Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

DOT1L as a therapeutic target for the treatment of DNMT3A-mutant acute myeloid leukemia.

Blood - 18 Aug 2016

Rau Rachel E, Rodriguez Benjamin A, Luo Min, Jeong Mira, Rosen Allison, Rogers Jason H, Campbell Carly T, Daigle Scott R, Deng Lishing, Song Yongcheng, Sweet Steve, Chevassut Timothy, Andreeff Michael, Kornblau Steven M, Li Wei, Goodell Margaret A

Abstract excerpt

Mutations in DNA methyltransferase 3A (DNMT3A) are common in acute myeloid leukemia and portend a poor prognosis; thus, new therapeutic strategies are needed. The likely mechanism by which DNMT3A loss contributes to leukemogenesis is altered DNA methylation and the attendant gene expression changes; however, our current understanding is incomplete. We observed that murine hematopoietic stem cells (HSCs) in which...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Adenosine
Share to Cell Cycle Checkpoints

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to DNA (Cytosine-5-)-Methyltransferases

Share to DNA Methyltransferase 3A

Share to Gene Expression Regulation, Leukemic

Share to Histone-Lysine N-Methyltransferase

Share to Phenylurea Compounds

Share to Tumor Stem Cell Assay

Source

Open in PubMed Open full text

Identifiers

PMID: 27335278
DOI: 10.1182/blood-2015-11-684225
PMCID: PMC4990856

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

DOT1L as a therapeutic target for the treatment of DNMT3A-mutant acute myeloid leukemia.PMID 27335278Read ↗

MLL partial tandem duplication leukemia cells are sensitive to small molecule DOT1L inhibitionSemantic proximity Read ↗

Histone H3 Lysine 79 Methyltransferase Dot1 Is Required for Immortalization by MLL OncogenesSemantic proximity Read ↗

Potent inhibition of DOT1L as treatment of MLL-fusion leukemiaSemantic proximity Read ↗

DOT1L Inhibition Sensitizes MLL-Rearranged AML to ChemotherapySemantic proximity Read ↗

The histone H3K79 methyltransferase Dot1L is essential for mammalian development and heterochromatin structure.Semantic proximity Read ↗

DNMT3A Haploinsufficiency Transforms FLT3ITD Myeloproliferative Disease into a Rapid, Spontaneous, and Fully Penetrant Acute Myeloid Leukemia.Semantic proximity Read ↗

hDOT1L Links Histone Methylation to LeukemogenesisSemantic proximity Read ↗

Leukemic transformation by the MLL-AF6 fusion oncogene requires the H3K79 methyltransferase Dot1lSemantic proximity Read ↗

Requirement for Dot1l in murine postnatal hematopoiesis and leukemogenesis by MLL translocationSemantic proximity Read ↗

DOT1L inhibits SIRT1-mediated epigenetic silencing to maintain leukemic gene expression in MLL-rearranged leukemia.Semantic proximity Read ↗

Early mammalian erythropoiesis requires the Dot1L methyltransferase.Semantic proximity Read ↗

Targeting histone methyltransferase and demethylase in acute myeloid leukemia therapySemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.