| Project/Area Number |
21390328
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Dermatology
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| Research Institution | Hamamatsu University School of Medicine (2010-2011)
University of Occupational and Environmental Health, Japan (2009) |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
NAKAMURA Motonobu 産業医科大学, 医学部, 准教授 (30303837)
SHIMAUCHI Takatoshi 浜松医科大学, 医学部, 講師 (90399204)
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| Project Period (FY) |
2009 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥14,560,000 (Direct Cost: ¥11,200,000、Indirect Cost: ¥3,360,000)
Fiscal Year 2011: ¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2010: ¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2009: ¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
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| Keywords | 皮膚T細胞リンパ腫 / AID / 成人T細胞白血病/リンパ腫 / マイクロRNA / 菌状息肉症 / セザリー症候群 / リンパ腫 / 皮疹 / HTLV-1 / 成人T細胞白血病 |
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| Research Abstract |
It has been reported that AID is involved in the development of virus-associated neoplasms. Moreover, microRNA-155 downregulates the expression of AID. On the other hand, point mutations of p53 have been reported in the patients with cutaneous T-cell lymphoma(CTCL) including ATLL. By real-time PCR analysis, we investigated the expression of AID and microRNA-155 in the peripheral blood of patients with mycosis fungoides, Sezary syndrome, and ATLL in a comparison with normal healthy subjects. We found that AID expression was higher in the peripheral blood lymphocytes and tumor-infiltrating cells in CTCL, especially ATLL. We isolated circulating CD4-, CD4+CD25-, and CD4+CD25+cells by MACS and examined the mRNA expression of AID and microRNA-155 in each fraction. In addition, skin specimens and lymph nodes from the patients were also tested. We found that AID expression was elevated with decreased expression of microRNA-155, particularly in ATLL, suggesting that AID and its regulatory microRNA are involved in the development of this virus-associated lymphoma.
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