PMID: 25750294Mar 10, 2015Paper

β-catenin Helices in the cytoplasm of sporadic and FAP duodenal adenomas

Anticancer Research
Carlos A RubioJenny Lindahl

Abstract

Initiation and progression in conventional adenomas is triggered by deregulation of Wnt/β-catenin signaling. In the absence of Wnt signal (off-state), β-catenin prevents phosphorylation of glycogen synthase kinase (GSK)-3β leading to aberrant nuclear accumulation in human tumors. While investigating the nuclear expression of β-catenin in biopsies from duodenal adenomas, we observed a non-previously reported phenomenon, namely the presence of β-catenin cytoplasmic helices (coils). Sections from 39 biopsies were immunostained with β-catenin: 25 from duodenal adenomas and the remaining 14 had normal duodenal mucosa (n=11) or polypoid gastric duodenal metaplasia (n=3). Eighteen out of the 25 duodenal adenomas (72%) showed β-catenin helices; in contrast, none of the 33 control biopsies (including those with normal duodenal mucosa, gastric duodenal metaplasia and normal mucosa adjacent to 19 adenomas) showed β-catenin helices (p<0.05). The review of diagnostic H&E-stained sections and of β-catenin-stained nuclei revealed that the dysplastic nuclei were arranged in a picket fence-like fashion along the basement membrane of the glands and not as loops within the dysplastic glands; the nuclei of the dysplastic glands were not forming pa...Continue Reading

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