| Project/Area Number |
09671341
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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 |
Digestive surgery
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| Research Institution | Tokyo Women's Medical University |
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Principal Investigator |
KAMEOKA Shingo T.W.M.C. Surgery II, Professor, 医学部・主任教授 (80101848)
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| Co-Investigator(Kenkyū-buntansha) |
NAGATA Hitoshi T.W.M.C. Surgery II, Assistant, 医学部, 助手 (90237529)
HAYASHI Tatsuhiro T.W.M.C. Surgery II, Assistant, 医学部, 助手 (70238111)
SAITO Noboru T.W.M.C. Surgery II, Assistant, 医学部, 助手 (10225724)
SOYAMA Koichi T.W.M.C. Surgery II, Assistant, 医学部, 助手 (30266754)
板橋 道朗 東京女子医科大学, 医学部, 助手 (10193418)
進藤 廣成 東京女子医科大学, 医学部, 助手 (80187567)
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| Project Period (FY) |
1997 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1999: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1998: ¥500,000 (Direct Cost: ¥500,000)
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| Keywords | Liver metastasis / Adhesion molecule / Laminin / Integrin / Extracellular matrix / type IV collagen / Urinary GGH / Metastasis inhibition / 細胞接着ドメイン / 血管新生阻害 / 転移予知 / ビトロネクチン / E-カドヘリン |
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| Research Abstract |
We investigated the mechanism and therapy of colorectal cancer metastasis according to the role of cell adhesion molecules. From 1990 to 1995, we assessed laminin, integrin and NCAM (neural cell adhesion molecule). This study was undertaken to investigate another molecule. Vitronectin and E-cadherin in 1997, urinary GGH (glucosyl - galactosyl - hydroxylysine) in 1998. GGH is a metabolic product from matrix collagenolysis by cancer invasion. And in 1999, we started inhibition therapy by the blocking of adhesion and the inhibition of neovascularization in a mouse hepatic metastasis model.
1. High level group of serum laminin and urinary GGH, and low level group of serum β1 integrin were risk factor of hepatic metastasis. Laminin and integrin β1 stain netgative group were also risk factor.
2. In the arterial infusion chemotherapy, some clinical cases were presented as a useful marker of metastatic change.
3. The inhibitory rate of combined therapy with cell-binding domain and angiogenesis inhibitor was about 60%. By these therapy, more effective inhibition and prolongation of survival period can be expected than in each treatment alone.
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