AML1-ETO Hijacks a Distal Enhancer of NAT10 to Reprogram Glutathione Metabolism and Sustain Leukemia Stem Cell Stemness

By
Emily Salmini
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Genetic ablation or pharmacological inhibition of NAT10 restricted the survival and self-renewal of LSCs in primary t(8;21) acute myeloid leukemia (AML) CD34+ cells, as well as in a retroviral AML1-ETO9a-driven t(8;21) AML mouse model.
[Proceedings of The National Academy of Sciences of The United States of America]
Abstract