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Wiley InterScience

Diseases of the Esophagus

Diseases of the Esophagus

Volume 20 Issue 1, Pages 36 - 41

Published Online: 5 Jan 2007

© 2010 International Society for Diseases of the Esophagus


The Official Journal of the International Society for Diseases of the Esophagus (ISDE) and the European Society of Esophagology (ESE)
International Society for Diseases of the Esophagus
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Original article
Is intestinal metaplasia a necessary precursor lesion for adenocarcinomas of the distal esophagus, gastroesophageal junction and gastric cardia?
P. Chandrasoma, K. Wickramasinghe, Y. Ma, T. DeMeester
The Departments of Surgical Pathology and Foregut Surgery, Keck School of Medicine and University of Southern California, Los Angeles, California, USA
Address correspondence to: Para Chandrasoma, MD, Department of Surgical Pathology, LAC+USC Medical Center, GH 16-905, 1200 N. State Street, Los Angeles, CA 90033. Email: ptchandr@usc.edu
Copyright © 2007 The Authors
Journal compilation © 2007 The International Society for Diseases of the Esophagus
KEYWORDS
adenocarcinoma • Barrett's esophagus • gastric cardia • intestinal metaplasia

ABSTRACT

SUMMARY. Adenocarcinoma of the distal esophagus and gastroesophageal junction are believed to arise in Barrett's esophagus with intestinal metaplasia. Whether adenocarcinoma can arise in columnar lined esophagus without intestinal metaplasia is in doubt. Whether adenocarcinoma of the gastric cardia arises in intestinal metaplasia of the gastric cardia is also in doubt. We aim to evaluate the relationship of size and stage of adenocarcinoma of the distal esophagus, gastroesophageal junction and gastric cardia to intestinal metaplasia and other types of columnar epithelium. Seventy-four patients who had esophagogastrectomy for adenocarcinomas in this region were examined histologically to assess the frequency of residual intestinal metaplasia in the surrounding epithelium. Tumors without residual intestinal metaplasia were evaluated for the presence of other columnar epithelia and correlated with tumor size and stage. Cardiac mucosa was present around all tumors. Residual intestinal metaplasia was present in 48 (65%) tumors, including 33/38 (87%) distal esophageal, 10/25 (45%) junctional and 5/11 (45%) gastric cardia tumors. The prevalence of intestinal metaplasia was 100% in all tumors that were less than 1 cm in maximum diameter and all intramucosal tumors. The prevalence of residual intestinal metaplasia decreased with increasing tumor size and stage. These data strongly support the contention that adenocarcinomas of this region, including those in the gastric cardia, arise in intestinal metaplastic epithelium. The absence of residual intestinal metaplasia in larger tumors is the result of tumor overgrowing the intestinal metaplasia from which it arose.


DIGITAL OBJECT IDENTIFIER (DOI)
10.1111/j.1442-2050.2007.00638.x About DOI

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