The incidence of esophageal cancer in the United States is approximately 13,000 cases per year. Adenocarcinoma of the esophagus (EAC) is the fastest growing solid malignancy, and it is now more frequent than esophageal squamous cell carcinoma (ESCC) in the United States. Although resection offers the best chance for cure, most patients who present with symptoms already have systemic disease and are incurable. The most important prognostic factor for esophageal cancer remains the stage of disease at the time of diagnosis. Currently, the best strategy for improving survival is early diagnosis followed by resection. Neoadjuvant chemoradiation is being used increasingly in the treatment of locally advanced disease. However, despite improvements in operative technique and postoperative care, the overall 5-year survival remains less than 15 percent, highlighting the need for novel diagnostic and treatment modalities.
Esophageal Squamous Cell Carcinoma
Nutritional deficiencies, including low levels of vitamins A, C, and riboflavin as well as minerals such as selenium, molybdenum, and zinc contribute to the pathogenesis of ESCC. High levels of nitrates and nitrites, found in pickled and preserved foods, are converted to N-nitrosamines and have been associated with ESCC. Several studies have linked alcohol and tobacco use with the development of esophageal cancer, and one study found ethanol to be associated with nearly 80 percent of esophageal cancers.1 Other predisposing conditions include long-standing achalasia, caustic injury, tylosis, and Plummer–Vinson syndrome.
Barrett metaplasia, and specifically intestinal-type columnar mucosa, is the precursor lesion to EAC. Microscopically, columnar epithelium is seen with mucosal glands that contain intestinal goblet cells (Fig. 16-1A). On endoscopy, Barrett mucosa appears as red, velvety areas between smooth, pale esophageal squamous mucosa (Fig. 16-2A). After the squamous epithelium is injured chronically by reflux, there is a metaplastic change to a columnar epithelium. With further injury and multiple genetic changes, progression occurs in a metaplasia–dysplasia–adenocarcinoma sequence.
Photomicrograph. A. Barrett mucosa showing columnar epithelium with mucosal glands containing intestinal goblet cells. B. High-grade dysplasia with nuclear atypia.
Endoscopic view. A. Barrett metaplasia with tongues of red, velvety mucosa extending above the gastroesophageal junction. B. A 5-cm distal esophageal adenocarcinoma extending to the gastroesophageal junction and ...