Reconstructing the disease model and epigenetic networks for MLL-AF4 leukemia.
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.
Zeisig
Bernd B
BB
Leukaemogenesis Team, Section of Haemato-Oncology, The Institute of Cancer Research, Sutton, Greater London, UK.
Cheung
Ngai
N
Yeung
Jenny
J
So
Chi Wai Eric
CW
D000818:Animals; D004195:Disease Models, Animal; D044127:Epigenesis, Genetic; D015973:Gene Expression Regulation, Leukemic; D011495:Histone-Lysine N-Methyltransferase; D006801:Humans; D015470:Leukemia, Myeloid, Acute / Q000235:genetics* / Q000473:pathology; D008745:Methylation; D008780:Methyltransferases / Q000037:antagonists & inhibitors / Q000502:physiology; D051788:Myeloid-Lymphoid Leukemia Protein / Q000502:physiology*; D015514:Oncogene Proteins, Fusion / Q000502:physiology*; D015452:Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / Q000235:genetics* / Q000473:pathology
C113855:MLL-AF4 fusion protein, human; D015514:Oncogene Proteins, Fusion; D051788:Myeloid-Lymphoid Leukemia Protein; C473477:DOT1L protein, human; C481527:Dot1l protein, mouse; D008780:Methyltransferases; D011495:Histone-Lysine N-Methyltransferase