Specific loss of chondromodulin-I gene expression in chondrosarcoma and the suppression of tumor angiogenesis and growth by its recombinant protein in vivo
Project/Area Number |
10671350
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Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Orthopaedic surgery
|
Research Institution | Niigata University |
Principal Investigator |
ENDO Naoto Niigata University School of Medicine, Department of Orthopaedic Surgery, Professor, 医学部, 教授 (10251810)
|
Co-Investigator(Kenkyū-buntansha) |
HANYU Tadamasa Niigata University School of Medicine, Department of Orthopedic Surgery, Associate Professor, 医学部, 助教授 (20189591)
高橋 栄明 新潟大学, 医学部, 教授 (50018397)
|
Project Period (FY) |
1998 – 1999
|
Project Status |
Completed (Fiscal Year 1999)
|
Budget Amount *help |
¥2,600,000 (Direct Cost: ¥2,600,000)
Fiscal Year 1999: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1998: ¥1,600,000 (Direct Cost: ¥1,600,000)
|
Keywords | Chondromodulin-I / Angiogenesis inhibitor / Tumor suppression / Tumor angiogenesis / 軟骨肉腫 / in situ hybricization / 抗腫瘍作用 |
Research Abstract |
Chondromodulin-I (ChM-I) was previously identified as an angiogenesis inhibitor in cartilage. In this study, we showed that the level of ChM-I transcripts was substantially reduced to 100 or even less in the lower-grade chondrosarcomas, in articular cartilage or other benign cartilaginous tumors. We implanted human chondrosarcoma OUMS-27 cells into the back of nude mice that reproducibly produced tumors with cartilaginous matrix. Tumor-induced angiogenesis was evident when the tumors were excised 30 days after implantation. However, the local administration of recombinant human ChM-I almost completely blocked vascular invasion and tumor growth in vivo. Moreover, ChM-I also inhibited the growth of HT-29 colon adenocarcinoma in vivo, implying its therapeutic potential for solid tumors.
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Report
(3 results)
Research Products
(4 results)