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from Part 3.1 - Molecular pathology: carcinomas
Published online by Cambridge University Press: 05 February 2015
Introduction
The incidence of esophageal carcinoma is increasing, with the incidence of esophageal adenocarcinoma increasing faster than any other malignancy in the United States (1). Estimates for 2013 predict 17990 new cases of esophageal carcinoma, accounting for 15210 deaths (2). While the incidence of squamous cell carcinoma of the esophagus is decreasing by 3.6% per year, the incidence of adenocarcinoma of the esophagus is increasing by 2.1% per year (3).
Adenocarcinoma of the esophagus
The most important risk factor for the development of adenocarcinoma of the esophagus is the presence of columnar-lined esophagus (CLE), or Barrett's esophagus (4). CLE is present in approximately 10% of patients with gastroesophageal reflux (5) and it is estimated that up to 90% of all esophageal adenocarcinomas arise from CLE. The presence of CLE is associated with an increased risk of adenocarcinoma by a factor of between 30 and 125 (4,6).
LOH data
Loss-of-heterozygosity (LOH) studies of specific oncogenes involved in the neoplastic progression of the esophagus have identiied important loss of function atmultiple sites (7–11). In a study performed on 23 cases of adenocarcinoma of the esophagus the chromosomal abnormalitieswith the highest incidence of LOH were 3p (64%), 5q (45%), 9p (52%), 11p (61%), 13q (50%), 17p (96%), 17q (55%), and 18q (70%; 71).
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