Evidence map›Paper›PMID 35172301›Full record

ArticleDigestion2022

The Origin of Epithelium with Low-Grade Atypia in Early Gastric Cancer.

Hiroaki Yamada, Hiroaki Kaneko, Hirofumi Kuwashima, Makoto Sugimori, Sho Tsuyuki, Katsuyuki Sanga, Kuniyasu Irie, Tomohiko Sasaki, Masaaki Kondo, Akio Miyake and 1 more

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Digestion, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.4field-weighted citation impact, top 40% 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

1 citing paper in PubMed, 2 citations in OpenAlex.

  1. 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

11 authors at 2 institutions in 1 country.

Hiroaki YamadaDepartment of Gastroenterology, Yokohama City University, Yokohama, Japan.
Hiroaki KanekoDepartment of Gastroenterology, Yokohama City University, Yokohama, Japan.
Hirofumi KuwashimaDepartment of Gastroenterology, Yokohama City University, Yokohama, Japan.
Makoto SugimoriDepartment of Gastroenterology, Yokohama City University, Yokohama, Japan.
Sho TsuyukiDepartment of Gastroenterology, Yokohama City University, Yokohama, Japan.
Katsuyuki SangaDepartment of Gastroenterology, Yokohama City University, Yokohama, Japan.
Kuniyasu IrieDepartment of Gastroenterology, Yokohama City University, Yokohama, Japan.
Tomohiko SasakiDepartment of Gastroenterology, Yokohama City University, Yokohama, Japan.
Masaaki KondoDepartment of Gastroenterology, Yokohama City University, Yokohama, Japan.
Akio MiyakeDivision of Pathological Diagnosis, Yokohama City University Hospital, Yokohama, Japan.
Shin MaedaDepartment of Gastroenterology, Yokohama City University, Yokohama, Japan.
Yokohama City University · JPYokohama City University Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionHelicobacter pylori (HP) infection causes chronic inflammation and atrophy of the gastric mucosa and thus a high risk of gastric cancer (GC). With the increasing success of HP infection treatment, a larger number of GCs that develop after eradication can be assessed. Several studies have shown that epithelium with low-grade atypia (ELA) is a frequent characteristic of these GCs, but the origin of this condition is unknown. In this study, we compared the mucin phenotype, cellular proliferation, and p53 staining in ELA and cancerous tissues obtained from patients with GC with and without HP eradication.

methodsThe study population consisted of 23 patients with GC that developed after successful HP eradication therapy (eradicated group) and 24 patients with GC and HP infection (infected group). The prevalence of ELA was determined by hematoxylin and eosin staining. Tumor tissue and ELA samples were further analyzed by immunohistochemical staining for Muc5AC, Muc2, p53, and Ki-67.

resultsThe ELA coverage rate was significantly higher in the eradicated group than in the infected group. Gastric-type mucin was frequently expressed by the ELA, and the mucin phenotypes of ELA and cancerous areas differed in 75% of cases. The Ki-67 labeling index was consistently lower in ELA than in the cancerous mucosa. Fourteen of 21 (66.7%) cancerous lesions, but only 3 ELA samples, were p53-positive.

conclusionIn most cases, ELA on the surfaces of GCs seems to have originated from normal gastric cells, not from cancer cells.

Indexed as

Helicobacter InfectionsHelicobacter pyloriStomach NeoplasmsEpitheliumGastric MucosaHumansKi-67 AntigenTumor Suppressor Protein p53Ki-67 AntigenTumor Suppressor Protein p53Epithelium with low-grade atypiaEradicationGastric cancerHelicobacter pylori

Identifiers

PMID35172301
PMCPMC9153352
OpenAlexW4213362809

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.