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


METHODS
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).


RESULTS
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 part of the β-catenin helices.


CONCLUSIONS
If these β-catenin coils are unrelated to an abnormal nuclear distribution at the base of the dysplastic glands, the rational explanation might be that the helices highlight changes taking place in the cytoplasm of affected glandular cells.


CONCLUSIONS
According to some authors, mutations in the β-catenin genes are always associated with a morphologically neoplastic course. It is herein proposed that β-catenin helices in duodenal adenomas might uncover a novel cytoplasmic phenomenon ensuing during the adenoma-carcinoma pathway.
Department of Pathology, Karolinska University Hospital, Stockholm, Sweden Carlos.Rubio@ki.se.
Carlos A
CA
Rubio
Department of Pathology, Karolinska University Hospital, Stockholm, Sweden.
Ann
A
Kaufeldt
Department of Pathology, Karolinska University Hospital, Stockholm, Sweden.
Rafat
R
Kohan
Department of Pathology, Karolinska University Hospital, Stockholm, Sweden.
Mariko
M
Ushoida
Department of Pathology, Karolinska University Hospital, Stockholm, Sweden.
Erika
E
Ezelius
Department of Pathology, Karolinska University Hospital, Stockholm, Sweden.
San
S
Björk
Department of Pathology, Karolinska University Hospital, Stockholm, Sweden.
Jenny
J
Lindahl
D000236:Adenoma / Q000737:chemistry* / Q000473:pathology; D011125:Adenomatous Polyposis Coli / Q000737:chemistry* / Q000473:pathology; D002467:Cell Nucleus / Q000737:chemistry; D003593:Cytoplasm / Q000737:chemistry*; D004379:Duodenal Neoplasms / Q000737:chemistry* / Q000473:pathology; D006801:Humans; D051176:beta Catenin / Q000032:analysis* / Q000502:physiology
C495270:CTNNB1 protein, human; D051176:beta Catenin
Duodenum adenomas; adenomas; cytoplasmic helices; β-catenin