ArticleCancer science2017
Degree of methylation burden is determined by the exposure period to carcinogenic factors.
Article in Cancer science, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- Gastric Cancer after <italic>Helicobacter pylori</italic> Eradication: Characteristics, Diagnosis, and Management.Digestion · 2025Review
- DNA Methylation Analysis.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Article
- Article
- TET repression and increased DNMT activity synergistically induce aberrant DNA methylation.The Journal of clinical investigation · 2020Article
- Accumulation of genetic and epigenetic alterations in normal cells and cancer risk.NPJ precision oncology · 2019Review
- Antibiotics suppress colon tumorigenesis through inhibition of aberrant DNA methylation in an azoxymethane and dextran sulfate sodium colitis model.Cancer science · 2019Article
- Novel epigenetic markers for gastric cancer risk stratification in individuals after Helicobacter pylori eradication.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2018Article
- Genetic and epigenetic alterations in normal tissues have differential impacts on cancer risk among tissues.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Degree of methylation burden is determined by the exposure period to carcinogenic factors.Cancer science · 2017Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aberrant DNA methylation accumulated in normal tissues, namely methylation burden, is associated with risk of carcinogenesis. The levels of methylation burden are known to be influenced by multiple factors, such as genetic factors and strengths of carcinogenic factors. However, the impact of the degree of exposure to a carcinogenic factor is still unclear. Here, using a Mongolian gerbil model of Helicobacter pylori (H. pylori)-induced gastritis, we aimed to clarify the impact of the degree of exposure on methylation burden in normal gastric tissues. DNA methylation levels of four CpG islands, HE6, SA9, SB5, and SD2, increased by H. pylori infection, depending upon the infection period. After eradication of H. pylori, DNA methylation levels decreased, but tended to be higher in gastric mucosae with a longer infection period. DNA molecules with dense methylation, but not those with sparse methylation, increased depending upon the infection period. DNA methylation levels of one of the four CpG islands, SA9, tended to be higher in gastric mucosae of gerbils infected with H. pylori, even 50 weeks after eradication than in those of non-infected gerbils. These results showed for the first time that the levels of methylation burden in normal tissues are influenced by the degree of exposure to a carcinogenic factor.
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