|
|
||||||||
Department of Cardiothoracic Surgery, The University of Southern California, Los Angeles, California
* Address correspondence to Dr DeMeester, Department of Cardiothoracic Surgery, The University of Southern California, Los Angeles, CA 90033 (Email: sdemeester@surgery.usc.edu).
Presented at the Minimally Invasive Thoracic Surgery Summit, New York, NY, June 8–9, 2007.
| The first 300 words of the full text of this article appear below. |
Adenocarcinoma of the esophagus has the fastest rising incidence of any cancer in the United States and develops as a consequence of chronic gastroesophageal reflux disease [1]. Barretts esophagus is the precursor lesion from which adenocarcinoma develops, and surveillance programs have led to the detection of high-grade dysplasia and early-stage adenocarcinoma in an increasing number of patients. High-grade dysplasia and intramucosal adenocarcinoma, although potentially lethal, are both curable lesions in most patients [2–4]; however, cure is dependent on complete removal of the neoplastic tissue. Until recently, this was reliably accomplished only with esophagectomy, but new technologies have been developed that allow endoscopic mucosal resection and ablation with preservation of the esophagus. The aim of this article is to explore current options for the management of Barretts high-grade dysplasia and intramucosal adenocarcinoma.
The first fundamental issue in the treatment of high-grade dysplasia and intramucosal adenocarcinoma is to cure the patient of the disease. Patients with only high-grade dysplasia are uniformly cured with esophagectomy because invasive cancer has not developed and will not develop after removal of all of the Barretts mucosa. However, a number of surgical series have demonstrated that despite extensive pre-resection biopsies, in 30% to 50% of patients thought only to have high-grade dysplasia, the resected specimen will in fact have an invasive cancer [5, 6]. In the absence of a visible ulcer or nodule on endoscopy, these occult adenocarcinomas have always been limited to the mucosa in our experience [5].
In contrast, if a lesion of any sort is seen endoscopically within the columnar-lined portion of the esophagus, that lesion is at high risk to be a cancer. Further, any visible lesion that on biopsy shows adenocarcinoma cannot be assumed to be limited to the mucosa, regardless of the size
This article has been cited by other articles:
![]() |
H. Pohl, B. Sirovich, and H. G. Welch Esophageal Adenocarcinoma Incidence: Are We Reaching the Peak? Cancer Epidemiol. Biomarkers Prev., June 1, 2010; 19(6): 1468 - 1470. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. A. Ajani Gastroesophageal Cancers: Progress and Problems J Natl Compr Canc Netw, October 1, 2008; 6(9): 813 - 814. [Abstract] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| ANN THORAC SURG | ASIAN CARDIOVASC THORAC ANN | EUR J CARDIOTHORAC SURG |
| J THORAC CARDIOVASC SURG | ICVTS | ALL CTSNet JOURNALS |