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H3K79 methylation profiles define murine and human MLL-AF4 leukemias.
MLL translocations, histone modifications and leukaemia stem-cell development.
HOXA9 is required for survival in human MLL-rearranged acute leukemias.
MLL-rearranged leukemia is dependent on aberrant H3K79 methylation by DOT1L.
Conditional MLL-CBP targets GMP and models therapy-related myeloproliferative disease.
MLL-rearranged B lymphoblastic leukemias selectively express the immunoregulatory carbohydrate-binding protein galectin-1.
MLL partial tandem duplication leukemia cells are sensitive to small molecule DOT1L inhibition.
Loss of BAP1 function leads to EZH2-dependent transformation.
Mixed-Lineage Leukemia Fusions and Chromatin in Leukemia.
A UTX-MLL4-p300 Transcriptional Regulatory Network Coordinately Shapes Active Enhancer Landscapes for Eliciting Transcription.
Murine Retrovirally-Transduced Bone Marrow Engraftment Models of MLL-Fusion-Driven Acute Myelogenous Leukemias (AML).
SETD2 alterations impair DNA damage recognition and lead to resistance to chemotherapy in leukemia.
The DOT1L inhibitor pinometostat reduces H3K79 methylation and has modest clinical activity in adult acute leukemia.
Therapeutic targeting of preleukemia cells in a mouse model of NPM1 mutant acute myeloid leukemia.
Novel inhibitors of the histone methyltransferase DOT1L show potent antileukemic activity in patient-derived xenografts.
Histone Lysine N Methyltransferase