics, Female, Fundamental and applied biological sciences. Psychology, Fusion Proteins, bcr-abl - genetics, Fusion Proteins, bcr-abl - metabolism, Gene Expression Profiling, Gene Expression Regulation, Leukemic - drug effects, General pharmacology, Hematologic and hematopoietic diseases, Humans, Imatinib Mesylate, Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy, Leukemia, Myelogenous, Chronic, BCR-ABL Positive - genetics, Leukemia, Myelogenous, Chronic, BCR-ABL Positive - pathology, Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis, Male, Medical sciences, Middle Aged, Molecular and cellular biology, Pharmacokinetics. Pharmacogenetics. Drug-receptor interactions, Pharmacology. Drug treatments, Piperazines - therapeutic use, Pyrimidines - therapeutic use