ArticleCancer cell2014
AF10 regulates progressive H3K79 methylation and HOX gene expression in diverse AML subtypes.
Article in Cancer cell, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 127 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
127 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Nucleosome Turnover Regulates Histone Methylation Patterns over the Genome.Molecular cell · 2019Pooled it
- Article
- PICALM::MLLT10 translocated leukemia.FEBS letters · 2026Review
- RBM15B recognizes H3K79me2 to guide selective mThe EMBO journal · 2026Article
- Ketogenic diet dampens excitatory neurotransmission by shrinking synaptic vesicle pools.Cell reports · 2026Article
- DOT1L provides transcriptional memory through PRC1.1 antagonism.Nature cell biology · 2026Article
- Targeting the Menin-KMT2A interaction in leukemia: Lessons learned and future directions.International journal of cancer · 2026Review
- Dysregulation of HOXA genes in acute myeloid leukemia and targeted therapy.NPJ precision oncology · 2025Review
- Histone modifications in the regulation of erythropoiesis.Annals of medicine · 2025Review
- Cystathionine γ-lyase downregulation promotes liver injury and necroptosis through reprogramming of methionine cycle.Redox report : communications in free radical research · 2025Article
- DOT1L as a Therapeutic Target: Insights into Epigenetic Regulation and Cancer Treatment.Biomolecules & therapeutics · 2025Review
- Chromatin Regulatory Targets for Anticancer Therapeutics.Chemical reviews · 2025Review
- Loss of DOT1L disrupts neuronal transcription, behavior, and leads to a neurodevelopmental disorder.medRxiv : the preprint server for health sciences · 2025Article
- Targeting chromatin modifying complexes in acute myeloid leukemia.Stem cells translational medicine · 2025Review
- NUP98 fusion proteins and KMT2A-MENIN antagonize PRC1.1 to drive gene expression in AML.Cell reports · 2024Article
- Chromatin structure in totipotent mouse early preimplantation embryos.The Journal of reproduction and development · 2024Review
- Structural variants involving MLLT10 fusion are associated with adverse outcomes in pediatric acute myeloid leukemia.Blood advances · 2024Article
- Venetoclax Combination Treatment of Acute Myeloid Leukemia in Adolescents and Young Adult Patients.Journal of clinical medicine · 2024Review
- Article
- The histone methyltransferase DOT1B is dispensable for stage differentiation and macrophage infection ofFrontiers in cellular and infection microbiology · 2024Article
67 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
- Commented on by
Authors and funding
20 authors.
Funding
Abstract
Homeotic (HOX) genes are dysregulated in multiple malignancies, including several AML subtypes. We demonstrate that H3K79 dimethylation (H3K79me2) is converted to monomethylation (H3K79me1) at HOX loci as hematopoietic cells mature, thus coinciding with a decrease in HOX gene expression. We show that H3K79 methyltransferase activity as well as H3K79me1-to-H3K79me2 conversion is regulated by the DOT1L cofactor AF10. AF10 inactivation reverses leukemia-associated epigenetic profiles, precludes abnormal HOXA gene expression, and impairs the transforming ability of MLL-AF9, MLL-AF6, and NUP98-NSD1 fusions-mechanistically distinct HOX-activating oncogenes. Furthermore, NUP98-NSD1-transformed cells are sensitive to small-molecule inhibition of DOT1L. Our findings demonstrate that pharmacological inhibition of the DOT1L/AF10 complex may provide therapeutic benefits in an array of malignancies with abnormal HOXA gene expression.
Indexed as
Identifiers
What OpenQuestion holds
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.