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The purpose of this study is to elucidate mechanisms whereby oxidative stress induced by acute reflux esophagitis: 1) activates p38 to regulate proteins that control the G1/S cell cycle checkpoint, and 2) activates HIFs (hypoxia inducible factors) to cause autocrine VEGF (vascular endothelial growth factor) signaling that triggers the EMT (epithelial-mesenchymal-transition) program in Barrett's esophagus.
Gastroesophageal reflux disease (GERD) and its complication, Barrett's esophagus (BE), are risk factors for esophageal adenocarcinoma. In BE, GERD causes inflammation with oxidative DNA damage and genomic instability that contributes to carcinogenesis. In BE, one response to oxidative stress is p38 pathway activation, which might protect against cancer development by initiating G1 arrest and enabling repair of DNA damage. Inflammation and oxidative stress also might induce epithelial-mesenchymal transition (EMT), the process in which epithelial cells acquire mesenchymal characteristics including the ability to migrate. This study will elucidate mechanisms whereby the oxidative stress of acute reflux esophagitis in BE activates p38 to regulate proteins controlling the G1/S cell cycle checkpoint, and activates HIFs to cause autocrine vascular endothelial growth factor (VEGF) signaling that triggers the EMT program.
Intervention Model: Single Group Assignment, Masking: Open Label, Primary Purpose: Basic Science
Cessation of Acid Suppressing Medications
Dallas VA Medical Center
Enrolling by invitation
Dallas VA Medical Center
Published on BioPortfolio: 2015-10-20T13:53:22-0400
Patients with Barrett's Esophagus are known to have excessive distal esophageal acid exposure comparable to patients with erosive esophagitis. A significant proportion of patients with BE ...
This is a multi-center study whose aim is to define the epidemiology and genetics of Barrett's esophagus and adenocarcinoma. The researchers have studied families affected with Barrett's e...
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To review recently published data on factors that predict the risk of progression of Barrett's esophagus (BE) to high grade dysplasia (HGD) or esophageal adenocarcinoma (EAC).
Barrett's esophagus (BE)-intestinal metaplasia in the esophagus-may progress to low-grade dysplasia (LGD), high-grade dysplasia (HGD), and ultimately, invasive esophageal adenocarcinoma (EAC). The cou...
In this review, we explore a paligenosis-based model to explain Barrett's esophagus development and progression: 'the cyclical hit model.'
MINI: The reported prevalence of new-onset or worsening gastroesophageal reflux disease after sleeve gastrectomy is controversial. Subsequent esophagitis and Barrett's esophagus can be serious uninten...
A condition with damage to the lining of the lower ESOPHAGUS resulting from chronic acid reflux (ESOPHAGITIS, REFLUX). Through the process of metaplasia, the squamous cells are replaced by a columnar epithelium with cells resembling those of the INTESTINE or the salmon-pink mucosa of the STOMACH. Barrett's columnar epithelium is a marker for severe reflux and precursor to ADENOCARCINOMA of the esophagus.
A 51-amino acid pancreatic hormone that plays a major role in the regulation of glucose metabolism, directly by suppressing endogenous glucose production (GLYCOGENOLYSIS; GLUCONEOGENESIS) and indirectly by suppressing GLUCAGON secretion and LIPOLYSIS. Native insulin is a globular protein comprised of a zinc-coordinated hexamer. Each insulin monomer containing two chains, A (21 residues) and B (30 residues), linked by two disulfide bonds. Insulin is used as a drug to control insulin-dependent diabetes mellitus (DIABETES MELLITUS, TYPE 1).
Disorders affecting the motor function of the UPPER ESOPHAGEAL SPHINCTER; LOWER ESOPHAGEAL SPHINCTER; the ESOPHAGUS body, or a combination of these parts. The failure of the sphincters to maintain a tonic pressure may result in gastric reflux of food and acid into the esophagus (GASTROESOPHAGEAL REFLUX). Other disorders include hypermotility (spastic disorders) and markedly increased amplitude in contraction (nutcracker esophagus).
A motility disorder of the ESOPHAGUS in which the LOWER ESOPHAGEAL SPHINCTER (near the CARDIA) fails to relax resulting in functional obstruction of the esophagus, and DYSPHAGIA. Achalasia is characterized by a grossly contorted and dilated esophagus (megaesophagus).
Cessation of the habit of using tobacco products for smoking or chewing, including the use of snuff.
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