ABSTRACT
Chronic myeloid leukaemia (CML) constitutes a clinical model for molecular detection and therapy surveillance of malignant disease, since this entity was the first leukaemia shown to be associated with a specific chromosomal rearrangement, the Philadelphia (Ph) translocation t(9;22)(q34;q11),1-3 which generates two chimeric genes: BCR/ABL4,5 on the derivative chromosome 22, and ABL/BCR on the derivative chromosome 9. BCR/ABL is transcribed and translated in most patients into a 210 kDa fusion protein with deregulated tyrosine kinase activity. ABL/BCR is expressed in about 60% of patients with CML, but probably lacks any biological function6 (for a review, see Thijsen et al7).
