ReviewGenes2025
Molecular Abnormalities and Carcinogenesis in Barrett's Esophagus: Implications for Cancer Treatment and Prevention.
Review in Genes, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed.
- Computational identification of rare pathogenic genomic variants in esophageal cancer markers: Transcript-level analysis, sequence-based insights, and structural-functional impacts of non-synonymous SNPs.Biochemistry and biophysics reports · 2026Article
- Associations Between Non-Genetic Risk Factors and DNA Methylation Alterations in Barrett's Esophagus and Its Progression to Esophageal Adenocarcinoma.International journal of molecular sciences · 2025Review
- The Interplay Between Esophageal Adenocarcinoma and Its Tumor Microenvironment: Toward Innovative Therapies.Cells · 2025Review
- Multidimensional mechanisms and therapies underlying gastroesophageal reflux disease: focus on immunity, signaling pathways, and the microbiota-gut-brain axis.Frontiers in immunology · 2025Review
- The Evolving Paradigm of Esophageal and Esophagogastric Junction Adenocarcinoma: Current Insights, Emerging Therapies, and Future Directions.Journal of cancer science and clinical therapeutics · 2025Article
- A New Survey about Dual-Acting PARP/COX-2 Inhibitors as Cancer Chemopreventive Agents.Iranian journal of pharmaceutical research : IJPRReview
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundBarrett's esophagus (BE) is described by the transformation of the normal squamous epithelium into metaplastic columnar epithelium, driven by chronic gastroesophageal reflux disease (GERD). BE is a recognized premalignant condition and the main precursor to esophageal adenocarcinoma (EAC). Understanding the molecular mechanisms underlying BE carcinogenesis is crucial for improving prevention, surveillance, and treatment strategies.
methodsThis narrative review examines the molecular abnormalities associated with the progression of BE to EAC.
resultsThis study highlights inflammatory, genetic, epigenetic, and chromosomal alterations, emphasizing key pathways and biomarkers. BE progression follows a multistep process involving dysplasia and genetic alterations such as TP53 and CDKN2A (p16) mutations, chromosomal instability, and dysregulation of pathways like PI3K/AKT/mTOR. Epigenetic alterations, including aberrant microRNA expression or DNA methylation, further contribute to this progression. These molecular changes are stage-specific, with some alterations occurring early in BE during the transition to high-grade dysplasia or EAC. Innovations in chemoprevention, such as combining proton pump inhibitors and aspirin, and the potential of antireflux surgery to halt disease progression are promising. Incorporating molecular biomarkers into surveillance strategies and advancing precision medicine may enable earlier detection and personalized treatments.
conclusionsBE is the primary preneoplastic condition for EAC. A deeper understanding of its molecular transformation can enhance surveillance protocols, optimize the management of gastroesophageal reflux inflammation, and refine prevention and therapeutic strategies, ultimately contributing to a reduction in the global burden of EAC.
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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.