Molecular analysis of platelet-dependent tumor cell proliferation
| Project/Area Number |
25830125
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Tumor therapeutics
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| Research Institution | Japanese Foundation for Cancer Research |
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Principal Investigator |
TAKAGI Satoshi 公益財団法人がん研究会, がん化学療法センター, 研究員 (20582240)
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| Research Collaborator |
SATO Shigeo
OH-HARA Tomoko
TAKAMI Miho
NODA Sachie
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2014: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 骨肉腫 / 血小板 / 血小板凝集 / PDGF / Akt / 癌 / 分子標的治療 |
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| Outline of Final Research Achievements |
In this study, we clarified the signal transduction pathway which was activated in cancer cells by the interaction with platelets and investigated the efficacy of inhibitors which target the identified pathway. We found that osteosarcoma cells could activate platelets via the direct cell-cell interaction and the PDGF-BB released by activated-platelets activated PDGFR-Akt axis in the osteosarcoma cells. Furthermore, we found that Sunitinib, a PDGFR inhibitor, and LY294002, a PI3K inhibitor, suppressed platelet-dependent sarcoma cells proliferation. These findings suggest that these inhibitors targeting PI3K-Akt axis and/or anti-platelet agents might be the anti-tumor drugs.
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Report
(3 results)
Research Products
(12 results)
