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

Cancer Cell. 2008 Nov 4;14(5):345-7. doi: 10.1016/j.ccr.2008.10.008.

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.

Publication types

  • Kommentar

MeSH terms

  • Animals
  • Disease Models, Animal*
  • Epigenesis, Genetic
  • Gene Expression Regulation, Leukemic*
  • Histone-Lysine N-Methyltransferase
  • Humans
  • Leukemia, Myeloid, Acute / genetics*
  • Leukemia, Myeloid, Acute / pathology
  • Methylation*
  • Methyltransferases / antagonists & inhibitors
  • Methyltransferases / physiology
  • Myeloid-Lymphoid Leukemia Protein / physiology*
  • Oncogene Proteins, Fusion / physiology*
  • Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics*
  • Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / pathology

Substances

  • MLL-AF4 fusion protein, human
  • Oncogene Proteins, Fusion
  • Myeloid-Lymphoid Leukemia Protein
  • DOT1L protein, human
  • Dot1l protein, mouse
  • Methyltransferases
  • Histone-Lysine N-Methyltransferase