| Project/Area Number |
26670556
|
|---|
| Research Category |
Grant-in-Aid for Challenging Exploratory Research
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Radiation science
|
|---|
| Research Institution | Kyoto University |
|---|
Principal Investigator |
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
田野 恵三 京都大学, 原子炉実験所, 准教授 (00183468)
宮武 伸一 大阪医科大学, 医学部, 特別職務担当教員(教授) (90209916)
|
|---|
| Project Period (FY) |
2014-04-01 – 2017-03-31
|
| Project Status |
Completed (Fiscal Year 2016)
|
| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
|
|---|
| 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 / 放射線治療生物学 / 低酸素腫瘍細胞 / HIF-1 alpha / ビグアナイド系抗糖尿病薬剤 / 急性低酸素領域 / 腫瘍血管正常化 |
|---|
| 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.
|
