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Comparison of the expression of β‐catenin in hepatocellular carcinoma in areas with high and low levels of exposure to aflatoxin B1
Author(s) -
Chen Ban Ke,
Singh Harjit,
Krishnan R.,
Fong Seow Heng
Publication year - 2004
Publication title -
journal of surgical oncology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.201
H-Index - 111
eISSN - 1096-9098
pISSN - 0022-4790
DOI - 10.1002/jso.20051
Subject(s) - hepatocellular carcinoma , aflatoxin , medicine , immunohistochemistry , beta catenin , hepatitis b virus , beta (programming language) , catenin , pathology , cancer research , gene , virus , virology , biology , wnt signaling pathway , biochemistry , food science , computer science , programming language
Background and Objectives Previous studies showed that the frequency of β‐catenin mutation was different in mice when induced by different chemicals. The aim of this study is to compare the expression of β‐catenin and p53 in hepatocellular carcinoma (HCC) from areas with exposure to high and low levels of aflatoxin B1 (AFB1). Methods Thirty‐five and twenty HCC samples from Guangxi and Malaysia, respectively, were studied. The expression of β‐catenin and p53 was determined by immunohistochemistry. Results The overexpression of β‐catenin was detected in 65.7% of HCC tissues and 37.1% in adjacent liver tissues samples from Guangxi, China. Similarly, overexpression of β‐catenin was also detected in 60.0% of HCC tissues and in 35.0% of adjacent liver tissues samples from Malaysia. The overexpression of p53 was detected in 42.9% of HCC specimens from Guangxi and in 25.0% of HCC specimens from Malaysia. There was a relationship between the expression of β‐catenin and hepatitis B virus (HBV) infection in the adjacent liver tissues in Guangxi, and between the expression of β‐catenin and p53 in HCC tissues in Malaysia. Conclusions The differences in the exposure to AFB1 did not affect the overexpression of β‐catenin in the development of HBV‐associated HCC. J. Surg. Oncol. 2004;86:157–163. © 2004 Wiley‐Liss, Inc.