| Project/Area Number |
05807129
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Cerebral neurosurgery
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| Research Institution | Sapporo Medical University School of Midicine, Department of Neurosurgery |
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Principal Investigator |
IBAYASHI Yukihiro Department of Neurosurgery, Sapporo Medical University, Assistant Professor, 医学部, 講師 (50193636)
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| Co-Investigator(Kenkyū-buntansha) |
OHTAKI Masafumi Department of Neurosurgery, Sapporo Medical University, Assistant Professor, 医学部, 講師 (90168964)
森本 繁文 札幌医科大学, 医学部, 助手 (80174449)
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| Project Period (FY) |
1993 – 1994
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| Project Status |
Completed (Fiscal Year 1994)
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| Budget Amount *help |
¥1,600,000 (Direct Cost: ¥1,600,000)
Fiscal Year 1994: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1993: ¥900,000 (Direct Cost: ¥900,000)
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| Keywords | glioma / immunotherapy / GM3 / GM2 / TLC / cell cycle / brain tumor / LAK cells / ganglioside |
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| Research Abstract |
The main objective of this project is to develop a novel immunotherapy for gliomas, in which glycolipid antigens are analyzed and quantified systematically and a set of appropriate antibodies would be selected according to the antigenic profile of an individual glioma. We first analyzed glycosphingolipid composition of 11 human glioma cell line, one melanoma cell line, and one fibroblast cell line. The glycosphingolipid composition of glioma cell line are different from that of normal nerve cell. We also found that a human glioma cell line U118MG could modulate glycosphingolipid expression via certain cytodines. We next analyzed the glycolipid antigens of 10 human gliomas, which were revealed to consist mainly of GM3 and GM2 . The reactivity of monoclonal antibodies against those gangliosides was examined next either as chemically isolated antigens or cell surface ones. The intensity of antibody binding was dose-dependent as the gangliosides were prepared on a thin-layr chromatographic plate, On the contrary, antibody reaction was more complex on the cell surface ; GM3 showed positive and negative threshould of antibody binding, and GM2 gave stronger reaction when GM3 co-existed nearly equally on the cell surface. We next analyzed cellcycle related glycolipids expression on a certain glioma. It was revealed that the total glycolipids were expressed nearly twice during mitosis, and nLc4Cer was significantly enhanced during that phase. The results may suggest better antibody react ions against the mitotic cells. In another experiment, we have found that the cell dendity greatly affects the level of antibody binding against GM3. There should be a variety of factors that influence the antibody reactions against glycolipid antigens. We are now focusing on the glycolipid analysis of surgical specimens of glioma tissue as well as on the factors participating in the antibody reactivity against those antigens.
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