The features of chronic myeloid leukemia (CML) are caused by a functionally overactive tyrosine kinase, Bcr-Abl, which is the product of the BCR-ABL gene consequent to a t(9;22)(q34;q11) reciprocal chromosomal translocation. The tyrosine kinase inhibitor imatinib has become the first-line treatment for CML, and has improved survival and may alter the natural course of the disease in many patients. However, advanced phase disease is still refractory to many treatments, and a better understanding of the molecular aspects of Bcr-Abl may yield new therapeutic avenues for drug discovery. In addition to the development of newer tyrosine kinase-targeted therapies, the emerging role of immunotherapy and exploitation of tyrosine kinase-independent pathways are promising aspects of translational research.
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