Analysis of the signal cross talk via CCL26 in the tumor microenvironment in osteosarcoma.
| Project/Area Number |
18K16666
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| Research Category |
Grant-in-Aid for Early-Career Scientists
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| Allocation Type | Multi-year Fund |
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| Review Section |
Basic Section 56020:Orthopedics-related
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| Research Institution | Oita University |
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Principal Investigator |
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| Project Period (FY) |
2018-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2019: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2018: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 骨肉腫 / 液性因子 / ケモカイン / 間葉系幹細胞 |
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| Outline of Final Research Achievements |
Osteosarcoma is the most common primary bone tumor, and advances in chemotherapy have improved survival rates, but there are still cases of distant metastasis, leading to poor prognosis. Recently, it has been established that the malignant trait of tumor cells does not only involve proliferative and metastatic activity but also the interaction between them and the normal cells surrounding them. Based on this perspective, we analyzed how osteosarcoma cells interact with different types of human mesenchymal stem cells. In this study, we elucidated the role of chemokine not only in terms of its mechanism in primary tumors but also in distant metastatic lesions, and we believe that our findings will contribute to the development of a new treatment strategy for osteosarcoma.
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| Academic Significance and Societal Importance of the Research Achievements |
過去30年にわたり骨肉腫に対する新薬は登場しておらず、現在の標準治療に用いられている抗癌剤は1970年代に開発された薬剤である。既存の抗癌剤の組み合わせや投与タイミングの改変、薬剤追加による治療成績の向上はもはや限界に達している。正常細胞と腫瘍細胞間のケモカインを介した相互作用に、どのような遺伝子が関与し、周辺環境を腫瘍細胞の生存や転移に有利な状態に変化させるか、が明らかになると考えられ、本研究の意義は極めて大きい。そのメカニズムを明らかにすることで、従来の化学療法とは全く異なる新しい治療法の開発に繋がる可能性があると考えている。
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Report
(3 results)
Research Products
(2 results)
