| Budget Amount *help |
¥156,000,000 (Direct Cost: ¥120,000,000、Indirect Cost: ¥36,000,000)
Fiscal Year 2014: ¥29,120,000 (Direct Cost: ¥22,400,000、Indirect Cost: ¥6,720,000)
Fiscal Year 2013: ¥30,550,000 (Direct Cost: ¥23,500,000、Indirect Cost: ¥7,050,000)
Fiscal Year 2012: ¥31,980,000 (Direct Cost: ¥24,600,000、Indirect Cost: ¥7,380,000)
Fiscal Year 2011: ¥31,720,000 (Direct Cost: ¥24,400,000、Indirect Cost: ¥7,320,000)
Fiscal Year 2010: ¥32,630,000 (Direct Cost: ¥25,100,000、Indirect Cost: ¥7,530,000)
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| Outline of Final Research Achievements |
Persistent inflammation is one of the major causes of onset of cancer development. Tumor virus infection plays significant roles in the process together with functions of virus-coded oncogenes. Hepatitis C virus (HCV) infection, despite of absence of a definitive viral oncogene, causes hepatocellular carcinoma (HCC) at high risk. Prevalence of the development of HCC by HCV infection is high when ALT level is kept high. This suggests that inflammatory cytopathic effect by HCV infection plays a role in cancer development. By analyzing HCV infected cells, presence of 2 new pathways were disclosed from which various cytokines and chemokines were produced; by cross talk with HCV infected hepatocytes and liver stellate cells, and by function of Apobec1 induced under aberrant physiological condition. These 2 mechanisms may be involved in altering inflammatory response that promotes cancer spiral.
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