Dysregulation of ?-Catenin Expression Correlates With Tumor Differentiation in Pancreatic Duct Adenocarcinoma

Background: β-Catenin functions as an integral part of the E-cadherin/catenin adhesion complex to maintain epithelial cell integrity. β-Catenin also functions as part of the Wnt signal transduction pathway to transmit growth-promoting signals to the nucleus via its interactions with Tcf/Lef transcri...

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Bibliographic Details
Published inAnnals of surgical oncology Vol. 10; no. 3; pp. 284 - 290
Main Authors Lowy, Andrew M., Fenoglio-Preiser, Cecilia, Kim, On Ja, Kordich, Jennifer, Gomez, Ana, Knight, Joy, James, Laura, Groden, Joanna
Format Journal Article
LanguageEnglish
Published New York Springer Nature B.V 01.04.2003
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Summary:Background: β-Catenin functions as an integral part of the E-cadherin/catenin adhesion complex to maintain epithelial cell integrity. β-Catenin also functions as part of the Wnt signal transduction pathway to transmit growth-promoting signals to the nucleus via its interactions with Tcf/Lef transcription factors. Previous reports have demonstrated altered β-catenin expression in numerous tumor types; however, reports regarding β-catenin expression in pancreatic cancer have been conflicting. Methods: β-Catenin expression was examined in 10 pancreatic cancer cell lines by Western and Northern analysis and by immunofluorescence. Expression was also examined by immunohistochemistry in 57 primary pancreatic cancers and 7 foci of carcinoma-in-situ. Results: Reduced expression of β-catenin was observed in 4 of 10 pancreatic cancer cell lines. Reduced membranous expression was noted in 32 pancreatic cancers (56%) and correlated with loss of tumor differentiation. Nuclear β-catenin expression was identified in two tumors (4%). β-Catenin expression was present in all seven foci of carcinoma-in-situ; however, nuclear expression was predominant in four of the seven cases. Conclusions: Alterations in β-catenin expression are common in pancreatic cancer; however, signaling and adhesion functions may be perturbed at different times during tumor progression. Therefore, dysregulation of β-catenin may contribute to the development and progression of this disease through distinct mechanisms.
ISSN:1068-9265
1534-4681
DOI:10.1245/ASO.2003.05.003