| Project/Area Number |
07457484
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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 | Niigata University |
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Principal Investigator |
NAKAJIMA Tamio Niigata University School of Dentistry Professor, 歯学部, 教授 (10014010)
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| Co-Investigator(Kenkyū-buntansha) |
NOMURA Tsutomu Niigata University Dental Hospital Assistant Professor, 歯学部・附属病院, 助手 (20228365)
SHINGAKI Susumu Niigata University School of Dentistry Associate Professor, 歯学部, 助教授 (30134943)
SAKU Takashi Niigata University School of Dentistry Professor, 歯学部, 教授 (40145264)
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| Project Period (FY) |
1995 – 1996
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| Project Status |
Completed (Fiscal Year 1996)
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| Budget Amount *help |
¥7,400,000 (Direct Cost: ¥7,400,000)
Fiscal Year 1996: ¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1995: ¥5,200,000 (Direct Cost: ¥5,200,000)
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| Keywords | Oral carcinoma / Lymph node metastasis / Basement membrane / 基底膜 / リンパ行性転移 / 血行性転移 / リンパ管侵襲 / 血管侵襲 / リンパ節転移 |
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| Research Abstract |
The mechanism of lymph node metastasis of oral carcinomas was studied using an animal model of squamous cell carcinoma with a high metastatic potential to lymph nodes in hamsters. On light microscopy, O-IN transplanted in the tonque caused lymphatic invasion with growth, but blood vessel invasion was not observed. Tumor cell clusters in lymphatic vessels were continuous with adjacent tumor cell nests and became disrupted into smaller pieces to be transported to lymph nodes. On electron microscopy, the endothelial injury caused by mechanical pressure from tumor growth was the characteristic feature common to both lymphatic and blood vessel invasions. Tumor cell nests penetrated into the lumen of both vessels through gaps of disrupted endothelial cells. The tumor cell nests invaded lymphatic vessels with their basement membrane on the surface and tumor cell clusters were maintained in a relatively large size, whereas they were disrupted into small pieces by neutrophils in blood vessels.
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This difference was most likely responsible for causing more frequent lymph node metastasis than hematogenous metastasis.
Immunostaining for laminin showed that the disruption of basement membrane became conspicuous, in particular at the invasion front, with the decrease of nest size and corresponding to the stage of lymph node metastasis. The expression of laminin mRNA and the activities of MMP-9 and MMP-3 were much stronger in metastatic cells than non-metastatic cells isolated from O-IN.The findings suggest that the disappearance of besement membrane associated is an essential sign for local invasion of tumor cells leading to lymphatic invasion and metastasis to regional lymph nodes. An inhibition experiment using TIMP is needed to confirm the interpretation.
On three-dimensional culture in collagen matrix gel, ACC2, a cell line established from human adenoid cell carcinoma and a metastatic cell line established from O-IN could be maintained for 6 and 14 days, respectively. Pseudocyst formation and secretion of HSPG,type I collagen and fibronectin were confirmed in ACC2. Deposition of basement membrane-like substance and components of extracellular matrix were observed in O-IN.
The results of this research were reported in international journals and meetings. Less
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