| Project/Area Number |
12671659
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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 |
Otorhinolaryngology
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| Research Institution | Hamamatsu University School of Medicine |
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Principal Investigator |
MINETA Hiroyuki Hamamatsu University School of Medicine, Dept of Otolaryngology, Associate Professor, 医学部, 助教授 (40190714)
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| Co-Investigator(Kenkyū-buntansha) |
BABA Satoshi Hamamatsu University School of Medicine, Dept of Pathology, Associate Professor, 医学部, 助教授 (10242760)
MISAWA Kiyoshi Hamamatsu University School of Medicine, Dept of Otolaryngology, Staff, 医学部・附属病院, 助手 (90334979)
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| Project Period (FY) |
2000 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2001: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 2000: ¥2,700,000 (Direct Cost: ¥2,700,000)
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| Keywords | Head and Neck / Angiogenesis / Angiostafin / Endostatin / 頭頚部癌 / VEGF |
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| Research Abstract |
We reported tat endostatin expression correlated with tumor size and p53 expression, but not lymph node status and prognosis, and that high endostatin expression correlated with high microvessel density in the primary tumor. Endogenous endostatin which may be upregulated by p53 gene dices not represent antiangiogenic phenotype of the primary tumor.
Endostatin inhibits iNOS activity, in thyroid anapiastic carcinoma, maxillary carcinoma, and lung carcinoma cell lines, 2. Inhibition of iNOS activity by endostatin may cause to antoangiogenesis.
We speculate a pathway of antiangiogic function of endostatin fron these results. Endostatin inhibits iNOS activity, leading to decrease of NO production in NOS expressed tumor cells. Loss of NO production may cause to antiangiogenesis through inhibition of VEGF and increase of p53 accumulation.
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