| Project/Area Number |
11672023
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Surgical dentistry
|
|---|
| Research Institution | Kanagawa Dental College |
|---|
Principal Investigator |
MATSUMOTO Goichi Kanagawa Dental College, Oral Surgery, Lectureship, 歯学部, 講師 (60199867)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
HIRATA Kazuya Kanagawa Dental College, Oral Surgery, Assistant, 歯学部, 助手 (80308311)
|
|---|
| Project Period (FY) |
1999 – 2000
|
| Project Status |
Completed (Fiscal Year 2000)
|
| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,900,000)
Fiscal Year 2000: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 1999: ¥2,500,000 (Direct Cost: ¥2,500,000)
|
|---|
| Keywords | angiostatin / gene therapy / squamous cell carcinoma / 血管新生 / (1)アンジオスタチン / (2)扁平上皮癌 / (3)VEGF / (4)VEGFR-2 / (5)血管新生 |
|---|
| Research Abstract |
Tumor growth is an angiogenesis dependent process and therapeutic strategies aimed at inhibiting angiogenesis are theoretically attractive. Angiostatin has been shown to potently inhibit endothelial proliferation in vitro and tumor growth in vivo. We now show that a shift in the balance of tumor angiogenesis by gene transfer of a cDNA coding for mouse angiostatin into mouse squamous cell carcinoma NRS-1 and SCC-VII cells supresses tumor growth in vivo. The inhibition of an angiostatin transfected tumor was accompained by a marked reduction in vascularity and the presence of many apoptotic tumor cells. However, transfected-angiostatin cDNA does not affect the expression of the VEGF and VEGF-R2 in the vascular endothelium. The inhibition mechanisms of neovascularization may be mediated independent of VEGF : VEGF-R2 complex. Our data may provide a useful approach for human oral cancer therapy by gene therapy with angiostatin.
|
