1990 Fiscal Year Final Research Report Summary
Hepatocacinogenesis in the liver of alcoholic cirrhosis
| Project/Area Number |
01480224
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Gastroenterology
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| Research Institution | Kansai Medical University (1990)
Toyama Medical and Pharmaceutical University (1989) |
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Principal Investigator |
INOUE Kyoichi Kansai Medical University, the third department of internal medicine, Professor, 医学部・第三内科, 教授 (10018335)
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| Co-Investigator(Kenkyū-buntansha) |
HIGUCHI Kiyohiro Toyama Medical and Pharmacentical University, the third department of internal m, 附属病院, 講師 (00135021)
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| Project Period (FY) |
1989 – 1990
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| Keywords | chronic hepatitis / liver cirrhosis / alcoholic liver injury / Hepato cellular carcinoma / DNA methylation / C-myc |
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| Research Abstract |
In order to investigate how chronic liver diseases, including liver cirrhosis and chronic hepatitis, are associated with hepatocarcinogenesis in terms of gene alteration, the methylation states of the c-myc and c-Ki-ras genes were examined in 34 liv13EA\ : er tissues from patiens with HCC, 18 HCC tissues and 31 control liver tissues. The methylation states were analyzed by the Southern hybridization method using the restriction endonuclease isoschizomers MspI and HpaII.The CCGG sites at the second exon of the c-myc gene tended to be more extensively hypomethylated both in chronic liver disease and in non-tumor tissues than in control livers. Whereas the CCGG sites of the c-Ki-ras, and the third exon of the c-myc gene tended to be hypomethylated13EA\ : only in HCC tissues in comparison with other tissue groups. These results suggest that chronic liver disease may be situated between normal liver and HCC based on the state of DNA methylation and associated with the development of HCC through hypom13EA\ : ethylation of the c-myc and/or c-Ki-ras gane. In relation to alcohol dringking hypomethylation and demethylation of c-myc were more frequently abserved. From these results it was concluded that alcohol drinking influences on the hepatocarcinogenes i13EA\ : s by hypomethylation and demethylation of oncogenes.
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