Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
10909076 | Leukemia Research | 2012 | 7 Pages |
Abstract
Clofarabine (CLO), a purine nucleoside analog with promising efficacy in acute myeloid leukemia (AML), inhibits the ribonucleotidereductase, p53R2. We have shown that p53R2 mRNA is up-regulated by decitabine (DEC), another drug with promising activity in AML. We developed a pharmacodynamic model to characterize the interaction between CLO and DEC on an AML cell line and down-regulated p53R2 protein to understand its role. These results confirm a role for p53R2 in both CLO and DEC mechanism of action, demonstrate synergism between these two drugs in this AML model and support the use of this combination in a future clinical trial.
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Authors
Karen E. Thudium, Sampa Ghoshal, Gerald J. Fetterly, Jason P. Den Haese, Adam R. Karpf, Meir Wetzler,