| Project/Area Number |
03670330
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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 |
内科学一般
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| Research Institution | Sapporo Medical College |
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Principal Investigator |
TSUJISAKI Masayuki Sapporo Med. College, Dept. of Int. Med., Instructor, 医学部, 助手 (50217311)
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| Co-Investigator(Kenkyū-buntansha) |
YACHI Akira Sapporo Med. College, Dept. of Int. Med., Prof., 医学部, 教授 (50045324)
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| Project Period (FY) |
1991 – 1992
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| Project Status |
Completed (Fiscal Year 1992)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1992: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1991: ¥1,400,000 (Direct Cost: ¥1,400,000)
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| Keywords | adhesion modecule / ICAM-1 / circulating antigen / cytotoxic mechanism / metastasis and invasion of cancer cells / ICAMー1 / モノクロ-ナル抗体 |
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| Research Abstract |
A new monoclonal antibody (MoAb) HA58 (IgGl) was prepared, which recognizes the binding site on the intercellular adhesion molecule-1 (ICAM-1) antigen to the lymphocyte function-associated antigen-1 (LFA-1). The double-determinant immunoassay (DDIA) was established with use of MoAb HA58 and another anti-ICAM-1, MoAb CL207, to detect the soluble, shedding ICAM-1 antigen. The incidence of positivity for ICAM-1 antigen in malignant diseases was higher than that in benign diseases or in healthy controls. Immunostaining of cancerous tissue with MoAb HA58 showed that the ICAM-1 antigen was expressed not only on malignant cells but also on stromal cells (mainly fibroblasts) near cancer nests, and the stromal cells immediately adjacent to cancer nests, in comparison to those cells farther away from the nests, have a higher ICAM-1 expression. We speculate that tumor cells activate T cells to produce cytokines (e.g.IFN-gamma), resulting in strong expression of the ICAM-1 on surrounding fibroblasts, as well as on tumor cells. Shedding ICAM-1 antigen may also block the attachment of cytotoxic T cells and/or NK cells to cancer cells, since LFA-1 could be blocked with soluble ICAM-1. This could be one of the escape mechanisms of cancer cells from the immunosurveillance system of the host.
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