Abstract
Chronic myelogenous leukemia (CML) is a clonal myeloproliferative disorder resulting from neoplastic transformation at the level of the pluripotent hematopoietic stem cell (1). The hallmark of CML is a shortened chromosome 22, termed the Philadelphia (Ph) chromosome, which results from a reciprocal translocation between chromosomes 9 and 22—t(9;22)(q34;q11) (2,3). Ph-positive CML is characterized by a multistep evolutionary course. The disease inexorably progresses from a benign or chronic phase lasting an average of 3.5 years to a terminal blast transformation phase (4). The invariably fatal outcome of CML cannot be altered by chemother-apeutic agents which control the proliferative thrust of the benign phase but do not affect the Ph chromosome. Although ablative chemoradiotherapy followed by allogeneic bone marrow transplantation can be curative, this option is only available to young patients with histocom-patible siblings. Therefore, exploration of other therapeutic approaches is warranted.