Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Genomic analysis of Barrett's esophagus after ablative therapy: Persistence of genetic alterations at tumor suppressor loci

19 Jul 2005

Abstract excerpt

Barrett's esophagus (BE) is a major predisposing factor for the development of esophageal adenocarcinoma. Current strategies for treatment of BE, both dysplastic and nondysplastic, include photodynamic therapy (PDT) and argon plasma coagulation (APC). However, the effect of ablative therapy at the genetic level is unclear. We performed loss of heterozygosity (LOH) analysis of BE in baseline and follow-up biopsy...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Esophageal and GI Pathology
Share to Esophageal Cancer Research and Treatment
Share to Helicobacter pylori-related gastroenterology studies

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 16032707
DOI: 10.1002/ijc.21302

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Genomic analysis of Barrett's esophagus after ablative therapy: Persistence of genetic alterations at tumor suppressor lociPMID 16032707Read ↗

Molecular genetic analysis of surveillance biopsy samples from Barrett's mucosa--significance of sampling.Semantic proximity Read ↗

Molecular Analysis of Persistent and Recurrent Barrett's Esophagus in the Setting of Endoscopic Therapy.Semantic proximity Read ↗

Clonal expansion and loss of heterozygosity at chromosomes 9p and 17p in premalignant esophageal (Barrett's) tissue.Semantic proximity Read ↗

Single nucleotide polymorphism-based genome-wide chromosome copy change, loss of heterozygosity, and aneuploidy in Barrett's esophagus neoplastic progression.Semantic proximity Read ↗

Loss of heterozygosity on chromosome 17p predicts neoplastic progression in Barrett's esophagus.Semantic proximity Read ↗

Genetic Mechanisms of TP53 Loss of Heterozygosity in Barrett's Esophagus: Implications for Biomarker ValidationSemantic proximity Read ↗

Detection of Mutations in Barrett's Esophagus Before Progression to High-Grade Dysplasia or Adenocarcinoma.Semantic proximity Read ↗

Persistence of Human Papillomavirus, Overexpression of p53, and Outcomes of Patients After Endoscopic Ablation of Barrett's Esophagus.Semantic proximity Read ↗

Molecular biologic assessment of Barrett's esophagus.Semantic proximity Read ↗

Molecular alterations of Barrett's esophagus on microdissected endoscopic biopsies.Semantic proximity Read ↗

Determination of the frequency of loss of heterozygosity in esophageal adenocarcinoma by cell sorting, whole genome amplification and microsatellite polymorphisms.Semantic proximity Read ↗

p16(INK4a) lesions are common, early abnormalities that undergo clonal expansion in Barrett's metaplastic epithelium.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.