Cytogenetic and molecular changes occur in the vast majority of CML patients during transition to blast crisis; however, the mechanism(s) whereby each specific secondary genetic alteration contributes to disease progression is still largely unclear (Fig. 2) (reviewed in Ref. 1) .
Conversely, growing evidence supports the importance of BCR-ABL in determining the phenotype of CML-BC cells (1), as increased BCR-ABL expression is a feature of CML-BC progenitors (1,15), and unrestrained BCR-ABL activity in CML-BC alters the expression of genes important for proliferation, survival, and maturation of myeloid progenitors (1). The cytogenetic and molecular changes observed in blast crisis CML might also be caused by the reported ability of the BCR-ABL oncoprotein to increase genomic instability (21,41).
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