Before the days of transplantation and tyrosine kinase inhibitor therapy, all cases of chronic myelogenous leukemia would inevitably proceed from chronic phase through accelerated and blast crisis, implying that there is a program of progression set in motion by unopposed BCR-ABL activity. Since then, much work has identified a plethora of genetic changes associated with progression, the common themes being changes in self-renewal, differentiation, and deregulation of apoptotic pathway. Some of the genes and pathways uncovered offer some progress for research on novel therapy for blast crisis.
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