ArticleCell reports2016
Promoter Hypomethylation and Expression Is Conserved in Mouse Chronic Lymphocytic Leukemia Induced by Decreased or Inactivated Dnmt3a.
Article in Cell reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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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
24 citing papers in PubMed, 35 citations in OpenAlex.
- Genome-Wide Methylation Profiling of Peripheral T-Cell Lymphomas Identifies TRIP13 as a Critical Driver of Tumor Proliferation and Survival.Epigenomes · 2024Article
- Genome-wide methylation profiling of Peripheral T-cell lymphomas identifies TRIP13 as a critical driver of tumor proliferation and survival.Research square · 2024Article
- Epigenetic regulation in hematopoiesis and its implications in the targeted therapy of hematologic malignancies.Signal transduction and targeted therapy · 2023Review
- Multiple Mechanisms of NOTCH1 Activation in Chronic Lymphocytic Leukemia: NOTCH1 Mutations and Beyond.Cancers · 2022Review
- Chinese Medicine Regulates DNA Methylation to Treat Haematological Malignancies: A New Paradigm of "State-Target Medicine".Chinese journal of integrative medicine · 2022Article
- Radiation therapy induces immunosenescence mediated by p90RSK.Frontiers in cardiovascular medicine · 2022Article
- Review
- Activation ofCancer research · 2021Article
- Functional and epigenetic phenotypes of humans and mice with DNMT3A Overgrowth Syndrome.Nature communications · 2021Article
- B1a and B2 cells are characterized by distinct CpG modification states at DNMT3A-maintained enhancers.Nature communications · 2021Article
- DNA Methyltransferases in Cancer: Biology, Paradox, Aberrations, and Targeted Therapy.Cancers · 2020Review
- DNA Methylation Associated With Diabetic Kidney Disease in Blood-Derived DNA.Frontiers in cell and developmental biology · 2020Article
- Catalytically inactive Dnmt3b rescues mouse embryonic development by accessory and repressive functions.Nature communications · 2019Article
- Article
- Genome-wide DNA methylation patterns of bovine blastocysts derived from in vivo embryos subjected to in vitro culture before, during or after embryonic genome activation.BMC genomics · 2018Article
- B-cell tumor development inBlood advances · 2018Article
- Base-Resolution Analysis of DNA Methylation Patterns Downstream ofG3 (Bethesda, Md.) · 2018Article
- Mature lymphoid malignancies: origin, stem cells, and chronicity.Blood advances · 2017Review
- Haploinsufficiency for DNA methyltransferase 3A predisposes hematopoietic cells to myeloid malignancies.The Journal of clinical investigation · 2017Article
- Epigenetic restriction of extraembryonic lineages mirrors the somatic transition to cancer.Nature · 2017Article
Corrections and comments
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Authors and funding
15 authors at 3 institutions in 1 country.
Funding
Abstract
DNA methyltransferase 3a (DNMT3A) catalyzes the formation of 5-methyl-cytosine in mammalian genomic DNA, and it is frequently mutated in human hematologic malignancies. Bi-allelic loss of Dnmt3a in mice results in leukemia and lymphoma, including chronic lymphocytic leukemia (CLL). Here, we investigate whether mono-allelic loss of Dnmt3a is sufficient to induce disease. We show that, by 16 months of age, 65% of Dnmt3a(+/-) mice develop a CLL-like disease, and 15% of mice develop non-malignant myeloproliferation. Genome-wide methylation analysis reveals that reduced Dnmt3a levels induce promoter hypomethylation at similar loci in Dnmt3a(+/-) and Dnmt3a(Δ/Δ) CLL, suggesting that promoters are particularly sensitive to Dnmt3a levels. Gene expression analysis identified 26 hypomethylated and overexpressed genes common to both Dnmt3a(+/-) and Dnmt3a(Δ/Δ) CLL as putative oncogenic drivers. Our data provide evidence that Dnmt3a is a haplo-insufficient tumor suppressor in CLL and highlights the importance of deregulated molecular events in disease pathogenesis.
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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.