Evidence map›Paper›PMID 25870690›Full record

ReviewJournal of medicine and life2014

Barrett esophagus: history, definition and etiopathogeny.

C Gindea, R Birla, P Hoara, A Caragui, S Constantinoiu

Open access · greenAbstract readHistorical ArticleReview
In one paragraph

Review in Journal of medicine and life, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.5field-weighted citation impact, top 27% 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

9 citing papers in PubMed, 31 citations in OpenAlex.

  1. Trial
  2. Barrett's esophagus: A review.World journal of gastrointestinal pathophysiology · 2025
    Review
  3. Mitochondrial clone tracing within spatially intact human tissues.bioRxiv : the preprint server for biology · 2025
    Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. 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

5 authors at 1 institution in 1 country.

C Gindea"Carol Davila" University of Medicine and Pharmacy, Bucharest; "Sf. Maria" Clinical Hospital, General and Esophageal Surgery Department, Bucharest, Romania.
R Birla"Carol Davila" University of Medicine and Pharmacy, Bucharest; "Sf. Maria" Clinical Hospital, General and Esophageal Surgery Department, Bucharest, Romania.
P Hoara"Carol Davila" University of Medicine and Pharmacy, Bucharest; "Sf. Maria" Clinical Hospital, General and Esophageal Surgery Department, Bucharest, Romania.
A Caragui"Carol Davila" University of Medicine and Pharmacy, Bucharest; "Sf. Maria" Clinical Hospital, General and Esophageal Surgery Department, Bucharest, Romania.
S Constantinoiu"Carol Davila" University of Medicine and Pharmacy, Bucharest; "Sf. Maria" Clinical Hospital, General and Esophageal Surgery Department, Bucharest, Romania.
Clinical Emergency Hospital Bucharest · RO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The injury of the esophageal epithelium may be determined by the reflux of the gastric acid in the esophagus. Barrett's esophagus (BE) is characterized by the replacement of the normal squamous epithelium with the columnar epithelium, when the healing of the lesion occurs. According to some studies, the incidence of the esophageal adenocarcinoma in patients with BE is of about 0,5% per year. The term Barrett's esophagus is subjected to interpretation nowadays, so it lacks the clarity needed for the clinical and scientific communication on the subject of columnar metaplasia of the esophageal mucosa. The major pathogenetic factor in the development of BE is represented by the reflux disease. The cellular origin of BE is controversial and it represents an issue that needs to be resolved because it will have implications in the putative molecular mechanisms underlying the metaplastic process. The epigenetic or genetic changes, which alter protein expression, function, and/ or activity, in post-mitotic cells to drive transdifferentiation or in stem/ progenitor cells such that they are reprogrammed to differentiate into columnar rather than squamous cells, are driven by the inflammatory environment created by chronic reflux. In order to be able to develop better therapeutic strategies for the patients with this disease, an increasing interest in understanding the pathogenesis of BE at the cellular and molecular level presents these days.

Indexed as

Barrett EsophagusCell DifferentiationHistory, 20th CenturyHumansSignal TransductionTranscription FactorsTranscription FactorsBarrett esophagusgastro-esophageal refluxpathogenesis

Identifiers

PMID25870690
PMCPMC4391409
OpenAlexW2417444488

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.