title: [New perspective in the treatment of chronic myeloid leukemia? gene silencing therapy].
abstract: Chronic myeloid leukemia is an incurable white blood cell disease with slow progression which affects myeloid stem cells. In the course of chromosome 22 shortening a fusion oncogene arises whose product, a Bcr-Abl oncoprotein, is a continuously expressed tyrosine kinase protein. Beside the opportunity of chemotherapy, stem cell therapy and interferon-a therapy, the application of tyrosine kinase inhibitors also became widespread in the treatment of the disease. Patients bearing the T315I point mutation, however, show resistance against all tyrosine kinase inhibitors, which can be managed by dose escalation or the combination of therapies. The discovery of RNA interference or gene silencing put the therapeutic opportunity of CML in new light. The in vitro application of anti-bcr-abl siRNA showed promising results in the causal treatment of the disease, feasible for identification of new genes associated to the disease, but we do not have sufficient evidence for the safety and efficacy of this method in human therapy.
authors.affiliation: Miskolci Egyetem Egészségügyi Kar, Nanobiotechnológiai és Regeneratív Medicina Tanszék, Hungary. evakisstoth@gmail.com
authors.forename: Éva
authors.initials: É
authors.lastname: Kiss-Tóth
authors.forename: Adrienn
authors.initials: A
authors.lastname: Juhászné Szalai
authors.forename: Péter
authors.initials: P
authors.lastname: Koska
authors.forename: János
authors.initials: J
authors.lastname: Szebeni
authors.forename: Emõke
authors.initials: E
authors.lastname: Kiss-Tóth
authors.forename: László
authors.initials: L
authors.lastname: Barkai
authors.forename: Bertalan
authors.initials: B
authors.lastname: Fodor
mesh_terms: D000818:Animals; D045744:Cell Line, Tumor; D019008:Drug Resistance, Neoplasm / Q000235:genetics; D016044:Fusion Proteins, bcr-abl / Q000037:antagonists & inhibitors / Q000235:genetics*; D020868:Gene Silencing / Q000187:drug effects; D015316:Genetic Therapy / Q000379:methods*; D006801:Humans; D015464:Leukemia, Myelogenous, Chronic, BCR-ABL Positive / Q000235:genetics* / Q000628:therapy*; D047428:Protein Kinase Inhibitors / Q000494:pharmacology / Q000627:therapeutic use; D011505:Protein-Tyrosine Kinases / Q000037:antagonists & inhibitors / Q000235:genetics
chemical_list: D047428:Protein Kinase Inhibitors; D011505:Protein-Tyrosine Kinases; D016044:Fusion Proteins, bcr-abl