Barrett's esophagus (BE) is a disease entity that is a sequela of chronic gastroesophageal reflux disease that may result in esophageal adenocarcinoma (EAC) due to columnar epithelial dysplasia. The histological degree of dysplasia is the sole biomarker frequently utilized by clinicians. However, the cost of endoscopy and the fact that the degree of dysplasia does not progress in many patients with BE diminish the effectiveness of histological grading as a perfect biomarker. Multiple or more quantitative biomarkers are required by clinicians since early diagnosis is crucial in esophageal adenocancers, which have a high mortality rate. The presence of epigenetic factors in the early stages of this neoplastic transformation holds promise as a predictive biomarker. In this review, current studies on DNA methylations, histone modifications, and noncoding RNAs (miRNAs) that have been discovered during the progression from BE dysplasia to EAC were collated.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10178512 | PMC |
| http://dx.doi.org/10.3390/ijms24097817 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Biologically-targeted discovery-replication scan identifies G×G interaction in relation to risk of Barrett's esophagus and esophageal adenocarcinoma.
HGG Adv
January 2025
Department of Epidemiology and Biostatistics, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Inherited genetics represents an important contributor to risk of esophageal adenocarcinoma (EAC), and its precursor Barrett's esophagus (BE). Genome-wide association studies have identified ∼30 susceptibility variants for BE/EAC, yet genetic interactions remain unexamined. To address challenges in large-scale G×G scans, we combined knowledge-guided filtering and machine learning approaches, focusing on genes with (A) known/plausible links to BE/EAC pathogenesis (n=493) or (B) prior evidence of biological interactions (n=4,196).
View Article and Find Full Text PDFContext-dependent effects of CDKN2A and other 9p21 gene losses during the evolution of esophageal cancer.
Nat Cancer
January 2025
Cancer Systems Biology Laboratory, The Francis Crick Institute, London, UK.
CDKN2A is a tumor suppressor located in chromosome 9p21 and frequently lost in Barrett's esophagus (BE) and esophageal adenocarcinoma (EAC). How CDKN2A and other 9p21 gene co-deletions affect EAC evolution remains understudied. We explored the effects of 9p21 loss in EACs and cancer progressor and non-progressor BEs with matched genomic, transcriptomic and clinical data.
View Article and Find Full Text PDFRefining risk assessment in Barrett's esophagus: addressing follow-up and diagnostic limitations.
J Gastroenterol
January 2025
Institute of Gastroenterology, Science and Technology Innovation Center, Guangzhou University of Chinese Medicine, Guangzhou, China.
Introduction: Endoscopic ablation is the mainstay treatment for dysplastic Barrett's esophagus (BE), of which radiofrequency ablation (RFA) and argon plasma coagulation (APC) are the most widely available options.
Objectives: We aimed to analyze the safety and outcomes of endoscopic ablation for BE within Polish centers.
Patients And Methods: We retrospectively analyzed data from three high-volume endoscopy units between 2002-2024.
The Mucosal Protection in the Treatment of Erosive Reflux Esophagitis: Mechanisms for Restoring Epithelial Permeability. A Randomized Clinical Trial.
J Gastrointestin Liver Dis
December 2024
Omsk State Medical University, Omsk, Russia.
Background And Aims: Gastroesophageal reflux disease (GERD) is widespread in the population and is characterized by the risk of developing Barrett's esophagus and associated adenocarcinoma. Key factors in the progression of the disease are not only the frequency and duration of reflux episodes, but also the resistance of the esophageal mucosa to aggressive reflux molecules. Assessment of the state of tight junction proteins, the rate of their recovery under the influence of various treatment regimens is an urgent task for choosing optimal approaches to curing patients with GERD.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!