2016 Fiscal Year Final Research Report
An attempt to improve the possibilities of controlling local tumors through taking it into account to increase the sensitivity of oxic quiescent tumor cells
| Project/Area Number |
26670556
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Radiation science
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| Research Institution | Kyoto University |
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Principal Investigator |
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Keywords | 休止期腫瘍細胞 / 酸素化休止期腫瘍細胞 / 低酸素領域 / 腫瘍内微小環境 / 中性子捕捉療法 / サリドマイド / p53 status / メトフォルミン |
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| Outline of Final Research Achievements |
Thalidomide released the acute hypoxia during tumor vascular normalization and suppressed distant lung metastasis from the local tumor.
Analysis of the relation with oxygen concentration during culturing using p53 wild-type and mutant tumor cells showed that the boron-10 uptake was significantly reduced in hypoxic culture compared with under normal oxygen and also markedly reduced in wild type tumor cells than in p53 mutant cells especially when BPA was used compared with BSH.
After establishment of HIF-1α deficient tumor cells, deficiency of HIF-1α was shown to enhance the sensitivity to metformin in culture under glucose depletion, markedly enhance the sensitivity to metformin in hypoxic culture, and remarkably improve the radio-sensitivity of solid tumor through combination with metformin.
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| Free Research Field |
放射線腫瘍学
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