Abstract
Mislocated enzymatic activity of DOT1L has been proposed as a driver of leukemogenesis in mixed lineage leukemia (MLL). The characterization of EPZ004777, a potent, selective inhibitor of DOT1L is reported. Treatment of MLL cells with the compound selectively inhibits H3K79 methylation and blocks expression of leukemogenic genes. Exposure of leukemic cells to EPZ004777 results in selective killing of those cells bearing the MLL gene translocation, with little effect on non-MLL-translocated cells. Finally, in vivo administration of EPZ004777 leads to extension of survival in a mouse MLL xenograft model. These results provide compelling support for DOT1L inhibition as a basis for targeted therapeutics against MLL.
Copyright © 2011 Elsevier Inc. All rights reserved.
MeSH terms
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Animals
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Cell Death / drug effects
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Cell Differentiation / drug effects
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Cell Line, Tumor
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Cell Proliferation / drug effects
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Dose-Response Relationship, Drug
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Enzyme Inhibitors / administration & dosage
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Enzyme Inhibitors / chemistry
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Enzyme Inhibitors / pharmacology*
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Gene Expression Profiling
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Gene Expression Regulation, Leukemic / drug effects
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Gene Rearrangement / drug effects
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Histone Methyltransferases
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Histone-Lysine N-Methyltransferase / antagonists & inhibitors
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Histones / metabolism
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Humans
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Leukemia, Biphenotypic, Acute / genetics
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Leukemia, Biphenotypic, Acute / pathology*
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Lysine / metabolism
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Methylation / drug effects
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Methyltransferases / antagonists & inhibitors*
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Methyltransferases / metabolism
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Mice
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Myeloid-Lymphoid Leukemia Protein / metabolism
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Oncogene Proteins, Fusion / metabolism
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Small Molecule Libraries / administration & dosage
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Small Molecule Libraries / chemistry
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Small Molecule Libraries / pharmacology*
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Xenograft Model Antitumor Assays
Substances
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Enzyme Inhibitors
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Histones
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Oncogene Proteins, Fusion
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Small Molecule Libraries
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Myeloid-Lymphoid Leukemia Protein
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DOT1L protein, human
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Histone Methyltransferases
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Methyltransferases
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Histone-Lysine N-Methyltransferase
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Lysine