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Peanut lectin-binding sites in polyps of the colon and rectum. Adenomas, hyperplastic polyps, and adenomas with in situ carcinoma.

Peanut lectin (PNA) has a specificity for the disaccharide beta-D-Gal-(1 leads to 3)-D-GalNac which is the purported antigenic determinant for the T blood group antigen (TAg). This TAg is considered the immediate precursor of the MN blood group substance. In normal colonic epithelium, PNA binds to the supranuclear (stalk) portion of epithelial cells. This corresponds to the detection of beta-DGal-(1 leads to 3)-D-GalNac in nascent oligosaccharide chains in the Golgi cisternae prior to addition of terminal sialic acid. Colonic carcinomas bind PNA in the "region" of the glycocalyx or in the apical portion of the cell, which represents incomplete glycoprotein synthesis. Eighty-two percent of tubular adenomas, 80% of villous adenomas, and 91% of adenomas with in situ cancer expressed PNA in a supranuclear distribution, reminiscent of normal colonic epithelium. This stalk distribution was seen in goblet cells. Twenty-five percent of tubular adenomas, 43% of villous adenomas and 60% of adenomas with in situ cancer (adenoma portion) expressed PNA in an apical cytoplasmic and/or glycocalyx pattern among nonmucinous columnar cells. In 80% of the cases, the in situ cancer itself expressed PNA in an apical cytoplasmic and/or glycocalyx pattern. Fetal and most colon cancer cells fail to produce mucin goblets and make incomplete glycoproteins. The cytologic localization of TAg by PNA corresponds to the cells' ability to produce mucin goblets. Most adenomas consist of goblet cells, localize TAg to the stalk, and probably make complete MN glycoprotein as does normal colonic epithelium. However, in adenomas, nonmucinous columnar cells localize TAg to the apical cytoplasm and/or glycocalyx region and represent incomplete blood group glycoprotein synthesis.

Adenoma↗

Differential activation of ornithine decarboxylase and tyrosine kinase in the rectal mucosa of patients with hyperplastic and adenomatous polyps.

Hyperplastic polyps are considered to be benign colonic lesions with almost no potential for malignant transformation. Recent reports have shown an increased association of hyperplastic polyps with adenomatous polyps and have advocated a full colonoscopy in patients who harbor hyperplastic polyps. Hyperproliferative mucosa is known to be associated with adenomatous polyps, but its relationship to hyperplastic polyps is unknown. In the present pilot study, it is determined whether a change in mucosal proliferative patterns is observed in patients who harbor only hyperplastic polyps or a history of hyperplastic polyps relative to those who harbor both hyperplastic polyps and adenomatous polyps by measuring ornithine decarboxylase and tyrosine kinase activity in macroscopically normal rectal mucosa. Fifteen patients had either adenomatous polyps proximally or harbored adenomatous polyps and hyperplastic polyps. Seven patients had hyperplastic polyps and 15 patients had a prior history of hyperplastic polyps with no polyps found during the current examination. The ornithine decarboxylase activity of the rectal mucosa with proximal adenomatous polyps or both polyp types was significantly higher than that of hyperplastic polyps, the history of hyperplastic polyps, or controls, and values for hyperplastic polyps and the history of hyperplastic polyps were similar to controls. On the other hand, tyrosine kinase activity in the rectal mucosa of patients with both or either polyp type was elevated without any significant difference between hyperplastic and adenomatous polyps. Thus, it is concluded that although increased ornithine decarboxylase activity in rectal mucosa suggests the presence of adenomatous polyps or a combination of adenomatous with hyperplastic polyps, increased tyrosine kinase activity suggests the presence of any type of polyp.

Colonic Polyps↗