Selective inactivation of hypomethylating agents by SAMHD1 provides a rationale for therapeutic stratification in AML

In acute myeloid leukemia, hypomethylating agents decitabine and azacytidine are used interchangeably. Here, the authors show that the major metabolite of decitabine, but not azacytidine, is subject to SAMHD1 inactivation, highlighting SAMHD1 as a potential biomarker and therapeutic target

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Auteurs principaux: Thomas Oellerich, Constanze Schneider, Dominique Thomas, Kirsten M. Knecht, Olga Buzovetsky, Lars Kaderali, Christoph Schliemann, Hanibal Bohnenberger, Linus Angenendt, Wolfgang Hartmann, Eva Wardelmann, Tamara Rothenburger, Sebastian Mohr, Sebastian Scheich, Federico Comoglio, Anne Wilke, Philipp Ströbel, Hubert Serve, Martin Michaelis, Nerea Ferreirós, Gerd Geisslinger, Yong Xiong, Oliver T. Keppler, Jindrich Cinatl
Format: article
Langue:EN
Publié: Nature Portfolio 2019
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Accès en ligne:https://doaj.org/article/95a48b4cc3c74d05b739c67d702815e2
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Résumé:In acute myeloid leukemia, hypomethylating agents decitabine and azacytidine are used interchangeably. Here, the authors show that the major metabolite of decitabine, but not azacytidine, is subject to SAMHD1 inactivation, highlighting SAMHD1 as a potential biomarker and therapeutic target