Project/Area Number |
21591221
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Hematology
|
Research Institution | Keio University |
Principal Investigator |
|
Co-Investigator(Kenkyū-buntansha) |
YANAGAWA Hiroshi 慶應義塾大学, 理工学部, 教授 (40327672)
山田 健人 慶應義塾大学, 医学部, 准教授 (60230463)
|
Co-Investigator(Renkei-kenkyūsha) |
YAMADA Taketo 慶應義塾大学, 医学部, 准教授 (60230463)
|
Project Period (FY) |
2009 – 2011
|
Project Status |
Completed (Fiscal Year 2011)
|
Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2011: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2010: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2009: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
|
Keywords | 多発性骨髄腫 / サリドマイド / 破骨細胞 / 増殖因子 / 骨髄異形成症候群(MDS) / In Vitro Virus法 / 骨病変 / in vitro virus法 |
Research Abstract |
To overcome multiple myeloma, we examined(1) molecular mechanism of anti-tumor effect of thalidomide,(2) molecular targeting of angiogenic growth factor and(3) inhibition of differentiation and activity of mouse osteoclasts using novel thalidomide derivative. We found that this compaoud directly binded to one of the essential factors for cell mitosis. Soluble receptor 1 for fibroblast growth factor could regulate proliferation of myeloma cells in vitro. It was also found that TC11 inhibited differentiation of osteoclats and absorption of bone matrix, suggesting potential therapeutic effect of TC11 on bone lesion in myeloma patients.
|