Abstract
INTRODUCTION Philadelphia positive chronic myelogenous leukemia (Ph1+ CML) is a myeloproliferative disorder of clonal origin, due to neoplastic transformation of a pluripotent stem cell, and characterized by excessive proliferation of hemopoietic precursors and expansion of the myeloid cellular mass1. In 90-95% of cases, the disease is associated with a chromosomal abnormality, the Ph1 chromosome, derived from a reciprocal translocation t(9;22) (q34;q11) between chromosomes 9 and 222. The translocation of the proto-oncogene c-abl from its normal location on chromosome 9 to the break-point cluster region (bcr) of chromosome 22 involves the formation of a chimeric gene (abl-bcr), the product of which is a protein with increased tyrosine-kinase activity3,4. It seems likely that the bcr rearrangement plays an important role in the pathogenesis of CML. Characteristically, the disease presents two phases: a “benign” or chronic phase lasting about 3 years, well controlled by chemotherapy, and a terminal blastic phase, refractory to chronic-phase treatments, invariably fatal in 3-6 months and frequently associated with cytogenetic abnormalities additional to the Ph1.
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