Chronic myeloid leukemia (CML) with the e19a2 transcript coding for p230 is typically associated with a benign clinical course unless accompanied at presentation with additional chromosomal abnormalities. We report here a case of CML with e19a2 who did not show additional chromosomal abnormalities at diagnosis, but progressed to the fatal advanced stage in approximately 2 years. The patient was initially treated with imatinib, which, however, could be administered only intermittently at reduced doses because of recurrent thrombocytopenia and fluid retention. Nine months after starting imatinib, fluorescence in situ hybridization (FISH) with the BCR/ABL-ES fusion probe revealed 96% and 3% of bone marrow cells with one and two BCR/ABL1 fusion signals, respectively. Two years after starting therapy, leukocytosis recurred and the bone marrow contained 8.2% large and bizarre myeloblasts. Cytogenetic analysis revealed double Ph clones as well as tetraploid cells with four to five Ph chromosomes. FISH analysis confirmed the presence of cells with two to five BCR/ABL1 fusion signals. The patient died of disease progression in 2 months. No point mutation was detected in the region coding for the BCR/ABL tyrosine kinase domain by sequence analysis. It is speculated that the amplification of the BCR/ABL1 fusion gene by duplication of Ph and tetraploidy led to the progression of CML with the e19a2 transcript.
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http://dx.doi.org/10.1016/j.cancergencyto.2010.01.018 | DOI Listing |
Leukemia
September 2024
Klinik für Innere Medizin II, Universitätsklinikum Jena, Comprehensive Cancer Center Central Germany, Campus Jena, Jena, Germany.
Sci Rep
March 2024
Division of Molecular Pathology, Department of Pathology, Hong Kong Sanatorium & Hospital, Happy Valley, Hong Kong.
Leukaemia of various subtypes are driven by distinct chromosomal rearrangement or genetic abnormalities. The leukaemogenic fusion transcripts or genetic mutations serve as molecular markers for minimal residual disease (MRD) monitoring. The current study evaluated the applicability of several droplet digital PCR assays for the detection of these targets at RNA and DNA levels (atypical BCR::ABL1 e19a2, e23a2ins52, e13a2ins74, rare types of CBFB::MYH11 (G and I), PCM1::JAK2, KMT2A::ELL2, PICALM::MLLT10 fusion transcripts and CEBPA frame-shift and insertion/duplication mutations) with high sensitivity.
View Article and Find Full Text PDFLeuk Res Rep
May 2023
Hematology Department, Fattouma Bourguiba University Hospital, Monastir, Tunisia.
Introduction: Chronic myeloid leukemia (CML) is characterized by Philadelphia chromosome resulting in the fusion between the BCR gene, located on chromosome 22, and the ABL gene on chromosome 9. The prognostic significance of BCR-ABL transcript variants in CML is controversial. The aim of the current study was to evaluate the clinico-hematological presentation and evolution of the disease, response to treatment and survival according to transcript type in chronic phase CML patients.
View Article and Find Full Text PDFBMC Med Genomics
July 2023
Centre for Haematology, Department of Immunology and Inflammation, Imperial College London, London, UK.
Background: Chronic myeloid leukaemia (CML) is one of the most well characterised human malignancies. Most patients have a cytogenetically visible translocation between chromosomes 9 and 22 which generates the pathognomonic BCR::ABL1 fusion gene. The derivative chromosome 22 ('Philadelphia' or Ph chromosome) usually harbours the fusion gene encoding a constitutively active ABL1 kinase domain.
View Article and Find Full Text PDFHematology
December 2023
Department of Hematology, Zhongda Hospital, Southeast University, Nanjing, People's Republic of China.
Myelodysplastic syndromes (MDS) refer to a set of clonal hematopoietic disorders with fusion transcript as disease progression. Breakpoint cluster region/abelson () fusion mostly occurs during the progressive phase from MDS to higher stages and acute leukemia transformation. Besides, it is extremely rare reported on the diagnosis of MDS.
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