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HOME > J Pathol Transl Med > Volume 42(4); 2008 > Article
Original Article Correlation of the Nuclear beta-catenin Expression with the Clinicopathological Parameters of Hepatocellular Carcinoma.
Hyoung Jong Kwak, Ha Na Choi, Sung Ho Hwang, Keum Ha Choi, Ho Sung Park, Kyu Yun Jang, Myoung Ja Chung, Myoung Jae Kang, Dong Geun Lee, Woo Sung Moon
Journal of Pathology and Translational Medicine 2008;42(4):208-214
DOI: https://doi.org/
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Department of Pathology, Chonbuk National University, Medical School, Institute for Medical Sciences and Center for Healthcare Technology Development, Jeonju, Korea. mws@chonbuk.ac.kr

Hepatocellular carcinoma (HCC) is the most common primary malignant tumor of the human liver. However, the molecular changes and mechanisms that regulate the development and progression of HCC remain unclear. Beta-catenin is known as a multi-functional protein that acts as a regulator of the cadherin-mediated cell-cell adhesion system and also in the Wingless/Wnt signal transduction pathway. The aim of this study was to investigate the expression of beta-catenin and its possible role in HCC.
We investigated the expression of beta-catenin, Ki-67, TP53, alpha-smooth muscle actin and CD34 by performing immunohistochemical staining for 61 specimens of HCC and their adjacent non-tumorous tissue. We also examined the relationship between the nuclear expression of beta-catenin and the clinicopathologic parameters.
The altered expression of beta-catenin was not detected in the nontumorous liver tissue. The nuclear expression of beta-catenin was observed in approximately 16% (10/61) of the HCC specimens. Double immunohistochemical staining for beta-catenin and E-cadherin showed a close relationship between nuclear translocation of beta-catenin and the loss of the membranous E-cadherin expression. Significant correlation was found between the nuclear translocation of beta-catenin and the tumor size, tumor necrosis and the presence of microvessel invasion and intrahepatic metastasis (p<0.05).
This data indicates that nuclear translocation of beta-catenin could play a role in the growth and progression of HCC.

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