Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2013: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2012: ¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
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Research Abstract |
DNA damage response genes in non-tumor lesions were associated with AP1 signaling which mediates the expression of many genes in CH-B-related HCC. In contrast, signal transducers and activators of transcription 1 and phosphatase and tensin homolog in non-tumor lesions were associated with early growth response protein 1 signaling that potentially promotes angiogenesis, fibrogenesis, and tumorigenesis in CH-C-related HCC. MicroRNAs were up- or down-regulated in cancerous tissue. These expression changes were confirmed as previously. Gene expression profiling of HCC and non-tumor lesions revealed the predisposing changes of gene expression in HCC. This approach has potential for the early diagnosis and possible prevention of HCC.
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