title: Role of epigenetics in chronic myeloid leukemia.
abstract: The efficacy of therapeutic modalities in chronic myeloid leukemia (CML) depends on both genetic and epigenetic mechanisms. This review focuses on epigenetic mechanisms involved in the pathogenesis of CML and in resistance of tumor cells to tyrosine kinase inhibitors leading to the leukemic clone escape and propagation. Regulatory events at the levels of gene regulation by transcription factors and microRNAs are discussed in the context of CML pathogenesis and therapeutic modalities.
authors.affiliation: Institute of Hematology and Blood Transfusion, U Nemocnice 1, Prague 2, 128 20, Czech Republic. katerina.machova@uhkt.cz
authors.forename: Katerina
authors.initials: K
authors.lastname: Machova Polakova
authors.forename: Jitka
authors.initials: J
authors.lastname: Koblihova
authors.forename: Tomas
authors.initials: T
authors.lastname: Stopka
mesh_terms: D000970:Antineoplastic Agents / Q000494:pharmacology / Q000627:therapeutic use; D019175:DNA Methylation; D019008:Drug Resistance, Neoplasm; D057890:Epigenomics; D016044:Fusion Proteins, bcr-abl / Q000037:antagonists & inhibitors / Q000235:genetics / Q000627:therapeutic use; D015973:Gene Expression Regulation, Leukemic / Q000187:drug effects; D006801:Humans; D015464:Leukemia, Myelogenous, Chronic, BCR-ABL Positive / Q000188:drug therapy / Q000235:genetics* / Q000473:pathology; D035683:MicroRNAs / Q000502:physiology*; D047428:Protein Kinase Inhibitors / Q000494:pharmacology / Q000627:therapeutic use
chemical_list: D000970:Antineoplastic Agents; D035683:MicroRNAs; D047428:Protein Kinase Inhibitors; D016044:Fusion Proteins, bcr-abl