| Project/Area Number |
15390367
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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 |
General surgery
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| Research Institution | YAMAGATA UNIVERSITY (2004)
Hokkaido University (2003) |
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Principal Investigator |
OKADA Futoshi Yamagata Univ., Grad.Sch.of Med.Sci, Asso.Prof., 大学院・医学系研究科, 助教授 (00250423)
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| Co-Investigator(Kenkyū-buntansha) |
KOBAYASHI Masonobu Hokkaido Univ., Inst.for Genetic Med., Asso.Prof., 遺伝子病制御研究所, 助教授 (80241321)
TODO Satoru Hokkaido Univ., Grad.Sch.of Med., Prof., 大学院・医学研究科, 教授 (60136463)
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| Project Period (FY) |
2003 – 2004
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| Project Status |
Completed (Fiscal Year 2004)
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| Budget Amount *help |
¥7,100,000 (Direct Cost: ¥7,100,000)
Fiscal Year 2004: ¥3,000,000 (Direct Cost: ¥3,000,000)
Fiscal Year 2003: ¥4,100,000 (Direct Cost: ¥4,100,000)
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| Keywords | ischemia-reperfusion / free radicals / carcinogenesis / tumor progression / 低酸素環境 / 低酸素インキュベーター |
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| Research Abstract |
In the present study, we aimed to verify that intrinsically produced free radicals in the ischemia-reperfusion environment are a causative factor of common cancers. For this purpose, we used several normal and pre-malignant cultured cell lines such as FPCK-1-1 (human, colonic adenoma cell), IEC 6 (rat, immortalized intestinal cell), NIH3T3 (mouse, immortalized fibroblast), Balb3T3 (mouse, immortalized fibroblast) and QR-32 (mouse, pre-malignant fibrosarcoma). We also utilized normoxic (21% O_2) and hypoxic (1% O_2) culture chambers to create an artificial environment of ischemia-reperfusion in the culture condition. By using those materials, we obtained the following results.
1)A large amount of free radicals were generated in the normal or pre-malignant cultured cells after the cells were transferred to normoxic condition from hypoxic condition.
2)Spontaneous tumorigenic conversion was observed in the immortalized mouse fibroblast cell lines after repeatedly cultured in normoxic and hypoxic conditions.
We are now determining the gene(s) responsible for the tumorigenic conversion.
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