| Project/Area Number |
24659644
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Single-year Grants |
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| Research Field |
Cerebral neurosurgery
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| Research Institution | University of Tsukuba |
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Principal Investigator |
TSUBOI Koji 筑波大学, 医学医療系, 教授 (90188615)
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| Co-Investigator(Renkei-kenkyūsha) |
OHNO Tadao 早稲田大学, 理工学術院, 客員教授 (90160580)
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
Fiscal Year 2013: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2012: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
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| Keywords | 悪性脳腫瘍 / 放射線 / 腫瘍免疫 / ERストレス / Celecoxib |
|---|
| Research Abstract |
We found that the anti-inflammatory drug celecoxib significantly enhanced the radiosensitivity of mouse glioblastoma cells GL261 by loading ER stress. Based on this, we established GL261 cells constitutively expressing monomeric Kusabira-Orange (GL261-mKO) that were used to generate a mouse thigh subcutaneous tumor model in syngenic albino C57BL/6 mice, in which tumor size can be monitored by an in vivo imaging system. In experiments with local X-ray irradiation (IR) to tumors in this system, the cure rate was significantly higher with the concomitant oral administration of 5mg/kg of celecoxib as compared to IR alone. Furthermore, the same tumor cells that were re-challenged to the brain in the cured mice were all rejected, while they grew rapidly in mice that showed tumor regrowth after IR. ELISPOT assay demonstrated that IFN-gamma level was significantly elevated in mice that rejected re-challenged tumor cells, indicating that anti-tumor cellular immunity was established.
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