2004 Fiscal Year Final Research Report Summary
A Study on Kinetics of Dendritic Cells and Vascular Endothelial Growth Factor in Squamous Cell Carcinoma of the Oral Cavity
| Project/Area Number |
14571797
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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 |
病態科学系歯学(含放射線系歯学)
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| Research Institution | Meikai University |
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Principal Investigator |
KUSAMA Kaoru Meikai University, School of Dentistry, Professor, 歯学部, 教授 (20130479)
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| Co-Investigator(Kenkyū-buntansha) |
SAKASHITA Hideaki Meikai University, School of Dentistry, Professor, 歯学部, 教授 (10178551)
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| Project Period (FY) |
2002 – 2004
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| Keywords | dendritic cell / oral cancer / squamous cell carcinoma / VEGF / TGF-β / IL-4 / GM-CSF / CD83 positive cell |
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| Research Abstract |
It has been shown that cancer cells themselves produce vascular endothelial growth factor (VEGF), which induces the formation of blood vessels, interferes with the differentiation and function of immune cells, and escape from the anti-tumor immune system of the host. In this study, high expression of VEGF was found in cancer cells of the oral squamous cell carcinomas, especially in the cases with metastasis to regional lymph nodes. The numbers of dendritic cells (DCs) decreased in the cases that cancer cells strongly expressed VEGF. S-100+ and CDla+ DCs decreased in the numbers in those cases, but CD83+ DCs increased. Although the differentiation of DCs from PBMCs was significantly inhibited by adding culture supernatants of human squamous cell lines and rhVEGF, the levels of CD83 protein and mRNA, and CD83 positive cells increased. ELISA revealed that VEGF and TGF-β were secreted by various cancer cells derived from oral squamous cell carcinomas (HSC-2, 3, 4, Ca9-22 and KB). The improvement of suppressive immune condition in cancer patients is one of keys for the effective order-made cancer treatment. Further immunohistochemical study revealed that the expression of VEGFR1, 2 and 3 was detected in cancer cells of the oral squamous cell carcinomas, suggesting the presence of an autocrine mechanism mediated by VEGF and VEGFR
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