ABSTRACT
The BCR/ABL tyrosine kinase, generated by the Philadelphia chromosome (Ph) translocation, is present in virtually all patients with chronic myeloid leukemia (CML) and has been demonstrated to be the causative agent of CML. BCR/ABL functions as a constitutively activated tyrosine kinase, and this kinase activity is required for the transforming function of BCR/ABL.1,2 Thus, BCR/ABL is an ideal candidate as a molecular target for a therapeutic agent, and an inhibitor of the BCR/ABL kinase would be predicted to be an effective and selective therapeutic agent for CML.
