Journal
CANCER CELL
Volume 14, Issue 5, Pages 355-368Publisher
CELL PRESS
DOI: 10.1016/j.ccr.2008.10.001
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Funding
- National Cancer Institute [K08CA92551, 5U01 CA105423, 5P01CA0684841]
- Leukemia & Lymphoma Society, and the Damon Runyon Cancer Research Foundation
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We created a mouse model wherein conditional expression of an MII-AF4 fusion oncogene induces B precursor acute lymphoblastic (ALL) or acute myeloid leukemias (AML). Gene expression profile analysis of the ALL cells demonstrated significant overlap with human MLL-rearranged ALL. ChIP-chip analysis demonstrated histone H3 lysine 79 (H3K79) methylation profiles that correlated with MII-AF4-associated gene expression profiles in murine ALLs and in human MLL-rearranged leukemias. Human MLL-rearranged ALLs could be distinguished from other ALLs. by their H3K79 profiles, and suppression of the H3K79 methyltransferase DOT1L inhibited expression of critical MLL-AF4 target genes. We thus demonstrate that ectopic H3K79 methylation is a distinguishing feature of murine and human MLL-AF4 ALLs and is important for maintenance of MLL-AF4-driven gene expression.
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