| Project/Area Number |
14570498
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Gastroenterology
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| Research Institution | Nara Medical University |
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Principal Investigator |
YOSHIJI Hitoshi Nara Medical University, 3rd Dept of Int Med, Research Associate, 医学部, 助手 (40336855)
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| Co-Investigator(Kenkyū-buntansha) |
IMAZU Hiroo Nara Medical University, 3rd Dept of Int Med, Research Associate, 助手 (60336857)
KOJIMA Hideyuki Nara Medical University, 3rd Dept of Int Med, Research Associate, 助手 (60326345)
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| Project Period (FY) |
2002 – 2003
|
| Project Status |
Completed (Fiscal Year 2003)
|
| Budget Amount *help |
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2003: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2002: ¥2,300,000 (Direct Cost: ¥2,300,000)
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| Keywords | Angiogenesis / VFGF / Hepatocellular Carcinoma / Angiotensin-II / Angiotensin-II / Tet system |
|---|
| Research Abstract |
In the current granted-project., we elucidated the in vivo role of vascular endothelial growth factor (VEGF) on hepatocellular carcinoma (HCC) development. We examined the combined effect of VEGF and basic fibroblast growth factor (bFGF), which is also known as a potent angiogenic factor in HCC, overexpression by means of a combination of a retroviral tetracycline (tet)-regulated gene expression system. We found that VEGF and bFGF synergistically increased tumor growth and angiogenesis in murine HCC cells, at least partly induction of VEGF by bFGF overexpression through VEGFR-2. We also found that clinically used angiotensin converting enzyme inhibitor (ACE-I), perindopril (PE) and interferon (IFN) at clinical compatible low doses significantly suppressed the HCC development and angiogenesis associated with suppression of VEGF. We reported these results in several journals, such as Hepatology and Clinical Cancer Research.
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