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Severe induction of aberrant DNA methylation by nodular gastritis in adults.

Author information

Affiliations

  • 1. Division of Epigenomics, National Cancer Center Research Institute, Tokyo, Japan.
      Authors
    • Sasaki A 1, 2
    • Takeshima H 1, 5
    • Yamashita S 1
    • Takeuchi C 1, 5
    • Fukuda M 1
    • Furuichi Y 1, 5
    • Ushijima T 1, 5
    (7 authors)
  • 2. Gastroenterology Medicine Center, Shonan Kamakura General Hospital, Kanagawa, Japan.
      Authors
    • Sasaki A 1, 2
    • Ichita C 2
    • Sumida C 2
    • Koizumi K 2
    (4 authors)
  • 3. Department of General Surgery, Shonan Kamakura General Hospital, Kanagawa, Japan.
      Authors
    • Kawachi J 3
    (1 author)
  • 4. Department of Diagnostic Pathology, Shonan Kamakura General Hospital, Kanagawa, Japan.
      Authors
    • Naito W 4
    (1 author)
  • 5. Department of Epigenomics, Institute for Advanced Life Sciences, Hoshi University, Tokyo, Japan.
      Authors
    • Takeshima H 1, 5
    • Ohashi Y 5
    • Takeuchi C 1, 5
    • Furuichi Y 1, 5
    • Ushijima T 1, 5
    (5 authors)
    • Show all (11)

ORCIDs linked to this article

Journal of Gastroenterology, 19 Mar 2024, 59(6):442-456
https://doi.org/10.1007/s00535-024-02094-y PMID: 38499886 

Abstract 

Background

Nodular gastritis (NG) is characterized by marked antral lymphoid follicle formation, and is a strong risk factor for diffuse-type gastric cancer in adults. However, it is unknown whether aberrant DNA methylation, which is induced by atrophic gastritis (AG) and is a risk for gastric cancer, is induced by NG. Here, we analyzed methylation induction by NG.

Methods

Gastric mucosal samples were obtained from non-cancerous antral tissues of 16 NG and 20 AG patients with gastric cancer and 5 NG and 6 AG patients without, all age- and gender-matched. Genome-wide methylation analysis and expression analysis were conducted by a BeadChip array and RNA-sequencing, respectively.

Results

Clustering analysis of non-cancerous antral tissues of NG and AG patients with gastric cancer was conducted using methylation levels of 585 promoter CpG islands (CGIs) of methylation-resistant genes, and a large fraction of NG samples formed a cluster with strong methylation induction. Promoter CGIs of CDH1 and DAPK1 tumor-suppressor genes were more methylated in NG than in AG. Notably, methylation levels of these genes were also higher in the antrum of NG patients without cancer. Genes related to lymphoid follicle formation, such as CXCL13/CXCR5 and CXCL12/CXCR4, had higher expression in NG, and genes involved in DNA demethylation TET2 and IDH1, had only half the expression in NG.

Conclusions

Severe aberrant methylation, involving multiple tumor-suppressor genes, was induced in the gastric antrum and body of patients with NG, in accordance with their high gastric cancer risk.

Full text links 

Read article at publisher's site: https://doi.org/10.1007/s00535-024-02094-y

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Funding 

Funders who supported this work.

Japan Agency for Medical Research and Development (2)

Japan Society for the Promotion of Science (2)

Princess Takamatsu Cancer Research Fund (1)