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KMID : 0614619920240030535
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Korean Journal of Gastroenterology
1992 Volume.24 No. 3 p.535 ~ p.546
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Dynamic expressions of proto-oncogenes in Chronic Hepatitis, Liver Cirrhosis and Hepatocellular Carcinoma
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이동후
박성수/신동호/노임환/권기운/유병무/강경원/이중달
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Abstract
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Liver cell replication is known to invlove a sequential activation of proto-oncogenes including c-myc and c-Ha-ras. These positive regulations of proliferative signal are thought to be counterbalanced by growth-constraining tumor suppressor
genes.
During the genesis of liver cell carcinoma both the qualitative and the quantitative changes in growth promoting proto-oncogenes were elucidated in animal models, And also mutational inactivation of suppressor genes such as p53 liberates the cell
from
the negative regulation, resulting in deregulated growth. Since there is strong corrleation between persistence of hepatitis B virus infection and the development of hepatocellular carcinoma, we attempted to investigate the dynamic changes of
proto-oncogenes and tumor suppressor gene in HBV DNA positive liver tissues among 8 chronic persistent hepatitis, 9 chronic active hepatitis, 12 liver cirrhosis, and 13 hepatocellular carcinomas, employing in situ hybridization and
immunohistochemistry.
Comparing to chronic hepatitis and liver cirrhosis, c-myc overexpression was heterogeneously distributed in hepatocellular carcinoma. Intensity of c-Ha-ras expressions was strong in hepatocellular carcinomas, liver cirrhosis, chronic active
hepatitis,
and chronic persistent hepatitis in orders. Whereas wild type of p53 was immunohistochemically detectable in all of the cases investigated, mutant gene deleted 9 amino acids adjacent to carboxyl terminal revealed in 37.5% of dchronic persistent
hepatitis, 33.3% of chronic active hepatitis or liver cirihosis, and 46.2% of hepatocelluar carcinomas, respectively. In conclusion, these data support that enhanced expression of positive growth promoting proto-oncogenes is related with
regeneration of
the liver and progression of tumor cell growth. And The various mutant genes of tumor suppressor might be emerged during the persistent replication of hepatocytes in HBV DNA positive chronic liver diseases, in cooperation with proto-oncogenes,
eventually resulting in development of hepatocellular carcinoma. This means, in turn, that HBV-related chronic liver diseases retained a malignant potential.
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KEYWORD
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