Evidence map›Paper›PMID 37298253›Full record

ReviewInternational journal of molecular sciences2023

Signaling Pathways in the Pathogenesis of Barrett's Esophagus and Esophageal Adenocarcinoma.

Ksenia Maslenkina, Liudmila Mikhaleva, Maxim Naumenko, Rositsa Vandysheva, Michail Gushchin, Dmitri Atiakshin, Igor Buchwalow, Markus Tiemann

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

12 citing papers in PubMed, 16 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Computing lifetime incidence of esophageal adenocarcinoma and age-specific prevalence of Barrett's esophagus.Diseases of the esophagus : official journal of the International Society for Diseases of the Esophagus · 2025
    Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. 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

8 authors at 3 institutions in 2 countries.

Ksenia MaslenkinaA.P. Avtsyn Research Institute of Human Morphology, Petrovsky National Research Center of Surgery, 119991 Moscow, Russia.ORCID 0000-0001-8083-9428
Liudmila MikhalevaA.P. Avtsyn Research Institute of Human Morphology, Petrovsky National Research Center of Surgery, 119991 Moscow, Russia.ORCID 0000-0003-2052-914X
Maxim NaumenkoA.P. Avtsyn Research Institute of Human Morphology, Petrovsky National Research Center of Surgery, 119991 Moscow, Russia.
Rositsa VandyshevaA.P. Avtsyn Research Institute of Human Morphology, Petrovsky National Research Center of Surgery, 119991 Moscow, Russia.
Michail GushchinA.P. Avtsyn Research Institute of Human Morphology, Petrovsky National Research Center of Surgery, 119991 Moscow, Russia.ORCID 0000-0002-1041-8561
Dmitri AtiakshinResearch and Educational Resource Centre for Immunophenotyping, Digital Spatial Profiling and Ultrastructural Analysis Innovative Technologies, Peoples' Friendship University of Russia Named after Patrice Lumumba, 117198 Moscow, Russia.ORCID 0000-0002-8347-4556
Igor BuchwalowResearch and Educational Resource Centre for Immunophenotyping, Digital Spatial Profiling and Ultrastructural Analysis Innovative Technologies, Peoples' Friendship University of Russia Named after Patrice Lumumba, 117198 Moscow, Russia.ORCID 0000-0003-1142-7483
Markus TiemannInstitute for Hematopathology, Fangdieckstr. 75a, 22547 Hamburg, Germany.
Research Institute of Human Morphology · RUPeoples' Friendship University of Russia · RUInstitut für Hämatopathologie Hamburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Barrett's esophagus (BE) is a premalignant lesion that can develop into esophageal adenocarcinoma (EAC). The development of Barrett's esophagus is caused by biliary reflux, which causes extensive mutagenesis in the stem cells of the epithelium in the distal esophagus and gastro-esophageal junction. Other possible cellular origins of BE include the stem cells of the mucosal esophageal glands and their ducts, the stem cells of the stomach, residual embryonic cells and circulating bone marrow stem cells. The classical concept of healing a caustic lesion has been replaced by the concept of a cytokine storm, which forms an inflammatory microenvironment eliciting a phenotypic shift toward intestinal metaplasia of the distal esophagus. This review describes the roles of the NOTCH, hedgehog, NF-κB and IL6/STAT3 molecular pathways in the pathogenesis of BE and EAC.

Indexed as

AdenocarcinomaBarrett EsophagusEsophageal NeoplasmsHumansSignal TransductionTumor MicroenvironmentBarrett’s esophaguscarcinogenesisdysplasiaesophageal adenocarcinomainflammatory signaling pathwaysintestinal metaplasiamutational loadp53

Identifiers

PMID37298253
PMCPMC10253447
OpenAlexW4378575602

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.