The radiobiological study of radio-sensitization targeting molecules and/or signal transduction pathways that are involved in cell adhesion.
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 |
Section | 一般 |
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) |
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)
|
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 |
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
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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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Report
(4 results)
Research Products
(52 results)
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[Journal Article] Rectal Bleeding After High-Dose-Rate Brachytherapy Combined with Hypofractionated External-Beam Radiotherapy for Localized Prostate Cancer : The Relationship Between Dose-Volume Histogram Parameters and the Occurrence Rate2012
Author(s)
Okamoto M, Ishikawa H, Ebara T, Kato H, Tamaki T, Akimoto T, Ito K, Miyakubo M, Yamamoto T, Suzuki K, Takahashi T, Nakano T.
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Journal Title
Int J Radiat Oncol Biol Phys.
Volume: 82(2)
Pages: 211-7
Related Report
Peer Reviewed
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[Journal Article] Multicenter Phase II Study of an Opioid-based Pain Control Program for Head and Neck Cancer Patients Receiving Chemoradiotherapy2011
Author(s)
Zenda S, Matsuura K, Tachibana H, Homma A, Kirita T, Monden N, Iwae S, Ota Y, Akimoto T, Otsuru H, Tahara M, Kato K, Asai M.
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Journal Title
Radiother Oncol
Volume: 101(3)
Pages: 410-4
Related Report
Peer Reviewed
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[Presentation] 前立腺癌2011
Author(s)
秋元哲夫
Organizer
日本医学放射線学会総会:教育講演
Place of Presentation
東京
Year and Date
2011-04-08
Related Report
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[Presentation] 前立腺癌2011
Author(s)
秋元哲夫
Organizer
日本医学放射線学会総会
Place of Presentation
横浜、神奈川県
Year and Date
2011-04-08
Related Report
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[Presentation] 分子標的治療2010
Author(s)
秋元哲夫
Organizer
日本癌治療学会
Place of Presentation
京都国際会館(京都府)
Year and Date
2010-10-29
Related Report
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[Presentation] 寡分割照射2010
Author(s)
秋元哲夫
Organizer
日本放射線腫瘍学会小線源治療部会第12回研究会
Place of Presentation
東京
Year and Date
2010-05-16
Related Report
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[Presentation] 寡分割照射2010
Author(s)
秋元哲夫
Organizer
日本放射線腫瘍学会小線源治療部会第12回研究会
Place of Presentation
六本木ガーデンコンファレンスセンター(東京都)
Year and Date
2010-05-16
Related Report
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