Evidence map›Paper›PMID 31290583›Full record

ArticlePathology international2019

Barretts's carcinogenesis.

Ken-Ichi Mukaisho, Shunpei Kanai, Ryoji Kushima, Takahisa Nakayama, Takanori Hattori, Hiroyuki Sugihara

Abstract read
In one paragraph

Article in Pathology international, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

17 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Trial
  3. How to Define the Gastroesophageal Junction.Digestive endoscopy : official journal of the Japan Gastroenterological Endoscopy Society · 2026
    Review
  4. Expression of therapy target molecules in esophagogastric junction and Barrett's adenocarcinoma.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2025
    Article
  5. Article
  6. Review
  7. Article
  8. Trefoil factor 1 inhibits the development of esophageal adenocarcinoma from Barrett's epithelium.Laboratory investigation; a journal of technical methods and pathology · 2022
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Inflammation-Induced Tumorigenesis and Metastasis.International journal of molecular sciences · 2021
    Review
  15. Article
  16. Review
  17. Review
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

6 authors.

Ken-Ichi MukaishoDivision of Molecular and Diagnostic Pathology, Department of Pathology, Shiga University of Medical Science, Otsu, Japan.
Shunpei KanaiDivision of Molecular and Diagnostic Pathology, Department of Pathology, Shiga University of Medical Science, Otsu, Japan.
Ryoji KushimaDivision of Diagnostic Pathology, Shiga University of Medical Science Hospital, Otsu, Japan.
Takahisa NakayamaDivision of Molecular and Diagnostic Pathology, Department of Pathology, Shiga University of Medical Science, Otsu, Japan.
Takanori HattoriDivision of Molecular and Diagnostic Pathology, Department of Pathology, Shiga University of Medical Science, Otsu, Japan.
Hiroyuki SugiharaDivision of Molecular and Diagnostic Pathology, Department of Pathology, Shiga University of Medical Science, Otsu, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Barrett's esophagus is considered a precancerous lesion of esophageal adenocarcinoma (EAC). Long-segment Barrett's esophagus, which is generally associated with intestinal metaplasia, has a higher rate of carcinogenesis than short-segment Barrett's esophagus, which is mainly composed of cardiac-type mucosa. However, a large number of cases reportedly develop EAC from the cardiac-type mucosa which has the potential to involve intestinal phenotypes. There is no consensus regarding whether the definition of Barrett's epithelium should include intestinal metaplasia. Basic researches using rodent models have provided information regarding the origins of Barrett's epithelium. Nevertheless, it remains unclear whether differentiated gastric columnar epithelium or stratified esophageal squamous epithelium undergo transdifferentiation into the intestinal-type columnar epithelium, transcommittment into the columnar epithelium, or whether the other pathways exist. Reflux of duodenal fluid including bile acids into the stomach may occur when an individual lies down after eating, which could cause the digestive juices to collect in the fornix of the stomach. N-nitroso-bile acids are produced with nitrites that are secreted from the salivary glands, and bile acids can drive expression of pro-inflammatory cytokines via EGFR or the NF-κB pathway. These steps may contribute significantly to carcinogenesis.

Indexed as

Barrett EsophagusCarcinogenesisEsophagusGastroesophageal RefluxHumansMetaplasiaStomachBarret's esophagusbile acid, gastroesophageal reflux, metaplasia

Identifiers

PMID31290583
PMCPMC6851828

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.