ArticleGenes & development2007
Dnmt3b promotes tumorigenesis in vivo by gene-specific de novo methylation and transcriptional silencing.
Article in Genes & development, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 150 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
150 citing papers in PubMed, 1 synthesis or guideline pooled it, 271 citations in OpenAlex.
- APC hypermethylation for early diagnosis of colorectal cancer: a meta-analysis and literature review.Oncotarget · 2017Pooled it
- DNMT1 loss leads to hypermethylation of a subset of late replicating domains by DNMT3A.PLoS genetics · 2026Article
- GABAAnnals of medicine · 2025Article
- Iron homeostasis and cell clonality drive cancer-associated intestinal DNA methylation drift in aging.Nature aging · 2025Article
- Integrating cell-free DNA methylation of SEPT9 and SFRP2 into a machine learning model for early diagnosis of HCC.Biomarkers in medicine · 2025Article
- In Vivo Reprogramming Highlights Epigenetic Regulation That Shapes Cancer Hallmarks.Cancer science · 2025Review
- A versatile in vivo platform for reversible control of transgene expression in adult tissues.Stem cell reports · 2025Article
- DNA methylation in mammalian development and disease.Nature reviews. Genetics · 2025Review
- The epigenetic landscape in intestinal stem cells and its deregulation in colorectal cancer.Stem cells (Dayton, Ohio) · 2024Review
- Epigallocatechin-3-Gallate Therapeutic Potential in Cancer: Mechanism of Action and Clinical Implications.Molecules (Basel, Switzerland) · 2023Review
- Pivotal role for S-nitrosylation of DNA methyltransferase 3B in epigenetic regulation of tumorigenesis.Nature communications · 2023Article
- DNMT3B overexpression downregulates genes with CpG islands, common motifs, and transcription factor binding sites that interact with DNMT3B.Scientific reports · 2022Article
- Dedifferentiation andMolecular medicine reports · 2022Review
- DNA Methyltransferase 3B-Mediated Intratumoral Heterogeneity and Therapeutic Targeting in Breast Cancer Recurrence and Metastasis.Molecular cancer research : MCR · 2022Article
- Article
- Review
- DNA Methyltransferase 3A Is Involved in the Sustained Effects of Chronic Stress on Synaptic Functions and Behaviors.Cerebral cortex (New York, N.Y. : 1991) · 2021Article
- Requirement of DNMT1 to orchestrate epigenomic reprogramming for NPM-ALK-driven lymphomagenesis.Life science alliance · 2021Article
- DNA methylation inhibitors: Retrospective and perspective view.Advances in cancer research · 2021Article
- Bacteria-related changes in host DNA methylation and the risk for CRC.Gut microbes · 2020Review
90 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
12 authors at 5 institutions in 2 countries.
Funding
Abstract
Increased methylation of CpG islands and silencing of affected target genes is frequently found in human cancer; however, in vivo the question of causality has only been addressed by loss-of-function studies. To directly evaluate the role and mechanism of de novo methylation in tumor development, we overexpressed the de novo DNA methyltransferases Dnmt3a1 and Dnmt3b1 in Apc Min/+ mice. We found that Dnmt3b1 enhanced the number of colon tumors in Apc Min/+ mice approximately twofold and increased the average size of colonic microadenomas, whereas Dnmt3a1 had no effect. The overexpression of Dnmt3b1 caused loss of imprinting and increased expression of Igf2 as well as methylation and transcriptional silencing of the tumor suppressor genes Sfrp2, Sfrp4, and Sfrp5. Importantly, we found that Dnmt3b1 but not Dnmt3a1 efficiently methylates the same set of genes in tumors and in nontumor tissues, demonstrating that de novo methyltransferases can initiate methylation and silencing of specific genes in phenotypically normal cells. This suggests that DNA methylation patterns in cancer are the result of specific targeting of at least some tumor suppressor genes rather than of random, stochastic methylation followed by clonal selection due to a proliferative advantage caused by tumor suppressor gene silencing.
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.