| Project/Area Number |
18591376
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Radiation science
|
|---|
| Research Institution | Tokyo Women's Medical University |
|---|
Principal Investigator |
AKIMOTO Tetsuo Tokyo Women's Medical University, School of Medicine, Associate Professor (10261851)
|
|---|
| Project Period (FY) |
2006 – 2007
|
| Project Status |
Completed (Fiscal Year 2007)
|
| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥300,000)
Fiscal Year 2007: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2006: ¥2,200,000 (Direct Cost: ¥2,200,000)
|
|---|
| Keywords | radiosensitivity / molecular target / DNA damage repair / radiation therapy / DNA損傷修復 / DNA二重鎖切断 / アポトーシス |
|---|
| Research Abstract |
We reported the correlation between changes in H2AX foci and radiosensitivity in various cancer cells, and demonstrated that repair system of radiation-induced DNA damage is closely associated with radioresponse or radiosensitivity of cancer cells. In addition, we explored the mechanism of thermal radiosensitization. The results of our study demonstrated that heat in combination with radiation decreased the formation of radiation-induced γH2AX foci and Nbsl, and preheating resulted in the increase in SF and decrease in the focus formation of γH2AX. Considering from the fact that γH2AX is a sensor for DNA damage site, the results of this study suggested the possibility that heat in combination with radiation would modify the repair process of radiation-induced DNA damage through masking of DNA damage site or inhibition of access of molecules that were involved in DNA damage repair to DNA damage site.
|
