Clinical application of TGF-beta signal in chronic hepatitis B
| Project/Area Number |
23701039
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Carcinogenesis
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| Research Institution | Kansai Medical University |
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Principal Investigator |
MURATA Miki 関西医科大学, 医学部, 助教 (10533416)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2013: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2012: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2011: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | Smad3リン酸化 / B型慢性肝炎 / TGF-β / Smad3 / 部位特異的リン酸化Smad単クローン抗体 / 肝発癌 |
|---|
| Research Abstract |
In our recent studies, HBV clearance at an early stage by anti viral therapy restored hepatocytic TGF-beta signaling from fibro carcinogenesis toward the tumor suppression. Moreover, low pSmad3C and high pSmad3L positivity were significantly predictive of human HCC development. We conclude that pSmad3L and pSmad3C can serve as a useful markers determining whether you can defend development of viral related HCC by antiviral therapy. Using an individua s phospho-Smad3 markers, clinicians may be able to achieve more effective chemoprevention and individualized therapy for HBV infected patients.
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Report
(4 results)
Research Products
(16 results)
