Endoscopic image demonstrates adenocarcinoma presenting as an erythematous exophytic mass occupying a portion of the lumen.
In this poorly differentiated adenocarcinoma, a sheet of pleomorphic cells lie underneath a largely unaffected squamous epithelium. Often in advanced cases, it may be difficult to distinguish squamous cell carcinoma from adenocarcinoma, as often, the metaplastic glandular epithelium may be completely effaced.
A higher power image demonstrating highly pleomorphic individual cells with obvious lack of cellular cohesion, growing in a sheet. In the non-diffuse type of gastric adenocarcinoma, glandular formation, but is often focal or absent in the diffuse type. All that reminds you of an adenocarinoma in this image are scattered signet ring cells.
Gastric brushings pre-operatively demonstrate pleomorphic cells in a loosely cohesive nature. Most of the aspirate contained debris.
Aspiration of a peri-esophageal lymph node several months post-operative shows numerous markedly enlarged round malignant cells with prominent nucleoli. Note the single cell nature of the cells, as in the original tumor.
Cell block of the node shows the same cells admixed with comparatively smaller normal lymphocytes.
These cells are strongly reactive for monoclonal CEA, confirming the impression of metastatic esophageal adenocarcinoma.
In the past, squamous cell carcinomas were the predominant malignancy in the esophagus, however, with the steady rise in incidence of esophageal adenocarcinomas, the rates of these two entities are now fairly equal. Unlike the development of squamous cell carcinoma is the esophagus, alcohol and smoking are not strongly associated risk factors. The majority of cases are attributed to the development of Barrett's mucosa, which is a complication of GERD. The risk of developing adenocarcinoma in the setting of Barrett's esophagus is about 1 cancer per 100 patient years of followup.1
The development of adenocarcinoma follows a sequence of esophagitis (GERD), intestinal metaplasia (Barrett's), dysplasia and finally carcinoma. There are molecular alterations associated with this sequelae, as Barrett's mucosa have higher proliferative activity and dysplastic cells have lost cell-cycle control. For example, overexpression and mutations of p53(tumor suppressor) have been identified, as well as amplication of c-ERB-B2 (oncogene) expression and nuclear translocation of B-catenin. In high-grade dysplasia, chromosomal abnormalities such as a chromosome 4 amplication is generally present.1
Generally affects patients over 40 (average age of diagnosis is 57), with a M:F ratio of 8:1, and incidence is four times higher in white men than black men. Presents with difficulty swallowing, weight loss, bleeding, chest pain. Symptoms related to GERD and sliding hiatal hernia such as heartburn, regurgitation and epigastric pain is present in less than half of diagnosed cases.
Resection +/- preop chemoradiation.
Poor. 14.5% 5-year survival in one large study.2 Resection of early cancers with limited invasion has a 5-year survival of 80%, however, most of these cancers are not identified until the disease is advanced.
1 Kumar V, Abbas AK, Fausto N. Robbins and Cotran Pathologic Basis of Disease. 7th Ed. Philadelphia, PA: Elsevier; 2005: 808-9.
2 Rosai, J. Rosai and Ackerman's Surgical Pathology. 9th Ed. Philadelphia, PA: Elsevier; 2004:624