| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2014: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Outline of Final Research Achievements |
Chronic liver inflammation and hepatic regeneration induced by host cellular immune responses can increase the risk of HCC development. To investigate the mechanisms of fibrocarcinogenesis in PBC, we studied 45 PBC not developing HCC (Stage I: 16, II:13, III:13, IV:3) and 6 PBC developing HCC. We performed inmmunohistochemical analysis using our phospho-Smad3 antibodies. As PBC livers progressed from chronic hepatitis through cirrhosis to HCC, hepatocytic linker phosphorylated Smad3 (pSmad3L) increased with fibrotic stage and C-terminal phosphorylated Smad3 (pSmad3C) decreased. We conclude chronic inflammation contributes directly to fibrocarcinogenesis by shifting hepatocytic Smad3-mediated signaling from tumor suppression to oncogenesis both in PBC. These data also suggest pSmad3L can be new biomarker for HCC and high pSmad3L group need careful surveillance for early detection of HCC.
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