Role of anchorage-independent growth regulation in tumor progression
Project/Area Number |
15K06829
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Tumor biology
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Research Institution | The University of Tokyo |
Principal Investigator |
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Project Period (FY) |
2015-04-01 – 2019-03-31
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Project Status |
Completed (Fiscal Year 2018)
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Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2017: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2016: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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Keywords | がん |
Outline of Final Research Achievements |
Anchorage-independent growth is characteristic for cancer cells, but the perspective of its regulatory mechanisms remains unclear. To address this, we focused on the molecule X which has been reported to control anchorage independent growth of cancer cells in vitro and tried to clarify the role of molecule X in vivo, especially in tumor progression. The analyses of X knockout mice revealed that molecule X expressed not only in cancer cells but also in host imuunesuppressive cells and increased the number of immunesuppressive cells. The molecule X also promoted tumor growth and lung metastasis in breast cancer model mice.
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Academic Significance and Societal Importance of the Research Achievements |
本研究により分子Xが、がん細胞だけでなくがん間質細胞にも発現し、腫瘍免疫を抑制することでがんの進展を促進していることが明らかとなった。分子Xはいわゆるがん精巣抗原であり、精巣以外の正常組織ではほとんど発現していないことから、分子Xを標的としてがん細胞とがん間質細胞の両者を制御することで、新たながん治療法の開発が期待される。
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Report
(5 results)
Research Products
(86 results)
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[Journal Article] Novel adherent CD11b+ Gr-1+ tumor-infiltrating cells initiate an immunosuppressive tumor microenvironment.2018
Author(s)
Tsubaki T, Kadonosono T, Sakurai S, Shiozawa T, Goto T, Sakai S, Kuchimaru T, Sakamoto T, Watanabe H, Kondoh G, Shinae Kizaka-Kondoh.
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Journal Title
Oncotarget
Volume: 9
Issue: 13
Pages: 11209-11226
DOI
Related Report
Peer Reviewed / Open Access / Int'l Joint Research
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[Journal Article] Mint3-mediated L1CAM expression in fibroblasts promotes cancer cell proliferation via integrin α5β1 and tumour growth.2017
Author(s)
Nakaoka HJ, Tanei Z, Hara T, Weng JS, Kanamori A, Hayashi T, Sato H, Orimo A, Otsuji K, Tada K, Morikawa T, Sasaki T, Fukayama M, Seiki M, Murakami Y, Sakamoto T.
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Journal Title
Oncogenesis
Volume: 6
Issue: 5
Pages: e334-e334
DOI
Related Report
Peer Reviewed / Open Access
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[Presentation] Control of metastatic niche formation by targeting APBA3/Mint3 in inflammatory monocytes2016
Author(s)
Toshiro Hara, Hiroki J. Nakaoka, Kouhei Mimura, Daisuke Hoshino, Masahiro Inoue, Fumitaka Nagamura, Yoshinori Murakami, Motoharu Seiki, and Takeharu Sakamoto
Organizer
Tenth AACR-Japanese Cancer Association Joint Conference
Place of Presentation
Hyatt Regency Maui (Maui, HI, USA)
Year and Date
2016-02-17
Related Report
Int'l Joint Research
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