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The Annals of Thoracic Surgery, Vol 57, 598-603, Copyright © 1994 by The Society of Thoracic Surgeons
DR Jones, AG Davidson, CL Summers, GF Murray and DC Quinlan
Diagnosis of the neoplastic progression in Barrett's esophagus using the
histologic classification of dysplasia is frequently difficult. The tumor
suppressor protein p53, when mutated, confers a promoter effect on cell
growth. The purpose of this study was to evaluate the applicability of p53
as an intermediate biomarker of malignancy in Barrett's esophagus. Archival
analysis of 100 biopsy specimens of Barrett's esophagus and 10 esophageal
adenocarcinomas were compared with 35 chronic esophagitis biopsy specimens.
Immunocytochemistry using an anti-p53 monoclonal antibody was performed and
elevated immunoreactivity quantitated microscopically. Data were analyzed
using a logistic regression model. Significant p53 immunoreactivity
occurred as follows: chronic esophagitis (0%), Barrett's esophagus without
dysplasia (10%), with low-grade dysplasia (60%), with high-grade dysplasia
(100%), and adenocarcinoma (70%). All cases of Barrett's esophagus were
significantly immunoreactive when compared with the chronic esophagitis
cases (p = 0.001). There was an increase in p53 immunoreactivity as the
histologic classification progressed toward adenocarcinoma (p = 0.001).
Progression to high-grade dysplasia may be predicted based on p53
immunoreactivity. These findings suggest a role for p53 as an intermediate
biomarker in Barrett's esophagus.
ARTICLES
Potential application of p53 as an intermediate biomarker in Barrett's esophagus
Department of Surgery, West Virginia University School of Medicine, Morgantown 26506-9238.
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