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Chronic Myeloid Leukaemia

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Chromosomal Translocations and Genome Rearrangements in Cancer

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Abstract

Chronic myeloid leukaemia (CML) was the first leukaemia associated with a unique genetic abnormality, the Philadelphia chromosome. This results from a reciprocal translocation between chromosomes 9 and 22, which generates the BCR-ABL1 fusion gene encoding a constitutively active tyrosine kinase. The complex intracellular signalling initiated by BCR-ABL1 is responsible for disease development, and targeted tyrosine kinase inhibitors have been the most successful therapeutic advance in CML. In this chapter, we review the implications of BCR-ABL1 signalling in CML, how this knowledge revolutionized CML treatment, and discuss approaches to further improving therapeutic response by the targeting of leukaemic stem cells.

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Authors and Affiliations

  1. Department of Haematology, Centre for Cancer Biology, SA Pathology, University of South Australia, Adelaide, Australia

    Debora A. Casolari

  2. Department of Haematology, Centre for Cancer Biology, University of Adelaide, Adelaide, Australia

    Junia V. Melo

Authors
  1. Debora A. Casolari
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  2. Junia V. Melo
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Correspondence to Junia V. Melo .

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Editors and Affiliations

  1. Dept. of Medicine, Section of Hematol./Oncol., University of Chicago, CHICAGO, Illinois, USA

    Janet D. Rowley

  2. Section of Hematology/Oncology, Comprehensive Cancer Center, University of Chicago, Chicago, Illinois, USA

    Michelle M. Le Beau

  3. Weatherall Inst. of Molecular Medicine MRC Molecular Haematology Unit, University of Oxford, Oxford, United Kingdom

    Terence H. Rabbitts

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Casolari, D.A., Melo, J.V. (2015). Chronic Myeloid Leukaemia. In: Rowley, J., Le Beau, M., Rabbitts, T. (eds) Chromosomal Translocations and Genome Rearrangements in Cancer. Springer, Cham. https://doi.org/10.1007/978-3-319-19983-2_7

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