Fucosyltransferase-producing sialyl Lea and sialyl Lex carbohydrate antigen in benign and malignant gastrointestinal mucosa

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Abstract
Background. Sialyl Lea antigen and sialyl Lex antigen are cancer‐associated carbohydrate antigens. Previous immunohistologic and immunochemical studies have shown that these antigens are preferentially expressed in gastric cancer and colonic cancer and that they possibly are related to the metastatic potential of the cancer cells. The biosynthesis of these antigens is completed by fucosyltransferases, but it has not been reported how fucosyltransferases control the expression of these carbohydrate antigens concerning the invasive potential of the cancer. Methods. The authors established an assay system for measuring the activity of α1 → 4 fucosyltransferase (sialyl Lea synthase) and α1 → 3 fucosyltransferase (sialyl Lex synthase) with a high‐pressure liquid chromatography system (HPLC). The activity was measured in various parts of normal and cancerous gastric and colonic tissue and compared with the expression of sialyl Lea, sialyl Lex, Lea, and Lex antigens determined in a solid‐phase enzyme‐linked immunosolvent assay (EIA). Results. Sialyl Lea synthase was detected in most normal or malignant mucosa of gastric and colonic tissues, regardless of anatomic locations. Sialyl Lex synthase activity generally was low in the normal gastric mucosa, whereas the activity was higher in 77% (7 of 9) of gastric cancer tissues than in corresponding normal tissues with enhanced expression of sialyl Lex antigen in most patients (5 of 7). In the large intestine, the activity of sialyl Lea synthase and sialyl Lex synthase was correlated. Although enhanced expression of sialyl Lex in colonic cancer was observed in 86% (12 of 14) of all patients, concomitant higher sialyl Lex synthase activity than that in normal tissue was observed in only 58% (7 of 12) of patients. Conclusions. The expression of sialyl Lea and sialyl Lex antigens in the stomach and the colon was not controlled solely by fucosyltransferases but by a more complicated system involving other glycosyltransferases. Cancer 1994; 73:1552–61.

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