ArticleBritish journal of cancer2017
Oxidative DNA damage induces hypomethylation in a compromised base excision repair colorectal tumourigenesis.
Article in British journal of cancer, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 25 citations in OpenAlex.
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- 8-Oxoguanine: A Lesion, an Epigenetic Mark, or a Molecular Signal?International journal of molecular sciences · 2025Review
- Inhibition of the LINE1-derivedMolecular therapy. Nucleic acids · 2025Article
- Reversal of perturbed DNA damage response and HIV latency by a histone methyltransferase inhibitor in virally suppressed individuals living with HIV.Frontiers in aging · 2025Article
- The role of SOD2 and NOS2 genes in the molecular aspect of bladder cancer pathophysiology.Scientific reports · 2023Article
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- Differential DNA methylation analysis ofWorld journal of gastroenterology · 2022Article
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- Global DNA hypomethylation of Alu and LINE-1 transposable elements as an epigenetic biomarker of anti-tuberculosis drug-induced liver injury.Emerging microbes & infections · 2021Article
- Evaluation of global and intragenic hypomethylation in colorectal adenomas improves patient stratification and colorectal cancer risk prediction.Clinical epigenetics · 2021Article
- The Interplay between Oxidative Stress, Inflammation and Angiogenesis in Bladder Cancer Development.International journal of molecular sciences · 2021Review
- The effects of flavonoids, green tea polyphenols and coffee on DMBA induced LINE-1 DNA hypomethylation.PloS one · 2021Article
- Current updates on the role of reactive oxygen species in bladder cancer pathogenesis and therapeutics.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2020Review
- Hypomethylation of LINE-1 repeat elements and global loss of DNA hydroxymethylation in vapers and smokers.Epigenetics · 2020Article
- Oxidative Damage in Sporadic Colorectal Cancer: Molecular Mapping of Base Excision Repair Glycosylases in Colorectal Cancer Patients.International journal of molecular sciences · 2020Review
- Epigenetic profiling of MUTYH, KLF6, WNT1 and KLF4 genes in carcinogenesis and tumorigenesis of colorectal cancer.BioMedicine · 2019Article
- When you're strange: Unusual features of the MUTYH glycosylase and implications in cancer.DNA repair · 2019Review
- The construction of intrahepatic cholangiocarcinoma model in zebrafish.Scientific reports · 2017Article
- Relationships among smoking, oxidative stress, inflammation, macromolecular damage, and cancer.Mutation research. Reviews in mutation researchReview
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundA compromised base excision repair (BER) promotes carcinogenesis by accumulating oxidative DNA-damaged products as observed in MUTYH-associated polyposis, a hereditary colorectal cancer syndrome marked by adenomas and cancers with an accumulation of 8-oxoguanine. Remarkably, DNA global demethylation has been shown to be mediated by BER, suggesting a relevant interplay with early colorectal tumourigenesis. To check this hypothesis, we investigated a cohort of 49 adenomas and 10 carcinomas, derived from 17 MUTYH-associated polyposis patients; as adenoma controls, we used a set of 36 familial adenomatous polyposis and 24 sporadic polyps.
methodsSamples were analysed for their mutational and epigenetic status, measured as global LINE-1 (long interspersed nuclear element) and gene-specific LINE-1 MET methylation by mass spectrometry and pyrosequencing.
resultsMUTYH-associated polyposis adenomas were strikingly more hypomethylated than familial adenomatous and sporadic polyps for both DNA demethylation markers (P=0.032 and P=0.007 for LINE-1; P=0.004 and P<0.0001 for LINE-1 MET, respectively) with levels comparable to those of the carcinomas derived from the same patients. They also had mutations due mainly to KRAS/NRAS p.G12C, which was absent in the controls (P<0.0001 for both sets).
conclusionsOur results show that DNA demethylation, together with specific KRAS/NRAS mutations, drives the early steps of oxidative damage colorectal tumourigenesis.
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