| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2014: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2013: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Outline of Final Research Achievements |
Acute hepatic injury in LEC rats is induced by oxidative stress due to an abnormal hepatic accumulation of copper. Cause of severe hepatitis is considered to be associated with hemolytic anemia. Vitamin E derivatives protect LEC rats from severe jaundice. During the process of the liver disease to hepatocellular carcinogenesis via acute hepatitis and chronic hepatitis in LEC rats, changes in expression of many genes were observed. More importantly, similar changes in expression of genes in the liver of LEC rats were shown to those in the progression of human liver tumors. Therefore, LEC rat is a useful animal model for investigation of target genes for tumor treatments of human hepatocellular carcinoma. Copper plays an important role in tumorigenesis, such as angiogenesis and metabolic regulation. A combination of treatment by copper-chelating agent and chemotherapy interacted synergistically and/or additively in induction of cell death in tumor cells in vitro.
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