ABSTRACT
Blast crisis is the terminal phase of chronic myeloid leukemia (CML), a clonal myeloproliferative disorder of the pluripotent hematopoietic stem cell, which typically evolves in three distinct clinical stages: chronic phase, accelerated phase, and blast crisis (reviewed in refs. 1,2). Blast crisis lasts only a few months and is characterized by the rapid expansion of myeloid or lymphoid differentiation-arrested blast cells (1,2). CML is consistently associated with an acquired genetic abnormality, the Philadelphia chromosome (Ph1), a shortened chromosome 22 resulting from a reciprocal translocation of the long arms of chromosomes 9 and 22 (1,2). This translocation generates the BCR-ABL fusion gene, which is translated in the p210 BCR-ABL oncoprotein of almost all CML patients (1,2).
