title: Sudden blastic crisis and additional chromosomal abnormalities during chronic myeloid leukemia in the imatinib era.
abstract: Imatinib has shown significant clinical and cytogenetic success in the treatment of chronic myeloid leukemia. Although resistance has been observed in a proportion of patients, sudden blastic crisis is a rare event during imatinib therapy. We describe a 24-year-old male patient with Philadelphia chromosome-positive chronic myeloid leukemia in chronic phase who developed sudden blastic crisis in the 24th month of imatinib therapy, with loss of complete cytogenetic response. At this time, the patient had splenomegaly, severe anemia, thrombocytopenia, and leukocytosis. Bone marrow aspirate revealed the presence of massive blastic infiltration with myeloid morphology. Flow cytometric analysis of the bone marrow cells showed positivity for CD45, CD34, CD13, CD33, CD19, CD41, CD61, and glycophorin-A. Trephine biopsy specimens showed 100% cellular marrow with diffuse infiltrate by blasts. A reticulin stain of the bone marrow biopsy section demonstrated severe diffuse fibrosis. Cytogenetic analysis by fluorescence in situ hybridization (FISH) revealed that 92% of the cells were positive for the BCR/ABL fusion signal and had increased copy numbers for chromosomes 8, 13, 19, and 21. The patient's prognosis was unfavorable. In conclusion, chronic myeloid leukemia remains complex and includes unanswered questions. The presented case with a rare event during imatinib therapy highlights the need for the continued monitoring of residual disease and the development of strategies to eliminate residual leukemia cells in patients showing a complete cytogenetic response.
authors.affiliation: Division of Hematology, Department of Internal Medicine, Uludag University School of Medicine Hospital, 16059 Gorukle, Bursa, Turkey. ridvanali@uludag.edu.tr
authors.forename: Ridvan
authors.initials: R
authors.lastname: Ali
authors.forename: Fahir
authors.initials: F
authors.lastname: Ozkalemkas
authors.forename: Vildan
authors.initials: V
authors.lastname: Ozkocaman
authors.forename: Tahsin
authors.initials: T
authors.lastname: Yakut
authors.forename: Hulya Ozturk
authors.initials: HO
authors.lastname: Nazlioglu
authors.forename: Ferah
authors.initials: F
authors.lastname: Budak
authors.forename: Murat
authors.initials: M
authors.lastname: Pekgoz
authors.forename: Serhat
authors.initials: S
authors.lastname: Korkmaz
authors.forename: Mutlu
authors.initials: M
authors.lastname: Karkucak
authors.forename: Tulay
authors.initials: T
authors.lastname: Ozcelik
authors.forename: Ahmet
authors.initials: A
authors.lastname: Tunali
mesh_terms: D000328:Adult; D000970:Antineoplastic Agents / Q000627:therapeutic use*; D001549:Benzamides; D001752:Blast Crisis / Q000175:diagnosis* / Q000473:pathology; D002869:Chromosome Aberrations; D020732:Cytogenetic Analysis; D006801:Humans; D000068877:Imatinib Mesylate; D017404:In Situ Hybridization, Fluorescence; D015464:Leukemia, Myelogenous, Chronic, BCR-ABL Positive / Q000175:diagnosis / Q000188:drug therapy* / Q000473:pathology*; D008297:Male; D010879:Piperazines / Q000627:therapeutic use*; D011743:Pyrimidines / Q000627:therapeutic use*
chemical_list: D000970:Antineoplastic Agents; D001549:Benzamides; D010879:Piperazines; D011743:Pyrimidines; D000068877:Imatinib Mesylate