Project/Area Number |
20592055
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Ophthalmology
|
Research Institution | Wakayama Medical University |
Principal Investigator |
MIYAZAKI Kenichi Wakayama Medical University, 医学部, 博士研究員 (40382329)
|
Co-Investigator(Kenkyū-buntansha) |
SAIKA Shizuya 和歌山県立医科大学, 医学部, 教授 (40254544)
OKADA Yuka 和歌山県立医科大学, 医学部, 講師 (50264891)
TOMOYOSE Katsuo 和歌山県立医科大学, 医学部, 助教 (00453176)
|
Project Period (FY) |
2008 – 2010
|
Project Status |
Completed (Fiscal Year 2010)
|
Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2010: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2009: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2008: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
|
Keywords | 小児悪性腫瘍 / Sonic hedgehog / Smad / Y79 / 網膜芽細胞腫 / 網膜芽細胞腫培養細胞株Y79 / ラット / 組織学 / Sonic hedeghog / Gli / トランスフォーミング成長因子ベータ / リン酸か |
Research Abstract |
The study was conducted for the purpose of development of a new strategy of treatment of retinoblastoma by targeting Sonic Hedgehog (Shh) signal. First, immunohistochemistry was carried out to examine the status of Shh signal and cell-growth related signals. Shh, Smoothened Patched and Gli-1 weere readily detected in retinoblastoma cells. Rb and Erk-1 was also observed. These findings suggest that Shh signal is active in retinoblastoma cells. A culture of a cell line established from retinoblastoma (Y79) was treated with cyclopamine and cell proliferation was assayed by using MTT assay. Although adding cyclopamine seemed to suppress cell proliferation of Y79 retinoblastome cell line, the data did not exhibit statistical significacy. Neovascularization is critical in tumor growth. We showed that blocking Shh signal by addition of cyclopamine inhibited neovascularization by cultured vascular endothelial cells cultured on the fibroblast layer. Finally, we implanted Y79 cells into the anterior chamber of a C57BL/6 mouse. However, the cells did not form tumor growth and settled arounf the anterior chamber angle. Further improvement of cell implantation is to be developed for the purpose of establishment of retinoblastoma mouse model.
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