Fig.15.7C ).Onlyafewareasofpalesquamousmucosaremainwithinthepredominantlymetaplastic,reddishmucosaofthedistalesophagus.(C)HistologicappearanceofthegastroesophagealjunctioninBarrettesophagus.Notethetransitionbetweenesophagealsquamousmucosa(lower right) andmetaplasticmucosacontaininggobletcells(upper). (Endoscopic image courtesy of Dr. Ira Hanan, The University of Chicago, Chicago, Illinois.) http://ebooksmedicine.net
Two morphologic variants account for a majority of esophageal cancers: adenocarcinoma and squamous cell carcinoma. Worldwide, squamous cell carcinoma is more common, but adenocarcinoma is on the rise. Other rare tumors are not discussed here.
Esophageal adenocarcinoma typically arises in a background of Barrett esophagus and long-standing GERD. Risk for development of adenocarcinoma is greater in patients with documented dysplasia and in those who use tobacco, are obese, or who have had previous radiation therapy. In the United States, esophageal adenocarcinoma occurs most frequently in whites and shows a strong gender bias, being seven times more common in men than in women. However, the incidence varies by a factor of 60-fold worldwide, with rates being highest in Western countries, including the United States, the United Kingdom, Canada, Australia, and the Netherlands, and lowest in Korea, Thailand, Japan, and Ecuador. In countries where esophageal adenocarcinoma is more common, the incidence has increased markedly since 1970, more rapidly than for almost any other cancer. As a result, esophageal adenocarcinoma, which represented less than 5% of esophageal cancers before 1970, now accounts for half of all esophageal cancers in some Western countries, including the United States.
Molecular studies suggest that the progression of Barrett esophagus to adenocarcinoma occurs over an extended period through the stepwise acquisition of genetic and epigenetic changes. This model is supported by the observation that epithelial clones identified in nondysplastic Barrett metaplasia persist and accumulate mutations during progression to dysplasia and invasive carcinoma. Chromosomal abnormalities and TP53 mutation are often present in the early stages of esophageal adenocarcinoma. Additional genetic changes and inflammation are thought to contribute to tumor progression.
(Fig.
15.11A ).Whileearlylesionsmayappearasflatorraisedpatchesinotherwiseintactmucosa,latertumorsmayformlargeexophyticmasses,infiltratediffusely,orulcerateandinvadedeeply.Onmicroscopicexamination,Barrettesophagusfrequentlyispresentadjacenttothetumor.Tumorstypicallyproducemucinandformglands(
Fig.15.11B
Fig. 15.11 Esophagealadenocarcinoma.(A)Adenocarcinomausuallyoccursdistallyand,asinthiscase,ofteninvolvesthegastriccardia.(B)Esophagealadenocarcinomagrowingasback-to-backglands.
Patients most commonly present with pain or difficulty in swallowing, progressive weight loss, chest pain, or vomiting. By the time signs and symptoms appear, the tumor usually has invaded submucosal lymphatic vessels. As a result of the advanced stage at diagnosis, the overall 5-year survival rate is less than 25%. By contrast, 5-year survival approximates 80% in the few patients with adenocarcinoma limited to the mucosa or submucosa.