ArticleCancer prevention research (Philadelphia, Pa.)2016
DNA Hypomethylation Contributes to Genomic Instability and Intestinal Cancer Initiation.
Article in Cancer prevention research (Philadelphia, Pa.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.
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81 citing papers in PubMed, 153 citations in OpenAlex.
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- The Future of Epigenetics: Emerging Technologies and Clinical Applications.ACS pharmacology & translational science · 2026Review
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- The expanding roles of homologous recombination proteins in genome stability.The EMBO journal · 2026Review
- CMAtlas: a comprehensive DNA methylation atlas for exploring epigenetic alterations in 34 human cancer types.Bioinformatics (Oxford, England) · 2026Article
- Genomic innovations in cancer prevention, diagnosis, prognosis and precision therapeutics.Frontiers in genetics · 2026Review
- Molecular mechanisms of air pollution-induced carcinogenesis and the emerging role of microplastics.Human genomics · 2025Review
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- Long interspersed nuclear element 1 methylation in non-small cell lung cancer: implications for diagnosis, prognosis, and therapeutic targeting.Cell communication and signaling : CCS · 2025Review
- Induction of DNA Demethylation: Strategies and Consequences.Epigenomes · 2025Review
- The relationship between epigenetic biomarkers and the risk of diabetes and cancer: a machine learning modeling approach.Frontiers in public health · 2025Article
- Methylation profiling in neuropathological tumors diagnosis: a comprehensive review.Frontiers in oncology · 2025Review
- A subset of Polycomb-targeted transcription factor genes become hypermethylated yet upregulated in colorectal cancer.Computational and structural biotechnology journal · 2025Article
- Article
- DNMT1 prolonged absence is a tunable cellular stress that triggers cell proliferation arrest to protect from major DNA methylation loss.Cellular and molecular life sciences : CMLS · 2024Article
- Interplay between epigenetics, senescence and cellular redox metabolism in cancer and its therapeutic implications.Redox biology · 2024Review
- How calorie restriction slows aging: an epigenetic perspective.Journal of molecular medicine (Berlin, Germany) · 2024Review
21 more citing papers are in PubMed but not listed here.
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3 authors at 1 institution in 1 country.
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Abstract
Intestinal cancer is a heterogeneous disease driven by genetic mutations and epigenetic changes. Approximately 80% of sporadic colorectal cancers are initiated by mutation and inactivation of the adenomatous polyposis coli (APC) gene, which results in unrestrained intestinal epithelial growth and formation of adenomas. Aberrant DNA methylation promotes cancer progression by the inactivation of tumor suppressor genes via promoter methylation. In addition, global DNA hypomethylation is often seen before the formation of adenomas, suggesting that it contributes to neoplastic transformation. Previous studies employed mice with a hypomorphic mutation in DNA methyltransferase 1 (Dnmt1), which exhibited constitutive global DNA hypomethylation and decreased tumorigenesis in the Apc(Min/+) mouse model of intestinal cancer. However, the consequences of intestinal epithelial-specific acute hypomethylation during Apc(Min/+) tumor initiation have not been reported. Using temporally controlled intestinal epithelial-specific gene ablation, we show that total loss of Dnmt1 in the Apc(Min/+) mouse model of intestinal cancer causes accelerated adenoma initiation. Deletion of Dnmt1 precipitates an acute response characterized by hypomethylation of repetitive elements and genomic instability, which surprisingly is followed by remethylation with time. Two months post-Dnmt1 ablation, mice display increased macroadenoma load, consistent with a role for Dnmt1 and DNA methylation in maintaining genomic stability. These data suggest that DNA hypomethylation plays a previously unappreciated role in intestinal adenoma initiation. Cancer Prev Res; 9(7); 534-46. ©2016 AACRSee related article by Lee and Laird, p. 509.
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