Evidence map›Paper›PMID 37962678›Full record

ArticleJournal of gastroenterology2024

Marked intestinal trans-differentiation by autoimmune gastritis along with ectopic pancreatic and pulmonary trans-differentiation.

Chihiro Takeuchi, Junichi Sato, Nobutake Yamamichi, Natsuko Kageyama-Yahara, Akiko Sasaki, Takemi Akahane, Rika Aoki, Shigemi Nakajima, Masayoshi Ito, Mitsue Yamamichi and 10 more

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

Article in Journal of gastroenterology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

8 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Integrative Analysis of Intestinal Transcriptomes UnderscoresBioinformatics and biology insights · 2026
    Article
  6. Article
  7. Review
  8. 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

20 authors at 9 institutions in 1 country.

Chihiro Takeuchi *Department of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo, 113-8655, Japan.
Junichi Sato *Department of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo, 113-8655, Japan.
Nobutake YamamichiDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo, 113-8655, Japan. nobutakeyamamichi@gmail.com.ORCID 0000-0002-5741-9887
Natsuko Kageyama-YaharaDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo, 113-8655, Japan.
Akiko SasakiDepartment of Gastroenterology, Medicine Center, Shonan Kamakura General Hospital, Kanagawa, Japan.
Takemi AkahaneDepartment of Gastroenterology, Nara Medical University, Nara, Japan.
Rika AokiTokushima Health Screening Center, Tokushima, Japan.
Shigemi NakajimaDepartment of General Medicine, Japan Community Healthcare Organization Shiga Hospital, Consortium for Community Medicine, Shiga University of Medical Science, Shiga, Japan.
Masayoshi ItoDepartment of Gastroenterology, Yotsuya Medical Cube, Tokyo, Japan.
Mitsue YamamichiDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo, 113-8655, Japan.
Yu-Yu LiuDivision of Epigenomics, National Cancer Center Research Institute, Tokyo, Japan.
Nobuyuki SakumaDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo, 113-8655, Japan.
Yu TakahashiDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo, 113-8655, Japan.
Yoshiki SakaguchiDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo, 113-8655, Japan.
Yosuke TsujiDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo, 113-8655, Japan.
Kouhei SakuraiDepartment of Pathology, Fujita Health University School of Medicine, Aichi, Japan.
Shuta TomidaCenter for Comprehensive Genomic Medicine, Okayama University Hospital, Okayama, Japan.
Keiko NiimiDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo, 113-8655, Japan.
Toshikazu UshijimaDivision of Epigenomics, National Cancer Center Research Institute, Tokyo, Japan.
Mitsuhiro FujishiroDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo, 113-8655, Japan.
The University of Tokyo · JPHoshi University · JPUniversity of Tokyo Hospital · JPFujita Health University · JPNara Medical University · JPOkayama University Hospital · JPShiga University of Medical Science · JPShonan Kamakura General Hospital · JPYotsuya Medical Cube · JP

Funding

Japan Society for the Promotion of Science 21H03178Princess Takamatsu Cancer Research Fund 19-25138
6 · The paper itself

Abstract

backgroundAutoimmune gastritis (AIG) is a prevalent chronic inflammatory disease with oncogenic potential that causes destruction of parietal cells and severe mucosal atrophy. We aimed to explore the distinctive gene expression profiles, activated signaling pathways, and their underlying mechanisms.

methodsA comprehensive gene expression analysis was conducted using biopsy specimens from AIG, Helicobacter pylori-associated gastritis (HPG), and non-inflammatory normal stomachs. Gastric cancer cell lines were cultured under acidic (pH 6.5) conditions to evaluate changes in gene expression.

resultsGastric mucosa with AIG had a unique gene expression profile compared with that with HPG and normal mucosa, such as extensively low expression of ATP4A and high expression of GAST and PAPPA2, which are involved in neuroendocrine tumorigenesis. Additionally, the mucosa with AIG and HPG showed the downregulation of stomach-specific genes and upregulation of small intestine-specific genes; however, intestinal trans-differentiation was much more prominent in AIG samples, likely in a CDX-dependent manner. Furthermore, AIG induced ectopic expression of pancreatic digestion-related genes, PNLIP, CEL, CTRB1, and CTRC; and a master regulator gene of the lung, NKX2-1/TTF1 with alveolar fluid secretion-related genes, SFTPB and SFTPC. Mechanistically, acidic conditions led to the downregulation of master regulator and stemness control genes of small intestine, suggesting that increased environmental pH may cause abnormal intestinal differentiation in the stomach.

conclusionsAIG induces diverse trans-differentiation in the gastric mucosa, characterized by the transactivation of genes specific to the small intestine, pancreas, and lung. Increased environmental pH owing to AIG may cause abnormal differentiation of the gastric mucosa.

Indexed as

Autoimmune DiseasesGastritisHelicobacter InfectionsHelicobacter pyloriCell TransdifferentiationGastric MucosaHumansPancreasAutoimmune gastritisDiverse trans-differentiationIncreased pHIntestinal differentiationMolecular epidemiology

Identifiers

PMID37962678
PMCPMC10810929
OpenAlexW4388653170

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.