| Project/Area Number |
08671369
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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 | HIROSHIMA UNIVERSITY |
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Principal Investigator |
YAMAGUCHI Oshiyuki Research Institute for Radiation Biology and Medicine, HIROSHIMA UNIVERSITY Assistant professor, 原爆放射能医学研究所, 講師 (10230377)
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| Co-Investigator(Kenkyū-buntansha) |
MIYAHARA Eiji Hiroshima University Medical Hospital, Medical stuff, 医学部・附属病院, 医員
野間 浩介 広島大学, 医学部・附属病院, 医員
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| Project Period (FY) |
1996 – 1998
|
| Project Status |
Completed (Fiscal Year 1998)
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| Budget Amount *help |
¥2,400,000 (Direct Cost: ¥2,400,000)
Fiscal Year 1998: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1997: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1996: ¥1,200,000 (Direct Cost: ¥1,200,000)
|
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| Keywords | CTL / T cell receptor (TCR) / malignant effusion / T細胞受容体 (TCR) |
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| Research Abstract |
Locoregional lymphocytes in the ascites caused from colon cancer were isolated and expanded with interleukin (IL)-2 to be potent effector cells against autologous tumor cells. They were CD4 and Fas-L positive, and produced TNF and IFN-gamma. Their cytotoxicity against autologous tumor cells was abrogated with anti-TCR V beta 20 as well as anti-TCR a alpha beta antibody. This TCR V beta 20 gene was cloned and the CDR3 sequence was identified. Molecular diagnosis for locoregional lymphocytes from cancer patients by PCR using the CDR3 sequence as a primer revealed that 3 of 4 patients with positive response to immunotherapy showed positive bands and 3 of 3 patients with negative response did negative ones. These evidences indicates the possibilities of cancer-specific immunotherapy using the TCR V beta 20 and molecular diagnosis for responder patients against cancer-specific immunotherapy.
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