title: [Imatinib therapy in chronic myeloid leukemia].
abstract: Chronic myeloid leukemia is a malignant clonal alteration of the pluripotent hemopoietic stem cell. The genetic hallmarks of the disease are the t(9,22) (Philadelphia chromosome), registered by conventional cytogenetics in more than 90% of all chronic myeloid leukemia cases and the active tyrosine kinase protein encoded by bcr-abl fusion gene. The constitutively active tyrosine kinase is currently accepted to be the cause of chronic myeloid leukemia. The introduction of imatinib has considerably changed the treatment of chronic myeloid leukemia. Prior studies demonstrated high rates of cytogenetic responses in all phases of the disease.
  
  
  METHODS
  The authors evaluated the cytogenetic and molecular responses of 21 chronic phase chronic myeloid leukemia patients who were consecutively admitted to their center. 13 of them were primarily treated with imatinib, and the other 7 were heavily pretreated with interferon alpha, cytarabine, all-trans-retinoic acid. Hydroxyurea pretreatment was routinely introduced in all patients until complete hematologic remission. Peripheral blood sample in every 3 months were collected for quantitative real-time polymerase chain reaction, and bone marrow aspirate in every 6 months for conventional cytogenetics.
  
  
  RESULTS
  Hematologic remission could have been achieved with hydroxyurea pretreatment in each patient. Complete cytogenetic remission at the 6th month and major molecular response at the 12th month were observed in each patient.
  
  
  CONCLUSIONS
  Imatinib treatment caused complete cytogenetic response and major molecular response in each chronic phase chronic myeloid leukaemia patient in our group. Hydroxyurea might have some effect on the rapid and deep cytogenetic and molecular responses, observed in the primary imatinib-treated group.
authors.affiliation: Kaposi Mór Oktatókórház Belgyógyászati Osztály, Kaposvár. egyedmiklos@yahoo.com
authors.forename: Miklós
authors.initials: M
authors.lastname: Egyed
authors.forename: Balázs
authors.initials: B
authors.lastname: Kollár
authors.forename: Péter
authors.initials: P
authors.lastname: Rajnics
authors.forename: Eva
authors.initials: E
authors.lastname: Karádi
authors.forename: András
authors.initials: A
authors.lastname: Matolcsi
mesh_terms: D000970:Antineoplastic Agents / Q000008:administration & dosage / Q000627:therapeutic use*; D001549:Benzamides; D004334:Drug Administration Schedule; D005260:Female; D006801:Humans; D006918:Hydroxyurea / Q000008:administration & dosage / Q000627:therapeutic use*; D000068877:Imatinib Mesylate; D015464:Leukemia, Myelogenous, Chronic, BCR-ABL Positive / Q000188:drug therapy* / Q000473:pathology; D008297:Male; D008875:Middle Aged; D019384:Nucleic Acid Synthesis Inhibitors / Q000008:administration & dosage / Q000627:therapeutic use*; D010879:Piperazines / Q000627:therapeutic use*; D016133:Polymerase Chain Reaction; D047428:Protein Kinase Inhibitors / Q000008:administration & dosage / Q000627:therapeutic use*; D011743:Pyrimidines / Q000627:therapeutic use*; D012074:Remission Induction; D016896:Treatment Outcome
chemical_list: D000970:Antineoplastic Agents; D001549:Benzamides; D019384:Nucleic Acid Synthesis Inhibitors; D010879:Piperazines; D047428:Protein Kinase Inhibitors; D011743:Pyrimidines; D000068877:Imatinib Mesylate; D006918:Hydroxyurea