ReviewImmunological reviews2015
TET proteins and 5-methylcytosine oxidation in hematological cancers.
Review in Immunological reviews, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 143 papers, 2 of them syntheses that pooled it.
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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
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Who cites it
143 citing papers in PubMed, 2 syntheses or guidelines pooled it, 196 citations in OpenAlex.
- Non-oncologic to oncologic drug: A systematic review of drug repurposing in cancer.Cancer chemotherapy and pharmacology · 2025Pooled it
- Pooled it
- Tumor cell-intrinsic TET3 restrains type I interferon signaling and anti-tumor immunity.Science China. Life sciences · 2026Article
- Regulatory function of ten‑eleven translocation‑2 in transcriptional mechanisms of demethylated myeloma cells.Molecular medicine reports · 2026Article
- TET Enzymes as Epigenetic Integrators in Intestinal Immunity, Inflammation, and Disease.Journal of personalized medicine · 2026Review
- Mammalian Proteome Profiling Reveals Readers and Antireaders of Strand-Symmetric and -Asymmetric 5-Hydroxymethylcytosine-Modifications in DNA.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The role of epigenetic modifications in hematological cancers.Frontiers in oncology · 2026Review
- Curcuminoids Activate TET Enzymes and Increase DNA Hydroxymethylation and Active Demethylation in Leukemia Cells.International journal of molecular sciences · 2025Article
- Loss of TET2 activity limits the ability of vitamin C to activate DNA demethylation in human HAP1 cells.Epigenetics & chromatin · 2025Article
- Retinoic acid and ascorbate synergize to suppress myeloid leukemia via TET2 activation.Cell reports · 2025Article
- Uncommon Evolution From Acute Myeloid Leukaemia toEJHaem · 2025Article
- TP53 and CDKN2A alterations define a poor prognostic subgroup in patients with nodal T follicular helper cell lymphoma.Leukemia · 2025Article
- Ten-Eleven Translocation Family Proteins: Structure, Biological Functions, Diseases, and Targeted Therapy.MedComm · 2025Review
- Neomorphic leukemia-derived mutations in the TET2 enzyme induce genome instability via a substrate shift from 5-methylcytosine to thymine.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Concomitant loss of TET2 and TET3 results in T cell expansion and genomic instability in mice.Communications biology · 2024Article
- IncreasedPharmaceuticals (Basel, Switzerland) · 2024Article
- The Role of DNMT Methyltransferases and TET Dioxygenases in the Maintenance of the DNA Methylation Level.Biomolecules · 2024Review
- Ultrasensitive detection of 5-hydroxymethylcytosine in genomic DNA using a graphene-based sensor modified with biotin and gold nanoparticles.Materials today. Bio · 2024Article
- TET proteins regulate Drosha expression and impact microRNAs in iNKT cells.bioRxiv : the preprint server for biology · 2024Article
- Article
83 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
6 authors at 4 institutions in 2 countries.
Funding
Abstract
DNA methylation has pivotal regulatory roles in mammalian development, retrotransposon silencing, genomic imprinting, and X-chromosome inactivation. Cancer cells display highly dysregulated DNA methylation profiles characterized by global hypomethylation in conjunction with hypermethylation of promoter CpG islands that presumably lead to genome instability and aberrant expression of tumor suppressor genes or oncogenes. The recent discovery of ten-eleven-translocation (TET) family dioxygenases that oxidize 5mC to 5-hydroxymethylcytosine (5hmC), 5-formylcytosine (5fC), and 5-carboxylcytosine (5caC) in DNA has led to profound progress in understanding the mechanism underlying DNA demethylation. Among the three TET genes, TET2 recurrently undergoes inactivating mutations in a wide range of myeloid and lymphoid malignancies. TET2 functions as a bona fide tumor suppressor particularly in the pathogenesis of myeloid malignancies resembling chronic myelomonocytic leukemia (CMML) and myelodysplastic syndromes (MDS) in human. Here we review diverse functions of TET proteins and the novel epigenetic marks that they generate in DNA methylation/demethylation dynamics and normal and malignant hematopoietic differentiation. The impact of TET2 inactivation in hematopoiesis and various mechanisms modulating the expression or activity of TET proteins are also discussed. Furthermore, we also present evidence that TET2 and TET3 collaborate to suppress aberrant hematopoiesis and hematopoietic transformation. A detailed understanding of the normal and pathological functions of TET proteins may provide new avenues to develop novel epigenetic therapies for treating hematological malignancies.
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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.