REVIEW

Chronic myeloid leukemia (CML) is characterized by the increased and un-regulated proliferation of mature granulocytes (neutrophils, eo-sinophils, and basophils) and their pre-cursors. Chronic myeloid leukemia is caused by the development of the Phil-adelphia chromosome (Ph), formed by the reciprocal translocation between chromosomes 9 and 22 that fuses the ABL gene to the breakpoint cluster region (BCR) gene; the fusion results in the dysregulated expression of the oncogenic BCR-ABL tyrosine kinase protein (Faderl et al., 1999). Chronic myeloid leukemia accounts for 20% of all diagnosed adult leukemias, with approximately 5,000 new cases diag-nosed each year in the United State