ArticleOncogene2019
An activating mutation of the NSD2 histone methyltransferase drives oncogenic reprogramming in acute lymphocytic leukemia.
Article in Oncogene, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 59 citations in OpenAlex.
- The SETD2 L1609P mutation found in leukemia disrupts methyltransferase activity and reduces histone H3K36 trimethylation.The Journal of biological chemistry · 2026Article
- DNA methylation landscapes in human cells and their chromatin determinants.Ageing and cancer research & treatment · 2026Article
- NSD Family-Mediated H3K36 Methylation in Human Cancer: Mechanisms and Therapeutic Opportunities.Biomedicines · 2025Review
- Chromatin Regulatory Targets for Anticancer Therapeutics.Chemical reviews · 2025Review
- Identification of potential methyltransferase NSD2 enzymatic inhibitors through a multi-step structure-based drug design.Molecular diversity · 2025Article
- Polycomb repressive complex 2 (PRC2) pathway's role in cancer cell plasticity and drug resistance.Functional & integrative genomics · 2025Review
- Single-cell DNA and surface protein characterization of high hyperdiploid acute lymphoblastic leukemia at diagnosis and during treatment.HemaSphere · 2025Article
- Recruitment of FBXO22 for targeted degradation of NSD2.Nature chemical biology · 2024Article
- Intestinal NSD2 Aggravates Nonalcoholic Steatohepatitis Through Histone Modifications.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Discovery of LLC0424 as a Potent and SelectiveJournal of medicinal chemistry · 2024Article
- NSD family proteins: Rising stars as therapeutic targets.Cell insight · 2024Review
- Epigenetic profiles of elevated cell free circulating H3.1 nucleosomes as potential biomarkers for non-Hodgkin lymphoma.Scientific reports · 2023Article
- Drug Discovery Targeting Nuclear Receptor Binding SET Domain Protein 2 (NSD2).Journal of medicinal chemistry · 2023Review
- NSD2 E1099K drives relapse in pediatric acute lymphoblastic leukemia by disrupting 3D chromatin organization.Genome biology · 2023Article
- Characterizing crosstalk in epigenetic signaling to understand disease physiology.The Biochemical journal · 2023Article
- Gain-of-Function Variomics and Multi-omics Network Biology for Precision Medicine.Methods in molecular biology (Clifton, N.J.) · 2023Article
- The architecture of clonal expansions in morphologically normal tissue from cancerous and non-cancerous prostates.Molecular cancer · 2022Article
- NSD2 as a Promising Target in Hematological Disorders.International journal of molecular sciences · 2022Review
- A Selective Histone Deacetylase Inhibitor Induces Autophagy and Cell Death via SCNN1A Downregulation in Glioblastoma Cells.Cancers · 2022Article
- Evaluation of the Effects of Exposure to Power-Frequency Magnetic Fields on the Differentiation of Hematopoietic Stem/Progenitor Cells Using Human-Induced Pluripotent Stem Cells.Bioelectromagnetics · 2022Article
Corrections and comments
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Authors and funding
14 authors at 4 institutions in 1 country.
Funding
Abstract
NSD2, a histone methyltransferase specific for methylation of histone 3 lysine 36 (H3K36), exhibits a glutamic acid to lysine mutation at residue 1099 (E1099K) in childhood acute lymphocytic leukemia (ALL), and cells harboring this mutation can become the predominant clone in relapsing disease. We studied the effects of this mutant enzyme in silico, in vitro, and in vivo using gene edited cell lines. The E1099K mutation altered enzyme/substrate binding and enhanced the rate of H3K36 methylation. As a result, cell lines harboring E1099K exhibit increased H3K36 dimethylation and reduced H3K27 trimethylation, particularly on nucleosomes containing histone H3.1. Mutant NSD2 cells exhibit reduced apoptosis and enhanced proliferation, clonogenicity, adhesion, and migration. In mouse xenografts, mutant NSD2 cells are more lethal and brain invasive than wildtype cells. Transcriptional profiling demonstrates that mutant NSD2 aberrantly activates factors commonly associated with neural and stromal lineages in addition to signaling and adhesion genes. Identification of these pathways provides new avenues for therapeutic interventions in NSD2 dysregulated malignancies.
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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.