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Related Concept Videos

Barrett Esophagus-I: Introduction01:21

Barrett Esophagus-I: Introduction

Barrett's esophagus is a medical condition where the esophageal mucosa is significantly damaged by stomach acid or other digestive fluids, often due to long-term exposure associated with gastroesophageal reflux disease (GERD). In GERD, a weakened or abnormally relaxed lower esophageal sphincter allows stomach acid to flow persistently into the esophagus.
This constant acid exposure transforms the esophagus's pink mucosal lining (stratified squamous epithelium) into a type of lining more similar...
Barrett Esophagus-II: Clinical Manifestations and Management01:21

Barrett Esophagus-II: Clinical Manifestations and Management

Individuals with Barrett's esophagus are often asymptomatic, but they may experience symptoms commonly associated with GERD, such as heartburn and acid regurgitation. Additional symptoms can include difficulty swallowing, chest pain, unintentional weight loss, blood in the stool (which may appear black, tarry, or bloody), and episodes of vomiting.
To diagnose Barrett's esophagus, healthcare providers often recommend an endoscopy for those showing symptoms of acid reflux. The procedure entails...
Peptic Ulcer Disease II: Pathophysiology01:24

Peptic Ulcer Disease II: Pathophysiology

Peptic ulcer disease develops when protective mechanisms of the gastrointestinal mucosa are overwhelmed by harmful factors, leading to localized erosions in the stomach or proximal duodenum. The main causes are Helicobacter pylori infection and chronic use of nonsteroidal anti-inflammatory drugs (NSAIDs).Helicobacter pylori–Induced InjuryBacterial Adaptation and Colonization:H. pylori is a spiral, Gram-negative bacterium adapted to the acidic stomach. and transmitted through oral-oral or...
Peptic Ulcer Disease II: Pathophysiology01:28

Peptic Ulcer Disease II: Pathophysiology

Peptic Ulcer Disease (PUD) is characterized by the development of ulcers in the stomach or duodenal mucosa. Its pathophysiology is complex, involving a balance between damaging and protective elements.
Damaging agents such as Helicobacter pylori, gastric acid, pepsin, and nonsteroidal anti-inflammatory drugs (NSAIDs) can weaken the mucosal defense, allowing hydrogen ions to infiltrate back and harm epithelial cells.
Peptic Ulcer Disease I: Introduction01:30

Peptic Ulcer Disease I: Introduction

Peptic Ulcer Disease (PUD) is characterized by mucosal excavation in the esophagus, stomach, pylorus, or duodenum. It can manifest as acute or chronic based on the extent and duration of mucosal involvement.
An acute ulcer, marked by superficial erosion and minimal inflammation, swiftly resolves upon identifying and addressing the underlying cause. In contrast, a chronic ulcer persists, potentially eroding through the muscular wall and forming fibrous tissue.
Peptic ulcers can also be...
Peptic Ulcer Disease I: Introduction01:25

Peptic Ulcer Disease I: Introduction

Peptic ulcer disease (PUD) involves breaks in the gastrointestinal tract's mucosal lining, primarily in the stomach and duodenum, with less frequent occurrences in the lower esophagus or near the pylorus.Ulcers can be acute or chronic. Acute ulcers are short-lived with minimal inflammation and heal quickly after the irritant is removed. Chronic ulcers persist, may recur, and often cause scarring due to ongoing tissue damage. Superficial erosions affect only the mucosal layer and are called...

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Related Experiment Video

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An Immunofluorescent Method for Characterization of Barrett’s Esophagus Cells
08:54

An Immunofluorescent Method for Characterization of Barrett’s Esophagus Cells

Published on: July 20, 2014

NSAIDs modulate clonal evolution in Barrett's esophagus.

Rumen L Kostadinov1, Mary K Kuhner, Xiaohong Li

  • 1Genomics and Computational Biology Graduate Program, University of Pennsylvania, Philadelphia, Pennsylvania, USA.

Plos Genetics
|June 21, 2013
PubMed
Summary
This summary is machine-generated.

Non-steroidal anti-inflammatory drugs (NSAIDs) significantly reduce the rate of somatic genomic abnormalities (SGAs) in Barrett's esophagus (BE) cells. This finding suggests NSAIDs may prevent esophageal adenocarcinoma (EA) by slowing cancer-driving genetic changes.

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Last Updated: May 10, 2026

An Immunofluorescent Method for Characterization of Barrett’s Esophagus Cells
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An Immunofluorescent Method for Characterization of Barrett’s Esophagus Cells

Published on: July 20, 2014

Surgical Models of Gastroesophageal Reflux with Mice
05:19

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Diagnosis of Neoplasia in Barrett’s Esophagus using Vital-dye Enhanced Fluorescence Imaging
06:55

Diagnosis of Neoplasia in Barrett’s Esophagus using Vital-dye Enhanced Fluorescence Imaging

Published on: May 11, 2014

Area of Science:

  • Oncology
  • Genetics
  • Pharmacology

Background:

  • Cancer develops through decades of clonal evolution driven by somatic genomic abnormalities (SGAs).
  • Non-steroidal anti-inflammatory drugs (NSAIDs) are known to reduce cancer risk, including progression from Barrett's esophagus (BE) to esophageal adenocarcinoma (EA).
  • The precise mechanisms by which NSAIDs exert their cancer chemopreventive effects remain incompletely understood.

Purpose of the Study:

  • To investigate the hypothesis that NSAIDs modulate cancer clonal evolution by decreasing the rate of SGA acquisition.
  • To quantify the rate of SGA acquisition in BE patients with and without NSAID use.

Main Methods:

  • Analysis of 161 BE biopsies from 13 individuals over 6.4-19 years using 1Million-SNP arrays to detect SGAs.
  • Comparison of SGA acquisition rates in individuals who initiated or discontinued NSAID use.
  • Quantification of the number and genomic impact of SGAs over time.

Main Results:

  • The estimated SGA rate was significantly lower when on NSAIDs (0.6 per genome/year) compared to off NSAIDs (7.8 per genome/year).
  • NSAID use was associated with a reduced rate of SGA acquisition in 11 out of 13 individuals.
  • Most BE patients maintained a stable level of SGAs, with occasional clonal expansions observed.

Conclusions:

  • NSAIDs are associated with a substantial reduction in the rate of somatic genomic abnormality acquisition in Barrett's esophagus.
  • This mechanism likely contributes to the cancer chemopreventive effects of NSAIDs against esophageal adenocarcinoma.
  • NSAIDs may represent a viable strategy for chemoprevention by stabilizing the genomic landscape of pre-cancerous lesions.