| Project/Area Number |
09671269
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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 |
General surgery
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| Research Institution | University of Occupational and Environmental Health |
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Principal Investigator |
YOSHINO Ichiro University of Occupational and Environmental Health, Medical Department Research Associate, 医学部, 助手 (40281547)
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| Co-Investigator(Kenkyū-buntansha) |
ICHIYOSHI Yuji University of Occupational and Environmental Health, Medical Department Assistan, 医学部, 講師 (50264031)
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| Project Period (FY) |
1997 – 1998
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| Project Status |
Completed (Fiscal Year 1998)
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| Budget Amount *help |
¥2,500,000 (Direct Cost: ¥2,500,000)
Fiscal Year 1998: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1997: ¥1,700,000 (Direct Cost: ¥1,700,000)
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| Keywords | Breast cancer / Cytotoxic T lymphocyte / Regional lymph node lymphocyte / HLA-A2 / Tumor antigen / Major histocompatibility antigen / 主要組織適合抗原 / 細胞障害性T細胞 / 癌抗原 |
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| Research Abstract |
In this study, we have induced the breast cancer-specific cytotoxic T lymphocytes (CTL) from regional lymph node lymphocytes (RLNL) of HLA A2-positive patients with breast cancer. Freshly isolated RLNL were stimulated with solid phase anti-CD3 monoclonal antibody followed by expansion with recombinant interleukin-2. Subsequently, the RLNL were stimulated with an irradiated HLA 0201 breast cancer cell line, MCF-7, at responder/stimulator ratio of 10/1 once a week for 2 weeks. The cultured RLNL exhibited specific lysis against MCF-7 in all 5 HLA A2-positive patients tested, but not in 2 HLA A2-negative patients. The cytotoxicity against MCF-7 was substantially inhibited by an addition of anti-HLA A2 mAb. In 3 out of the 5 HLA A2-positive patients, the anti-MCF-7 CTL also exhibited a substantial level of reactivity against PC-9, an HLA A0206-positive lung adenocarcinoma cell line. Inversely, anti-PC-9-speciflc CTL was inducible by multiple stimulations of the RLNL with PC-9 cells in 2 out of the 3 patients. These results suggested that several common tumor antigens might exist among HLA A2-positive breast cancers, some of which may be shared with lung adenocarcinomas.
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