| Project/Area Number |
08457544
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Surgical dentistry
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| Research Institution | Kanazawa University |
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Principal Investigator |
YAMAMOTO Etsuhide School of Medicine, Kanazawa University, Professor, 医学部, 教授 (00092445)
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| Co-Investigator(Kenkyū-buntansha) |
KAWASHIRI Shuichi School of Medicine, assistant, 医学部, 助手 (30291371)
KUMAGAI Shigehiro Attached hospital, School of Medicine, Lecturer, 医学部・附属病院, 講師 (00215013)
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| Project Period (FY) |
1996 – 1998
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| Project Status |
Completed (Fiscal Year 1998)
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| Budget Amount *help |
¥6,700,000 (Direct Cost: ¥6,700,000)
Fiscal Year 1998: ¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 1997: ¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1996: ¥3,000,000 (Direct Cost: ¥3,000,000)
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| Keywords | DMBA induced tongue cancer / mode of invasion / architecture of tumor vessel / proliferating cell nuclear antigen / vasucular endothelial cell growth factor / vessel density / positive rate / oral squamous cell carcinoma / 口腔扁平上皮癌 / 浸潤 / リンパ節転移 / 基質分解酵素 / マトリックスメタロプロテナーゼ / 正所性移植モデル / 浸潤像 / 基底膜 / 細胞膜接着 / 増殖細胞核抗原 |
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| Research Abstract |
The vascular architecture of DMBA (9, 10-dimethyl I, 2-benzanthracene) induced tongue carcinoma in the hamster was examined. Changes in tumor vessels and their significance during growth of invasive oral squamous cell carcinoma was observed. Tongue cancer was induced by abrading the right margin of the tongue of each hamster with an endodontic barbed broach and subsequently applying 1.0 % DMBA dissolved in aceton, three times a week, at the same site. After macroscopic detection of cancer and the signs of cachexia (weight loss, etc.), Indian-ink was infused into the ascending aorta of each animal under general anesthesia. Tissue was harvested from each animal and made into a transparent specimen, 100 p m in thickness, for examination of vasucular architecture. The mode of cancer invasion was Grade I in 8 animals, Grade 2 in 8, Grade 3 in 23, and Crade 4C in 5. Macroscopic tumor growth mode was exophytic in 36 animals and endophytic in 8 animals. Each mode of cancer invasion was associa
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ted with characteristic vascular architecture. That is, low invasive cancers (Grade I and 2) showed dendriform vascularization and a marked increase in vessel density as they underwent exophitic growth. Grade 3 invasive cancei shbwed rings of blood vessels forming during the coume of invasion by alveolar tumor foci. Diffusely invasive cancer (Grade 4C) showed destruction of exisdng blood vessels and a decrease in vessel density. As fumor invasion progressed ; the vessel density decreased (p<0.05). The vessel density was significantly lower in cases of exophytic cancer than in cases of endophytic cancer (p<0.01). The PCNA (proliferating cell nuclear antigen) of cancer cells, which is an indicator of tumor proliferation potential, was more frequently positive as tumor invasion bccame more severe. That is, the PCNA positive rate in Grade I or 2 animals differed significantly from that in Grade 3 or 4C animals (p<0.05). The PCNA positive rate decreased as vessel density increased (p<0.05). Thus, the vessel density was not proportional to the tumor proliferation potential. The expression of vascular endothelial growth factor (VEGF) was seen more frequently as tumor invasion progressed (p<0.05), but the expression of VEGF did not correlate with the vessel density. These results suggested that the changes of the tumor vessel were dependent on the mode of cancer invasion and proliferation. Less
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