M William, BasemWoost, PhilipMahfouz, RedaBrister, LaurenCaimi, PaoloCampagnaro, EricaCooper, BrendaM Lazarus, HillardSaunthararajah, YogenJG de Lima, MarcosV Komanduri, KrishnaJacobberger, James2020-03-172020-03-1720151083-8791https://doi.org/10.1016/j.bbmt.2014.11.507https://cutt.ly/QtjV5YsMSA Google ScholarDisease relapse is a major cause of treatment failure following alloSCT for acute myeloid leukemia (AML). Azacitidine has shown efficacy in treating, and preventing, post-transplant relapse in patients with AML. Post-SCT azacitidine administration is challenging due to the possibility of myelosuppression and an incomplete understanding of the optimal dose and schedule. DNMT1 is responsible for genome methylation in S phase and degraded after bonding irreversibly to substituted DNA. Hence, the DNMT1 level may be an attractive pharmacodynamic (PD) endpoint for azacitidine therapyenDNA Methyltransferase-1 (DNMT1)DNACytometricPharmacodynamicAzacitidineHypomethylatingAllogeneic Hematopoietic Stem Cell Transplantation (AlloSCT)Articlehttps://doi.org/10.1016/j.bbmt.2014.11.507