| Project/Area Number |
02670477
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Dermatology
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| Research Institution | Kobe University |
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Principal Investigator |
ICHIHASHI Masamitu Kobe Univ. School of Medicine, Associate Professor, 医学部, 助教授 (00030867)
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| Co-Investigator(Kenkyū-buntansha) |
HAYASHIBE K. Kobe Univ. School of Medicine, Assistant, 医学部, 助手 (40198875)
UEDA M. Kobe Univ. School of Medicine, Assistant, 医学部, 助手 (20176598)
船坂 陽子 神戸大学, 医学部, 助手 (30209150)
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| Project Period (FY) |
1990 – 1991
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| Project Status |
Completed (Fiscal Year 1992)
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| Budget Amount *help |
¥1,900,000 (Direct Cost: ¥1,900,000)
Fiscal Year 1991: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 1990: ¥800,000 (Direct Cost: ¥800,000)
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| Keywords | ultraviolet light / DNA repair / cyclobutane dimer / (6-4)photoproduct / xeroderma pigmentosum / carcinogenesis / 単クロ-ン抗体 / DNA損傷 / (6ー4)光生成物 / シクロブタン型2量体 |
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| Research Abstract |
UV-induced DNA damages are considered to play an essential role in induction of skin cancers, since xeroderma pigmentosum (XP) patients with defective DNA repair exhibit early and high incidence of skin cancers.
[Aim] To understand a biological role of repairs of UV-induced (6-4) photoproducts [(6-4)], repair kinetics for both (6-4) and cyclobutane dimers (P_y R_y ) were comparatively studied using normal and repair-defective XP fibroblasts.
[Results & Discussion] Repair kinetics of (6-4) of normal and XPs were much faster than those of P_y R_y ・ Approximately 70% and 60% (6-4) were removed in the first 6h in normal and XP70TO (E) cells, respectively. After 10J/m^2 UVC exposure, 40% P_y R_y was removed in normal cells during 6h after radiation, whereas only 15% was removed in XP E cells. Repair of (6-4) of XP46KO (F) at 12h and 24h. after radiation were as low as 10% and 20% of normal subject, respectively. Repair of P_y R_y of XP F assayed by UDS, however, was as high as 60% of normal 24h after irradiation. These results together with intermediate UV sensitivity of XP E and F cells, and late onset of skin cancers of XP E and F subjects suggest that P_y R_y may play a major role in UV killing and carcinogenesis in comparison with (6-4), although not yet compelling.
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