Reconstructing the disease model and epigenetic networks for MLL-AF4 leukemia.

Abstract	The lack of a proper animal model has impeded understanding of the molecular mechanism of leukemia associated with the MLL-AF4 fusion. In this issue of Cancer Cell, Krivtsov et al. report a much-improved murine Mll-AF4 model and propose a molecular link with H3K79 methylation mediated by the histone methyltransferase DOT1L.
Authors	Bernd B Zeisig, Ngai Cheung, Jenny Yeung, Chi Wai Eric So
Journal	Cancer cell (Cancer Cell) Vol. 14 Issue 5 Pg. 345-7 (Nov 04 2008) ISSN: 1878-3686 [Electronic] United States
PMID	18977321 (Publication Type: Journal Article, Comment)
Chemical References	MLL-AF4 fusion protein, human Oncogene Proteins, Fusion Myeloid-Lymphoid Leukemia Protein DOT1L protein, human Dot1l protein, mouse Methyltransferases Histone-Lysine N-Methyltransferase
Topics	Animals Disease Models, Animal Epigenesis, Genetic Gene Expression Regulation, Leukemic Histone-Lysine N-Methyltransferase Humans Leukemia, Myeloid, Acute (genetics, pathology) Methylation Methyltransferases (antagonists & inhibitors, physiology) Myeloid-Lymphoid Leukemia Protein (physiology) Oncogene Proteins, Fusion (physiology) Precursor B-Cell Lymphoblastic Leukemia-Lymphoma (genetics, pathology)

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