ABSTRACT
Chronic myeloid leukemia (CML) is a disease in which the acquisition of the Philadelphia chromosome (Ph) translocation is a universal change present in all of the cells of the population of leukemia cells and in over 95% of the patients in whom the clinical phenotype of CML is present.1 Analysis of the junction point of the fusion chromosome between chromosomes 9 and 22 has shown that a chimeric protein, p210 BCR/ABL, is generated by the chromosomal translocation.1 Detailed comparisons of the p210 BCR/ABL protein and its normal homologue, the p145 c-ABL kinase, have indicated that this translocation changes the intracellular location of the kinase from the nucleus and plasma membrane2 to the cytoplasmic fraction.3 In contrast to the p145 c-ABL kinase, which induces cell cycle arrest and apoptosis when overexpressed in cells,4 overexpression of p210 BCR/ABL generates apoptosis rescue and continuous cycling of the myeloid cell.
