2022-05-272022-05-272009-12Ali, R. vd. (2009). "Sudden blastic crisis and additional chromosomal abnormalities during chronic myeloid leukemia in the imatinib era". International Journal of Clinical Oncology, 14(6), 545-550.1341-9625https://doi.org/10.1007/s10147-009-0884-5https://link.springer.com/article/10.1007/s10147-009-0884-5http://hdl.handle.net/11452/26745Imatinib 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, C1361, 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.eninfo:eu-repo/semantics/closedAccessOncologyBlastic crisisChronic myeloid leukemiaCytogenetic responseImatinibChronic myelogenous leukemiaBone-marrow fibrosisMesylate therapyMyelocytic-leukemiaChronic-phasebcr-ablTransformationProgressionResistanceOptionsAdultAntineoplastic agentsBlast crisisChromosome aberrationsCytogenetic analysisHumansIn situ hybridization, fluorescenceLeukemia, myelogenous, chronic, BCR-ABL positiveMalePiperazinesPyrimidinesArticle0002724637000142-s2.0-7294909088954555014619967494OncologyChronic Myeloid Leukemia; Imatinib; Protein Tyrosine Kinase InhibitorBCR ABL proteinCD19 antigenCD33 antigenCD34 antigenCD45 antigenCD61 antigenCytarabineDaunorubicinFibrinogen receptorGlycophorin AImatinibMicrosomal aminopeptidaseReticulinAcute kidney failureAdultAnemiaArticleBlast cellBlast cell crisisBone marrow biopsyBone marrow cellCase reportCell infiltrationCell structureChromosome 13Chromosome 19Chromosome 21Chromosome 8Chromosome aberrationChronic myeloid leukemiaContinuous infusionCytogeneticsDeathDisseminated intravascular clottingDrug dose increaseDyspneaFatigueFlow cytometryFluorescence in situ hybridizationHumanHuman tissueKaryotypingLeukapheresisLeukocyte countLeukocytosisMaleMyelofibrosisPallorPhiladelphia 1 chromosomePriority journalPrognosisPurpuraSplenomegalyStainingThrombocytopeniaTreatment durationTreatment responseTumor lysis syndrome