| Project/Area Number |
14570831
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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 |
Dermatology
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| Research Institution | Kansai Medical University |
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Principal Investigator |
ISEI Taiki (2003) Kansai Medical University, Department of Dermatology, Assistant Professor, 医学部, 講師 (90223049)
橋本 洋子 (2002) 関西医科大学, 医学部, 講師 (70257955)
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| Co-Investigator(Kenkyū-buntansha) |
HORIO Takeshi Kansai Medical University, Department of Dermatology, Professor, 医学部, 教授 (90026914)
爲政 大幾 関西医科大学, 医学部, 講師 (90223049)
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| Project Period (FY) |
2002 – 2003
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| Project Status |
Completed (Fiscal Year 2003)
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| Budget Amount *help |
¥3,300,000 (Direct Cost: ¥3,300,000)
Fiscal Year 2003: ¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 2002: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Keywords | ultraviolet radiation / carcinogenesis / DNA damage / tumor immunity / xeroderma pigmentosum / XPAマウス |
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| Research Abstract |
XPA gene-deficient mice display dermatologic abnormalities similar to human XP, such as enhanced UV-induced acute inflammation and high incidence of UVB-induced skin cancer. We have previously reported that UVB-induced immunosuppression of contact hypersensitivity was greatly enhanced in XPA mice. To determine whether the enhancement of immunosuppression is involved in easy development of UVB-induced skin cancer in XPA mice, we examined the effects of UVB radiation on tumor rejection in XPA mice. First, UVB-induced skin tumors were transplanted to recipient mice. Non-irradiated XPA recipient mice, as well as wild type mice, rejected the tumors 4 weeks after the transplantation. When tumors were engrafted in the skin irradiated with 100-200mJ/cm^2 of UVB, 50%(20/40) and 10%(4/42) of the tumors were transplantable to the XPA and to the wild type mice, respectively. Second, to fix the number of transplanted cells, tumor cell line of UVB-induced SCC in XPA mice was injected into the recipient subctaneously. No difference in the development of tumors was observed between the non-irradiated XPA and wild type mice, and tumor disappeared 4 weeks after inoculation. When tumor cell were inoculated into UVB irradiated skin, tumor grew progressively in 60%(12/20) of the XPA mice, but only in 4%(1/23) of wild type mice. These data suggests that enhanced UVB-induced impairment of tumor rejection could be partially involved in the cancer development of XP patients.
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