| Project/Area Number |
04454297
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Radiation science
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| Research Institution | Tokai University |
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Principal Investigator |
MORI Tomoyuki Tokai U.V., Sch.of Medicine, Professor, 医学部, 教授 (70055896)
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| Co-Investigator(Kenkyū-buntansha) |
FUKUHARA Noboru Tokai U.V., Sch.of Medicine, Assistant Prof., 医学部, 助手 (70218949)
TAMAI Yoshifumi Tokai U.V., Sch.of Medicine, Assistant Prof., 医学部, 助手 (90207225)
MAEZAWA Hiroshi Tokai U.V., Sch.of Medicine, Associate Prof., 医学部, 講師 (00138653)
OHIZUMI Yukio Tokai U.V., Sch.of Medicine, Associate Prof., 医学部, 講師 (30024813)
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| Project Period (FY) |
1992 – 1994
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| Project Status |
Completed (Fiscal Year 1994)
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| Budget Amount *help |
¥5,800,000 (Direct Cost: ¥5,800,000)
Fiscal Year 1994: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 1993: ¥1,600,000 (Direct Cost: ¥1,600,000)
Fiscal Year 1992: ¥2,900,000 (Direct Cost: ¥2,900,000)
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| Keywords | Oncogene / Radiosensitivity / Tumor cells / 放射線治療 |
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| Research Abstract |
Radiation sensitivity of five tumor cell lines (FM3A,3LL,EMT-6, FSa-II and SCC-VII) of mouse in vitro was examined with clonogenic assay after irradiation with Co-60 gamma-rays. EMT-6 cells were most resistant in these cell lines. Three cell lines (FM3A,3LL and SCC-VII) had the similar sensitivity and were more sensitive than FSa-II cells. Expression of two oncogenes, c-myc and R-ras, in cells in vitro was examined by northern blot hybridization analysis. Expression of c-myc gene was detected but the level of c-myc mRNA in cells did not correlate to the radioresistancy of cells. Expression of R-ras did not detected in the present study. Analysis of other genes (Ha-ras, jun, raf, etc.) is undergoing. Radiosensitivity of both normal and SV40-transformed keratinocytes was examined with clonogenic assay in a serum-free medium. Transformed keratinocytes was more sensitive than normal one. Expression of wild p53 oncogene, which may cause G1 arrest after irradiation, was inhibited in transformed cells. Therefore the repair of DNA damages may suppressed in transformed cells.
The present study could not confirm the role of specific oncogene on radiosensitivity of cells and tumors. The role of wild p53 gene in rumor cells is remained to analyze.
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