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44 - Esophageal cancer

from Part 3.1 - Molecular pathology: carcinomas

Published online by Cambridge University Press:  05 February 2015

By
DuyKhanh P. Ceppa  and
Thomas A. D’Amico
Edited by
Edward P. Gelmann ,
Charles L. Sawyers  and
Frank J. Rauscher, III
DuyKhanh P. Ceppa
Affiliation:
Division ofhoracic Surgery, Indiana University School of Medicine, Indianapolis, IN, USA
Thomas A. D’Amico
Affiliation:
Division of horacic Surgery, Duke University Health System, Durham, NC, USA
Edward P. Gelmann
Affiliation:
Columbia University, New York
Charles L. Sawyers
Affiliation:
Memorial Sloan-Kettering Cancer Center, New York
Frank J. Rauscher, III
Affiliation:
The Wistar Institute Cancer Centre, Philadelphia
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Summary

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).

Type
Chapter
Information
Molecular Oncology
Causes of Cancer and Targets for Treatment
 , pp. 526 - 531
Publisher: Cambridge University Press
Print publication year: 2013

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