ArticleCancer cell2011
MLL-rearranged leukemia is dependent on aberrant H3K79 methylation by DOT1L.
Article in Cancer cell, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 546 papers.
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Who cites it
546 citing papers in PubMed, 888 citations in OpenAlex.
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- Detection of MEN1 resistance mutations in cell-free DNA from acute leukemia patients treated with menin inhibitors.Blood cancer journal · 2026Article
- PAF1C restores transcription after DNA damage independently of promoting histone mark deposition.EMBO reports · 2026Article
- A Perturb-seq map of a differentiation hub reveals synergistic vulnerabilities in KMT2A-rearranged acute myeloid leukemia.Leukemia · 2026Article
- The hidden regulators: Non-coding RNAs in KMT2A-rearranged acute lymphoblastic leukemia.International journal of cancer · 2026Review
- Current perspectives on KMT2A fusion proteins and menin inhibition in paediatric acute myeloid leukaemia.The FEBS journal · 2026Review
- Multiomic analysis of clonal development reveals new regulators of leukemic cell growth.Genes & development · 2026Article
- PICALM::MLLT10 translocated leukemia.FEBS letters · 2026Review
- RBM15B recognizes H3K79me2 to guide selective mThe EMBO journal · 2026Article
- chromIDEAS reveals epigenetic dynamics via multi-dimensional clustering of chromatin states.Nucleic acids research · 2026Article
- SKIDA1 sustains MLL::ENL-expressing hematopoietic progenitors during neonatal stages and promotes B-lineage priming.Blood neoplasia · 2026Article
486 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 4 institutions in 2 countries.
Funding
Abstract
The histone 3 lysine 79 (H3K79) methyltransferase Dot1l has been implicated in the development of leukemias bearing translocations of the Mixed Lineage Leukemia (MLL) gene. We identified the MLL-fusion targets in an MLL-AF9 leukemia model, and conducted epigenetic profiling for H3K79me2, H3K4me3, H3K27me3, and H3K36me3 in hematopoietic progenitor and leukemia stem cells (LSCs). We found abnormal profiles only for H3K79me2 on MLL-AF9 fusion target loci in LSCs. Inactivation of Dot1l led to downregulation of direct MLL-AF9 targets and an MLL translocation-associated gene expression signature, whereas global gene expression remained largely unaffected. Suppression of MLL translocation-associated gene expression corresponded with dependence of MLL-AF9 leukemia on Dot1l in vivo. These data point to DOT1L as a potential therapeutic target in MLL-rearranged leukemia.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.