ReviewDigestive diseases and sciences2018
Origins of Metaplasia in the Esophagus: Is This a GE Junction Stem Cell Disease?
Review in Digestive diseases and sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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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.
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.
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Who cites it
10 citing papers in PubMed, 12 citations in OpenAlex.
- Esophageal cancer: from pathogenesis to precision therapies.Signal transduction and targeted therapy · 2026Review
- Listening to the Past, Shaping the Future: A Data-mining Based and Visual Analysis of Five Decades of Gastric Carcinogenesis Research.Biological procedures online · 2025Article
- Therapeutic Effect of Polaprezinc on Reflux Esophagitis in the Rat Model.Digestive diseases and sciences · 2023Article
- Mechanisms and pathophysiology of Barrett oesophagus.Nature reviews. Gastroenterology & hepatology · 2022Review
- Targeted Hsp70 fluorescence molecular endoscopy detects dysplasia in Barrett's esophagus.European journal of nuclear medicine and molecular imaging · 2022Article
- Impact of the Tumor Microenvironment for Esophageal Tumor Development-An Opportunity for Prevention?Cancers · 2022Review
- CXCR4 peptide-based fluorescence endoscopy in a mouse model of Barrett's esophagus.EJNMMI research · 2022Article
- Molecular Profile of Barrett's Esophagus and Gastroesophageal Reflux Disease in the Development of Translational Physiological and Pharmacological Studies.International journal of molecular sciences · 2020Article
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Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The incidence of esophageal adenocarcinoma (EAC) and its precursor lesion Barrett's esophagus (BE) has been increasing steadily in the western world in recent decades. Understanding the cellular origins of BE and the conditions responsible for their malignant transformation would greatly facilitate risk assessment and identification of patients at risk of progression, but this topic remains a source of debate. Here, we review recent findings that have provided support for the gastroesophageal junction (GEJ) as the main source of stem cells that give rise to BE and EAC. These include both gastric cardia cells and transitional basal cells. Furthermore, we discuss the role of chronic injury and inflammation in a tumor microenvironment as a major factor in promoting stem cell expansion and proliferation as well as transformation of the GEJ-derived stem cells and progression to EAC. We conclude that there exists a large amount of empirical support for the GEJ as the likely source of BE stem cells. While BE seems to resemble a successful adaptation to esophageal damage, carcinogenesis appears as a consequence of natural selection at the level of GEJ stem cells, and later glands, that expand into the esophagus wherein the local ecology creates the selective landscape for cancer progression.
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Registered trials
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.