Review Article

Hsp90 Inhibitors for the Treatment of Chronic Myeloid Leukemia

Figure 4

BCR-ABL functioning in the presence and absence of Hsp90 inhibitors. (a) In CML cells, Hsp90 levels are elevated. Hence oncoprotein BCR-ABL binds to Hsp90 for stabilization and maturation. Hence, stabilized BCR-ABL then activates many signaling pathways leading to CML cells survival, progression, and malignancy. (b) Blocking Hsp90 chaperone activity by employing Hsp90 inhibitors results in BCR-ABL degradation via ubiquitin proteasome pathway.
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