Mechanism of hepatocarcinogenesis by mitochondria DNA analysis and its clinical signifianoe

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The patterns of point mutation and deletion of mitochondria DNA in cancerous tissues and noncancerous hepatic tissues in patients with hepatocellular carcinoma and without the carcinoma. Although the number of such changes were limited in normal liver, the number of the changes were significantly higher in the carcinoma tissues and noncancerous hepatic tissues in patients with hepatocellular carcinoma. The number of the changes increased as the differentiation. Persistent chronic hepatitis C affects the mitochondria DNA because the number of the changes increased as the progression of hepatitis. Although the degree of hepatic fibrosis was not correlated with the changes of point mutation and deletion of mitochondria DNA, the prevalence of muticentric carcinogenesis was correlated with the changes. These findings suggest that the number of the changes was correlated with the potential of hepatocarcinogenesis. The prevalence of multicentric carcinogenesis was correlated with platelet count In patients with low platelet count less than 10^4/mm^3, it is necessary to pay attention of the development of multicentric carcinogenesis. Some patients with intrahepatic cholangiocarcinoma were infected with hepatitis C, indicating that hepatitis C infection. affect the development of intrahepatic cholangiocarcinoma. The evaluation of the potential of hepatocarcinogenesis is useful to detect the carcinoma.