Adenocarcinomas of the colon arise from
adenomatous polyps. We hypothesized that
sucrase-
isomaltase (SI), a
glycoprotein hydrolase, found in normal small intestine, fetal colon, and colon
carcinomas is a marker associated with progression of
adenomatous polyps with dysplasia to
adenocarcinomas. To examine this hypothesis, we performed immunostaining using a polyclonal antihuman SI antibody in 32
adenomatous polyps with varying degrees of dysplasia. In addition,
sucrase enzyme activity was determined in three sets of simultaneously harvested
polyps,
cancer, and adjacent normal mucosa from the same patient. All severely dysplastic
polyps (6/6) exhibited SI staining. Most
polyps (85%) with 3+ staining (i.e., greater than 10% of
polyp positive for SI) had severe dysplasia, whereas those with mild dysplasia had either 1% to 5% staining or no staining in 95% of the cases. These data indicate that the extent of SI immunostaining in
polyps correlates with the degree of dysplasia (p = 0.0001).
Sucrase-
isomaltase activity in the
polyps was 18.1 +/- 1.8 mU/mg (mean +/- SD); in adjacent
carcinoma SI activity was 29.1 +/- 1.8 mU/mg. Adjacent mucosa showed no activity in all cases. In summary, our results suggest that SI expression correlates with the progression of dysplastic
adenomatous polyps to
carcinoma.
Sucrase-
isomaltase expression may be useful as a
clinical marker to improve our prognostic capabilities in patients with dysplastic lesions of the colon, that is,
inflammatory bowel disease.