1990 Volume 21 Issue 1 Pages 53-63
Esophageal carcinoma in rats was experimentally induced with the oral administration of N-methylbenzylamine and sodium nitrate. In addition to the conventional morphological findings, lectin binding patterns were examined by light and transmission electron microscopy employing horseradish peroxidase (HRP)-labeling methods, and compared among the normal esophageal epithelium, papilloma, dysplasia, carcinoma in situ and invasive carcinoma. Lectins used were concanavalin A (Con A), wheat germ agglutinin (WGA), Ricinous comnaunis agglutinin (RCA), peanut agglutinin (PNA), soybean agglutinin (SBA), Dolichos biflorus agglutinin (DBA), Ulex europeus agglutinin-1 (UEA-1). By light microscopy, ConA, W GA and RCA stained positively the cells of all layers of the normal esophageal epithelium, and those of papilloma, dysplasia, carcinoma in situ and invasive carcinoma as well. PNA stained positively the cells in the middle layer of the normal esophageal epithelium and papilloma. However, PNA stained positively all the cells of dysplasia and part of the cells of carcinoma in situ and invasive carcinoma. SBA and UEA-1 stained positively the cells in the middle and superficial layers of the normal epophageal epithelium and papilloma. In dysplasia and carcinoma in situ but not in invasive carcinoma, SBA and UEA-1 appeared to lose their bindings. DBA binding was negative in all the tissues. By electron microscopy, lectin bindings were proved to be positive mainly in the plasma membrane and Golgi membranes. In addition, ConA binding was positive also in nuclear membranes and endoplasmic reticulum. By comparing the progression of carcinoma with the change in lectin binding patterns, especially when stained with PNA, SBA and UEA-1, it is possible to estimate that dysplasia is a precancerous condition in the esophageal epithelium. Therefore, PNA seems to be especially useful for diagnosing the esophageal carcinoma.
