| Project/Area Number |
21591620
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Radiation science
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| Research Institution | 独立行政法人国立がん研究センター (2011)
Tokyo Women's Medical University (2009-2010) |
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Principal Investigator |
AKIMOTO Tetsuo 独立行政法人国立がん研究センター, 臨床開発センター, 部長 (10261851)
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| Project Period (FY) |
2009 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2011: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2010: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2009: ¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
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| Keywords | 放射線感受性 / 放射線 / 分子標的 / 接着因子 / 放射線抵抗性 / 接着分子 / 放射線生物 / 放射線応答 |
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| Research Abstract |
A purpose of this study is to achieve "the radiosensitive sensibilization that we determine a radioresistant factor due to the cell adhesion mechanism of the cancer cell, and targeted the molecules and signal transduction". We are involved in the control of cellular infiltration and the metastasis of the cancer cell secondary to last year and examine it mainly on Dyasdherin which is an adhesion factor providing it controlling a function of E-cadherin to minus number and a correlation with the radiation sensitivity and obtain the following results this year. Using the human cancer cell cultured cell which varied in radiation sensitivity, we examined manifestation of Dyasdherin and cellular proliferative capacity and radiation sensitivity in vitro. As a result, the proliferation potency that assumed a growth marker an index if manifestation of Dyasdherin is high is high, and radiation sensitivity tend to be low. The manifestation enhance the change after the radiation that there is not o
… More
f the things in the localization temporarily when we examine a change of the Dyasdherin manifestation with 2) irradiation. With a change of these 3) manifestation, we confirm that the activation of the signal acts in concert with EGFR and is activated. These results are places continuing a study more now to determine the mechanism and associated signaling pathway with a thing suggesting the possibility that a cell adhesion factor is associated with the radiation reply of the cancer cell. Particularly, we pay attention to the relations with the radiation reply of a cell growth factor receptor and the cancer cell which we are parallel and examine. Activation of EGFR and HER2 and the localized change(from the cell surface to a nucleus) are induced by irradiation, but the localized change is adorned when we inhibit the activation. As a result, we confirm that we inhibit a DNA lesion repairing process by the radiation and are involved in a radiosensitive change(radiosensitive augmentation). We examined a mediator about activation and cell death of these signal transduction and the survival mainly on the crosstalk with the signal which was due to a cell adhesion factor. Molecules and signal transduction working primary by this analysis find and confirm it how the radiation reply of the cancer cell changes by the activation inhibition and manifestation suppression and we examine the likelihood as the treatment target and are going to report it. Less
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