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Chronic myeloid leukaemia (CML) is a myeloproliferative neoplasm caused by a translocation between chromosome 9 and 22, denoted as t(9;22)(q34;q11.2), involving the fusion of the breakpoint cluster region (BCR) gene on chromosome 22q11.2 and the Abelson gene (ABL1) on chromosome 9q34. This translocation is known as the Philadelphia chromosome.1,2 The resultant fusion oncogene, BCR-ABL1, encodes a tyrosine kinase that drives clonal proliferation of haematopoietic stem cells and mainly affects the granulocytic lineage.1,2 Tyrosine kinase inhibitors (TKI) target and suppress the BCR-ABL1 tyrosine kinase and have revolutionised the outcome of CML. Imatinib was the first available TKI, with nilotinib and dasatinib developed later as more potent second-generation agents.3,4

Chronic myeloid leukaemia in the South African public health setting: Are we reaching the European LeukemiaNet targets for frontline therapy?