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Chronic myeloid leukaemia with BCR–ABL fusion genes located to both chromosomes 9, cyclic leukocytosis and nodal T-lymphoblastic transformation – durable complete remission following imatinib therapy

Leukemia volume 19, pages 671–673 (2005)Cite this article

TO THE EDITOR

The causative molecular event in chronic myeloid leukaemia (CML) is the formation of a BCR–ABL fusion gene, leading to expression of a constitutively active BCR–ABL tyrosine kinase. In most cases, the BCR–ABL fusion gene results from the translocation t(9;22), which creates a shortened chromosome 22 known as the Philadelphia (Ph) chromosome. Clinically, CML is characterised by three phases: chronic, accelerated and blastic phase. In one-third of blastic phases, the blast cells are lymphoid, usually of B-cell type. T-lymphoblastic transformation is a rare event.1

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Authors and Affiliations

  1. Department of Haematology, Herlev Hospital, University of Copenhagen, Herlev, Denmark

    I H Dufva, H Karle & H E Johnsen

  2. John F. Kennedy Institute, Glostrup, Denmark

    K Brondum-Nielsen

  3. Department of Clinical Genetics, The Cytogenetic Laboratory, Section of Haematology/Oncology, Rigshospitalet, Copenhagen, Denmark

    M K Andersen

  4. Tissue Typing Laboratory, Department of Clinical Immunology, Rigshospitalet, Copenhagen, Denmark

    H O Madsen

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  1. I H Dufva
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  2. H Karle
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Correspondence to I H Dufva.

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Dufva, I., Karle, H., Brondum-Nielsen, K. et al. Chronic myeloid leukaemia with BCR–ABL fusion genes located to both chromosomes 9, cyclic leukocytosis and nodal T-lymphoblastic transformation – durable complete remission following imatinib therapy. Leukemia 19, 671–673 (2005). https://doi.org/10.1038/sj.leu.2403662

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