Evidence map›Paper›PMID 27718135›Full record

ReviewGastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association2017

Mechanisms for the induction of gastric cancer by Helicobacter pylori infection: aberrant DNA methylation pathway.

Masahiro Maeda, Hiroshi Moro, Toshikazu Ushijima

Open access · bronzeAbstract readReview
PubMed Publisher
In one paragraph

Review in Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed, 2 pooled it
9.4field-weighted citation impact, top 2% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

73 citing papers in PubMed, 2 syntheses or guidelines pooled it, 140 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Genes · 2026
    Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. Review
  11. Concurrent hypermethylation of CpG islands and hypomethylation of CpG-poor regions are associated with gastric cancer risk after Helicobacter pylori eradication.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2025
    Article
  12. Review
  13. World journal of gastrointestinal oncology · 2025
    Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. Environmental factors in gastric carcinogenesis and preventive intervention strategies.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2025
    Review
  20. Review

13 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 3 institutions in 2 countries.

Masahiro MaedaDivision of Epigenomics, National Cancer Center Research Institute, Tokyo, Japan.
Hiroshi MoroDivision of Epigenomics, National Cancer Center Research Institute, Tokyo, Japan.
Toshikazu UshijimaDivision of Epigenomics, National Cancer Center Research Institute, Tokyo, Japan. tushijim@ncc.go.jp.
Epigenomics (Germany) · DEKyoto University · JPTokyo National Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multiple pathogenic mechanisms by which Helicobacter pylori infection induces gastric cancer have been established in the last two decades. In particular, aberrant DNA methylation is induced in multiple driver genes, which inactivates them. Methylation profiles in gastric cancer are associated with specific subtypes, such as microsatellite instability. Recent comprehensive and integrated analyses showed that many cancer-related pathways are more frequently altered by aberrant DNA methylation than by mutations. Aberrant DNA methylation can even be present in noncancerous gastric mucosae, producing an "epigenetic field for cancerization." Mechanistically, H. pylori-induced chronic inflammation, but not H. pylori itself, plays a direct role in the induction of aberrant DNA methylation. The expression of three inflammation-related genes, Il1b, Nos2, and Tnf, is highly associated with the induction of aberrant DNA methylation. Importantly, the degree of accumulated aberrant DNA methylation is strongly correlated with gastric cancer risk. A recent multicenter prospective cohort study demonstrated the utility of epigenetic cancer risk diagnosis for metachronous gastric cancer. Suppression of aberrant DNA methylation by a demethylating agent was shown to inhibit gastric cancer development in an animal model. Induction of aberrant DNA methylation is the major pathway by which H. pylori infection induces gastric cancer, and this can be utilized for translational opportunities.

Indexed as

DNA MethylationEpigenesis, GeneticGastric MucosaHelicobacter InfectionsHelicobacter pyloriHumansStomach NeoplasmsAberrant DNA methylationEpigenetic cancer risk diagnosisHelicobacter pylori infection

Identifiers

PMID27718135
OpenAlexW2528940457

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.