Literature DB >> 15040026

Expression of transforming growth factor-alpha and hepatitis B surface antigen in human hepatocellular carcinoma tissues and its significance.

Jing Zhang1, Wen-Liang Wang, Qing Li, Qing Qiao.   

Abstract

AIM: To evaluate the expression of transforming growth factor-alpha (TGF-alpha) and hepatitis B surface antigen (HBsAg) in human hepatocellular carcinoma (HCC) tissues and its significance.
METHODS: Seventy specimens of HCC tissues were detected by immunohistochemical method. Five specimens of normal human liver tissues were used as control.
RESULTS: The TGF-alpha positive expression rates in HCC and its surrounding tissues were 74.3%(52/70) and 88.1%(52/59), respectively. TGF-alpha positive granules were mainly in the cytoplasm and fewer existed on the karyotheca. The TGF-alpha positive expressing rate in well differentiated HCC was significantly higher than that in moderately and poorly differentiated HCC (P<0.05). The TGF-alpha positive expression also was observed in intrahepatic bile ducts (part of those were hyperplastic ducts). The HBsAg positive expression rates in HCC and its surrounding tissues were 21.4%(15/70) and 79.7%(47/59), respectively. HBsAg positive granules were in the cytoplasm, inclusion and on the karyotheca. There was a prominent positive correlation between TGF-alpha and HBsAg expression in HCC surrounding tissues (P<0.05, gamma=0.34). TGF-alpha was usually existed with HBsAg in regenerated and/or dysplastic liver cells. In the five normal liver tissues, TGF-alpha and HBsAg were not detectable in hepatocytes and bile ducts.
CONCLUSION: Hepatitis B virus infection is closely related with hepatocarcinogenesis. The overexpression of TGF-alpha in the liver seems to be associated with the regeneration of hepatocytes injured by HBsAg. The continued expression of TGF-alpha might lead to dysplasia of liver cells and development of HCC. Furthermore, TGF-alpha might play a role in morphogenesis and regeneration of intrahepatic bile ducts.

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Year:  2004        PMID: 15040026      PMCID: PMC4726998          DOI: 10.3748/wjg.v10.i6.830

Source DB:  PubMed          Journal:  World J Gastroenterol        ISSN: 1007-9327            Impact factor:   5.742


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