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Most chemotherapy agents act by damaging the DNA of cancer cells, thus leading to cell death. CPX-351, a liposomal cytarabine–daunorubicin formulation, is one such example that has been approved by the U.S. Food and Drug Administration (FDA) and the European Medicines Agency (EMA) for its use in patients with secondary acute myeloid leukemia (AML). Despite the great potential of frontline chemotherapeutic agents, a proportion of patients with AML relapse following treatment, indicating the need for improved regimens for this subset of patients.1,2
At the Virtual Edition of the 25th European Hematology Association (EHA) Annual Congress, Yuki Nishida et al.1 presented a poster with promising preclinical data on the combinatory use of CPX-351 with the DNA repair inhibitor, M3814. More specifically, M3814 inhibits the actions of the DNA-dependent protein kinase catalytic subunit (DNA-PKcs), which plays a key role in DNA double-strand break repair. The authors hypothesized that DNA damage, induced by CPX-351, together with DNA repair inhibition by M3814, might provide a stronger anti-leukemic strategy than DNA damage alone.
Both the in vitro and in vivo data of this study indicate that, when combined, CPX-351 and M3814 lead to superior anti-leukemic effects compared with CPX-351 chemotherapy alone. The combination treatment was well tolerated in vivo and, together with its observed promising efficacy, is paving the way for the further clinical investigation of DNA damage and DNA repair inhibitor combinations for the treatment of AML.
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