The p53 orbit in chronic myeloid leukemia: time to move to patient care

Chronic myeloid leukemia (CML) is the paradigm of precision medicine in cancer. CML was the first disease to be effectively treated with selective drug designed to inhibit the causative BCR-ABL oncoprotein activity. BCR-ABL tyrosine kinase inhibitor (TKI), imatinib, was the first FAD approved tyrosine kinase as standard treatment of a specific cancer. However, CML also highlighted TKIs limits: the development of resistance, due to mutations, and the inability to completely eradicate the disease, due to TKI insensitiveness of CML stem cells. Lastly, CML was also shown to be effectively targeted by strategies designed to modulate tumor suppressors. Here, we comment the impressive and recently published combinatorial therapy with p53 and c-Myc modulators in CML stem cells.