Evidence map›Paper›PMID 19568874›Full record

ArticleEnvironmental health and preventive medicine2008

DNA methylation: a marker for carcinogen exposure and cancer risk.

Takeshi Nakajima, Shotaro Enomoto, Toshikazu Ushijima

Open access · bronzeAbstract read
In one paragraph

Article in Environmental health and preventive medicine, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
0.8field-weighted citation impact, top 30% 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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. PMEnvironmental health and preventive medicine · 2020
    Article
  5. Review
  6. Gut and liver · 2016
    Article
  7. Methylation status of theOncology letters · 2016
    Article
  8. Article
  9. Article
  10. Article
  11. Epigenetic alterations in gastric cancer (Review).Molecular medicine reports · 2015
    Review
  12. Review
  13. Elevated risk of recurrent colorectal neoplasia withMolecular and clinical oncology · 2013
    Article
  14. Environmental toxicants, epigenetics, and cancer.Advances in experimental medicine and biology · 2013
    Review
  15. Characterization of DNA hypermethylation in two cases of peritoneal mesothelioma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2012
    Article
  16. Article
  17. Article
  18. Article
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 2 institutions in 1 country.

Takeshi NakajimaCarcinogenesis Division, National Cancer Center Research Institute, 5-1-1 Tsukiji, Chuo-ku, Tokyo, 104-0045, Japan.
Shotaro Enomoto
Toshikazu Ushijima
Genesis Research Institute · JPNational Cancer Center Hospital East · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancers arise as a consequence of multiple genetic and epigenetic alterations. Many genes aberrantly methylated in cancers have been identified in recent years, and their use in cancer diagnosis and therapy is currently under investigation. During our genome-wide screening for a novel tumor-suppressor gene in gastric cancers, we found that only a small amount of aberrant methylation was present, even in non-cancerous gastric mucosae. A subsequent large-scale analysis of the gastric mucosae of healthy individuals and gastric cancer patients using quantitative methylation-specific PCR (qMSP) revealed that Helicobacter pylori infection potently induced aberrant DNA methylation in non-cancerous gastric mucosae and that these high methylation levels can decrease following cessation of the H. pylori infection. Helicobacter pylori infection induced the methylation of specific genes among 48 genes that can be methylated in gastric cancer cell lines. Most importantly, the methylation levels in the gastric mucosae of individuals without H. pylori infection correlated with their risk of gastric cancer. These findings show that a field for cancerization is formed by H. pylori infection and that this field can be measured using DNA methylation as a marker. The concept of an "epigenetic field for cancerization" has been also demonstrated for colon and breast cancers, and it is possibly present for other cancers and other diseases. Applied knowledge of epigenetic changes in human diseases has now started to make an impact on the prevention, diagnostics, and therapeutics of these diseases.

Identifiers

PMID19568874
PMCPMC2698244
OpenAlexW1986736445

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.