Evidence map›Paper›PMID 14705821›Full record

ArticleDigestive diseases and sciences2003

Gastric carcinogenesis by duodenal reflux through gut regenerative cell lineage.

Ken-Ichi Mukaisho, Koichi Miwa, Hitomi Kumagai, Masamichi Bamba, Hiroyuki Sugihara, Takanori Hattori

Abstract read
PubMed Publisher
In one paragraph

Article in Digestive diseases and sciences, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

17 citing papers in PubMed, 35 citations in OpenAlex.

  1. How to Define the Gastroesophageal Junction.Digestive endoscopy : official journal of the Japan Gastroenterological Endoscopy Society · 2026
    Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Barretts's carcinogenesis.Pathology international · 2019
    Article
  7. Article
  8. Article
  9. Article
  10. Barrett's esophagus and animal models.Annals of the New York Academy of Sciences · 2011
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. 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

6 authors at 2 institutions in 1 country.

Ken-Ichi MukaishoDepartment of Pathology, Shiga University of Medical Science, Seta-tsukinowa-cho, Ohtsu, Shiga, 520-2192, Japan. mukaisho@belle.shiga-med.ac.jp
Koichi Miwa
Hitomi Kumagai
Masamichi Bamba
Hiroyuki Sugihara
Takanori Hattori
Shiga University of Medical Science · JPKanazawa University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

To elucidate the histogenesis of gastric stump cancer, we performed an operation in rats to make all duodenal contents flow back into the glandular stomach. The subjects were 41 rats, and sequential morphological changes of the duodenogastric stoma and the incidence of stump cancers were studied. Serial sections around the stoma were studied with mucin stains such as paradoxical concanavalin A (Con A), galactose oxidase Schiff (GOS), and high-iron diamine-Alcian blue (HID-AB). An immunohistochemical study on cell proliferation with bromodeoxyuridine (BrdU) was also done. At week 30, pyloric gland type cells positive for Con A first appeared at the base of the intestinal crypts and the fundic glands adjacent to the anastomosis. These glands became large with time, resulting in formation of cystically dilated glands. These gland cells were partially stained with GOS, and then they retained a proliferative activity. These changes seemed to resemble "gastritis cystica profunda" in human remnant stomachs. At 50 and 80 weeks, adenocarcinomas were observed in 4 of 10 rats (40.0%) and in 16 of 21 rats (76.2%), respectively. We have noted that the early change of cystic proliferation of mucous glands resembled the so-called "ulcer associated cell lineage (UACL)" described by others, but our characteristic finding was not only pyloric but also foveolar metaplasia. This pyloric-foveolar metaplasia subsequently led to development of glands with intestinal-type goblet cells, which looked like incomplete intestinal metaplasia. This sequence was different from UACL, and very recently, we proposed a concept of "gut regenerative cell lineage (GRCL); from pyloric-foveolar to with goblet cell metaplasia in regeneration," common to all parts of the gut, and the stump cancer appeared to arise from GRCL.

Indexed as

AdenocarcinomaAnimalsCell LineageDisease Models, AnimalDuodenogastric RefluxGastric MucosaGastric StumpMaleRatsRats, WistarRegenerationStomach Neoplasms

Identifiers

PMID14705821
OpenAlexW2018901065

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.