1993 Fiscal Year Final Research Report Summary
Changes of cytokines and their gene expression in the process of carcinogenesis of oral precancerous lesions
Project/Area Number |
04454511
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Research Category |
Grant-in-Aid for General Scientific Research (B)
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Allocation Type | Single-year Grants |
Research Field |
外科・放射線系歯学
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Research Institution | Showa University |
Principal Investigator |
NAGUMO Masao Showa University, School of Dentistry, Professor, 歯学部, 教授 (70013993)
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Co-Investigator(Kenkyū-buntansha) |
YAGAMI Kimitoshi Showa University, School of Dentistry, Lecturer, 歯学部, 助手 (00210211)
IWASE Masayasu Showa University, School of Dentistry, Assistant Professor, 歯学部, 講師 (50193743)
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Project Period (FY) |
1992 – 1993
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Keywords | precancerous lesions / carcinogenesis / cytokines / gene expression / Langerhans cell / cell proliferation / c-myc |
Research Abstract |
We investigated localization of cytokines and the expression of their genes in the specimens that were obtained from cancer patients whose cancer resions were developed from precancerous lesions or status, such as leukoplakia and papiloma. Changes of the numbers of Langerhans cells (LC) and HLA-DR antigen positive LC were also estimated before and after carcinogenesis. Further, the effect of cytokines (TNF-alpha, TGF-beta, IFN-gamma) or their combinations on cell proliferation of a oral cancer cell line (NA) was tested and the relationship between cell proliferation and the expression of protooncogenes (c-myc, ras) was estimated. The results obtained were as follows : 1.The localization of TGF-alpha was increased with development to cancer, whereas TGF-beta was decreased with carcinogenesis. The increase of TGF-alpha was well correlated with that of PCNA which is now thought to be good marker of cell proliferation. 2.The Expression of TGF-alpha mRNA was increased with carcinogenesis. 3.The numbers of LC and HLA-DR antigen positive LC were increased with carcinogenesis. 4.The combination of TNF-alpha and TGF-beta or TNF-alpha and IFN-gamma inhibited cell proliferation of NA cells aditively or synergistically. The inhibition of cell proliferaton seemed to be brought about by the downregulation of c-myc mRNA expression.
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