DNA Changes as a Risk Factor for Barrett's Esophagus in Patients With Barrett's Esophagus, Gastroesophageal Reflux, or Gastrointestinal Bleeding
Recruitment status was Active, not recruiting
RATIONALE: A study that evaluates DNA changes and other disease-related health information in patients with Barrett's esophagus, gastroesophageal reflux, or gastrointestinal bleeding may help doctors learn more about the risk factors for Barrett's esophagus.
PURPOSE: This clinical trial is looking at DNA changes and other disease-related health information as risk factors for Barrett's esophagus in patients with Barrett's esophagus, gastroesophageal reflux, or gastrointestinal bleeding.
Genetic: gene expression analysis
Genetic: polymorphism analysis
Other: immunoenzyme technique
Other: laboratory biomarker analysis
Other: physiologic testing
Other: study of socioeconomic and demographic variables
Procedure: study of high risk factors
|Official Title:||Molecular Epidemiology of Barrett's Esophagus|
- Polymorphisms in detoxifying enzyme systems such as glutathione S-transferases (e.g., mu, theta, pi)
- Polymorphisms in other xenobiotic metabolism pathways (e.g., CYP1A1, CYP2E1, CYP3A4/5, NQO1, mEH, NAT-2)
- Polymorphisms in inflammatory gene pathways (e.g., MPO, MnSOD, IGF, IGFBF3, Il1-beta)
- Polymorphisms in DNA repair genes or the p53 pathways (e.g., ERCC2, XRCC1, p53, p73, CCND1, p21)
|Study Start Date:||August 2005|
- Assess the role of several genetically determined factors that, in combination with CagA status, cigarette smoking, alcohol, and diet to varying degrees, result in an increased risk for Barrett's esophagus.
OUTLINE: This is a controlled study.
Patients complete questionnaires about demographics, medical history, smoking and alcohol history, current medications, frequency and chronicity of gastroesophageal reflux symptoms, and diet history.
Blood and tissue are collected and analyzed by DNA-based assays and enzyme-linked immunosorbent assay for CagA status and polymorphisms in detoxifying enzyme systems, other xenobiotic metabolism pathways (e.g., CYP1A1, CYP2E1, CYP3A4, CYP3A5, NQO, NAT-2), inflammatory gene pathways (e.g., IGF, IGFBF3), and in DNA repair genes or p53 pathways (e.g., XRCC1, p53 gene).
PROJECTED ACCRUAL: A total of 350 patients will be accrued for this study.
|United States, Massachusetts|
|Harvard School of Public Health|
|Boston, Massachusetts, United States, 02115|
|Massachusetts General Hospital Cancer Center|
|Boston, Massachusetts, United States, 02114|
|Principal Investigator:||David C. Christiani, MD||Massachusetts General Hospital|