| Project/Area Number |
10670455
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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 | The University of Tokyo |
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Principal Investigator |
MAEKAWA Hisato The University of Tokyo, Faculty of Medicine, Assistant, 医学部・附属病院, 助手 (10301102)
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| Co-Investigator(Kenkyū-buntansha) |
TSUKAMOTO Kazuhisa The University of Tokyo, Faculty of Medicine, Assistant, 医学部・附属病院, 助手 (20251233)
MITSUI Hiroshi The University of Tokyo, Faculty of Medicine, Assistant, 医学部・附属病院, 助手 (30239280)
MARUYAMA Toshiyuki The University of Tokyo, Faculty of Medicine, Assistant, 医学部・附属病院, 助手 (30219571)
SAKATA Youichi Jichii University School of Medicine, Thoroloil Haemolais, Assistant Professor, 血液研究部門止血血栓, 助教授 (40129028)
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| Project Period (FY) |
1998 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥3,200,000 (Direct Cost: ¥3,200,000)
Fiscal Year 1999: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1998: ¥2,300,000 (Direct Cost: ¥2,300,000)
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| Keywords | angiostatin / hepatocellular carcinoma / plasminogen / coagulation & fibrinolysis |
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| Research Abstract |
Because of the hyper-vascularity of hepatocellular carcinoma, several methods that utilize its vascularity have been investigated as for its diagnosis and treatment. Recently, several proteins of which suppress the growth of microvascular-endothelial cells, including angiostatin, have been isolated and their clinical studies have started. And at the same time correlations between the proteins and blood coagulation and fibrin6lysis have been told.
In this project, we reconfirmed the activity of suppression of the growth of microvascular-endothelial cells at first and determined the presence of angiostatin in the supernatant of rat hepatocyies, and human liver cancer originated cells, HepG2, HLF, HuHi-7 and Alexander cells. After the determinations, we examined the correlation between angiostatin and macrophage metalloproteinase-12 which was assumed to contribute the conversion of plasminogen to angiostatin in vivo. Because we could not find the significance correlation by RT-PCR of macrophage metalloproteinase-12 in the cells, we hypotheses the contribution of other enzymes that cancer cells produced, any events occurring on the site of inflammation or blood coagulation and fibrinolysis.
Next we determined the presence of angiostatin in plasma of the patients of hepatocellular carcinoma to find its presence in about 30% of the patients. And we could not find any correlation between the presence of angiostatin and thrombin-ATIII complex or plasmin-anti-plasmin complex, representative marker for the disorder of blood coagulation and fibrinolysis.
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