Evidence map›Paper›PMID 40925382›Full record

ArticleCell genomics2025

Single-cell analysis of Barrett's esophagus and carcinoma reveals cell types conferring risk via genetic predisposition.

Marten C Wenzel, Pouria Dasmeh, Patrick S Plum, Ann-Sophie Giel, Sascha Hoppe, Marek Franitza, Christoph Jonas, René Thieme, Yue Zhao, Dominik Heider and 10 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell genomics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–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

4 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Current Concepts for Diagnosing Non-Dysplastic and Dysplastic Barrett's Esophagus.Gastrointestinal endoscopy clinics of North America · 2026
    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

20 authors.

Marten C WenzelInstitute of Pathology, Faculty of Medicine and University Hospital Cologne, University of Cologne, Cologne, Germany.
Pouria DasmehInstitute of Human Genetics, University Hospital of Marburg, Marburg, Germany; Department of Chemistry and Chemical Biology, Harvard University, Boston, MA, USA; Institute for Evolutionary Biology and Environmental Studies, University of Zurich, Zurich, Switzerland.
Patrick S PlumInstitute of Pathology, Faculty of Medicine and University Hospital Cologne, University of Cologne, Cologne, Germany; Department of General, Visceral, Cancer and Transplantation Surgery, Faculty of Medicine and University Hospital Cologne, University of Cologne, Cologne, Germany; Department of Visceral, Transplant, Thoracic and Vascular Surgery, University Hospital of Leipzig, Leipzig, Germany.
Ann-Sophie GielInstitute of Human Genetics, University Hospital of Marburg, Marburg, Germany.
Sascha HoppeInstitute of Pathology, Faculty of Medicine and University Hospital Cologne, University of Cologne, Cologne, Germany.
Marek FranitzaCologne Center for Genomics, University of Cologne, Cologne, Germany.
Christoph JonasInstitute of Pathology, Faculty of Medicine and University Hospital Cologne, University of Cologne, Cologne, Germany.
René ThiemeDepartment of Visceral, Transplant, Thoracic and Vascular Surgery, University Hospital of Leipzig, Leipzig, Germany.
Yue ZhaoDepartment of General, Visceral, Cancer and Transplantation Surgery, Faculty of Medicine and University Hospital Cologne, University of Cologne, Cologne, Germany.
Dominik HeiderDepartment of Data Science in Biomedicine, Faculty of Mathematics and Computer Science, Philipps-University of Marburg, Marburg, Germany; Institute of Medical Informatics, University of Münster, Münster, Germany.
Claire PallesInstitute of Cancer and Genomic Sciences, University of Birmingham, Birmingham, UK.
Rebecca Claire FitzgeraldMedical Research Council (MRC) Cancer Unit, Hutchison-MRC Research Centre, University of Cambridge, Cambridge, Cambridgeshire, UK.
Christiane J BrunsDepartment of General, Visceral, Cancer and Transplantation Surgery, Faculty of Medicine and University Hospital Cologne, University of Cologne, Cologne, Germany.
Reinhard BuettnerInstitute of Pathology, Faculty of Medicine and University Hospital Cologne, University of Cologne, Cologne, Germany.
Alexander QuaasInstitute of Pathology, Faculty of Medicine and University Hospital Cologne, University of Cologne, Cologne, Germany.
Ines GockelDepartment of Visceral, Transplant, Thoracic and Vascular Surgery, University Hospital of Leipzig, Leipzig, Germany.
Carlo MajInstitute of Human Genetics, University Hospital of Marburg, Marburg, Germany.
Seung-Hun ChonDepartment of General, Visceral, Cancer and Transplantation Surgery, Faculty of Medicine and University Hospital Cologne, University of Cologne, Cologne, Germany.
Johannes SchumacherInstitute of Human Genetics, University Hospital of Marburg, Marburg, Germany. Electronic address: johannes.schumacher@uni-marburg.de.
Axel M HillmerInstitute of Pathology, Faculty of Medicine and University Hospital Cologne, University of Cologne, Cologne, Germany; Center for Molecular Medicine Cologne, University of Cologne, Cologne, Germany. Electronic address: ahillmer@uni-koeln.de.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inherited genetic variants contribute to Barrett's esophagus (BE) and esophageal adenocarcinoma (EAC), but it is unknown which cell types are involved in this process. We performed single-cell RNA sequencing of BE, EAC, and paired normal tissues and integrated genome-wide association data to determine cell-type-specific genetic risk and cellular processes that contribute to BE and EAC. The analysis reveals that EAC development is driven to a greater extent by local cellular processes than BE development and suggests that one cell type of BE origin (intestinal metaplasia cells) and cellular processes that control the differentiation of columnar cells are of particular relevance for EAC development. Specific subtypes of fibroblasts and endothelial cells likely contribute to BE and EAC development, while dendritic cells and CD4

Indexed as

AdenocarcinomaBarrett EsophagusEsophageal NeoplasmsGenetic Predisposition to DiseaseSingle-Cell AnalysisFibroblastsGenome-Wide Association StudyHumansBarrett’s esophaguscancer developmentesophageal adenocarcinomagenetic riskgenome-wide association studyintestinal metaplasiapartitioned heritabilitysingle-cell RNA sequencing

Identifiers

PMID40925382
PMCPMC12790991

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.