| Project/Area Number |
23590418
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Human pathology
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| Research Institution | Kawasaki Medical School |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
AKIYAMA Takashi 川崎医科大学, 医学部, 准教授 (80294411)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2011: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | スフィンゴシン-1-リン酸 / 受容体 / 悪性リンパ腫 / 低酸素 / FTY720 / リンパ腫 / STAT3 / HTLV-1 / 異種移植片 / 低酸素環境 / スフィンゴシン-1-リン酸受容体 / 白血病 |
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| Research Abstract |
In this study, we found that sphingosine-1-phosphate receptor 1 (S1PR1) was expressed in 12% of 183 diffuse large B-cell lymphoma (DLBCL) cases, in particular, as high as 56% in primary testicular DLBCL. However, the S1PR1 expression status was not associated with STAT3 activation. S1PR1 was also expressed in 20% of 25 adult T-cell leukemia/lymphoma (ATLL) cases. S1PR1 expression of HTLV-1-infected T cell lines was elevated under hypoxic condition. FTY720, functional antagonist of S1PR1, inhibited activation of STAT3,suppressed cell proliferation, and induced apoptosis of HTLV-1-infected T cell lines in vitro. FTY720 (10mg/kg) treatment did not induce significant suppression of S1PR1 expression nor tumor growth in SCID xenograft model of HTLV-1-infected T cell line HUT102. induce significant suppression of S1PR1 expression nor tumor growth in SCID xenograft model of HTLV-1-infected T cell line HUT102.
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