| Project/Area Number |
20590593
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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 |
Laboratory medicine
|
|---|
| Research Institution | Fukuoka University |
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Principal Investigator |
KUROKI Masahide Fukuoka University, 医学部, 教授 (40122692)
|
|---|
| Co-Investigator(Renkei-kenkyūsha) |
SHIBAGUCHI Hirotomo 福岡大学, 医学部, 講師 (60295061)
TANAKA Toshihiro 福岡大学, 医学部, 講師 (00398314)
|
|---|
| Project Period (FY) |
2008 – 2010
|
| Project Status |
Completed (Fiscal Year 2010)
|
| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2010: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2009: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2008: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
|
|---|
| Keywords | 癌 / 免疫学 / バイオテクノロジー / モノクローナル抗体 / MK-1 |
|---|
| Research Abstract |
Using the ELISA for MK-1, we found that MK-1 is useful for some malignant tumors. A human monoclonal anti-MK-1 antibody, M13-57, revealed antibody-dependent cell-mediated cytotoxicity and complement-dependent cytotoxicity against MK-1-expressing cells, suggesting that this antibody may be useful for antibody-based therapy of cancer. Also, a chimeric T-cell antigen receptor consisting of M13-57 scFv, CD28 and CD3 ζ induced a wild-type T-cell receptor-like molecular event upon MK-1 binding, suggesting that this may be useful for cancer therapy.
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