Project/Area Number |
15390431
|
Research Category |
Grant-in-Aid for Scientific Research (B)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Cerebral neurosurgery
|
Research Institution | Department of Neurosurgery, Graduate School of Medical Science, Kanazawa University, Kanazawa |
Principal Investigator |
WATANABE Takuya (2005) Kanazawa University, Department of Neurosurgery, Graduate School of Medical Science, Assistant, 医学系研究科, 助手 (90399775)
山下 純宏 (2003-2004) 金沢大学, 医学系研究科, 教授 (90026948)
|
Co-Investigator(Kenkyū-buntansha) |
喜多 大輔 金沢大学, 医学部附属病院, 助手 (10377385)
渡邉 卓也 金沢大学, 医学系研究科, 助手
|
Project Period (FY) |
2003 – 2005
|
Project Status |
Completed (Fiscal Year 2005)
|
Budget Amount *help |
¥14,200,000 (Direct Cost: ¥14,200,000)
Fiscal Year 2005: ¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2004: ¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2003: ¥7,400,000 (Direct Cost: ¥7,400,000)
|
Keywords | glioma invasion / matrix metalloproteinase / extracellular matrix / Testican / Crk 1 / Apaf-1 / TP53 / ADAMTS / AT / RT / hSNF5 / INI1 / cyclin D1 / γ-catenin / ADAMTS-5 / brevican / microcatheter fence-post / LOH 1p,19q / glioma / deep-Seated gliobiastoma / TP53 mutation / invasion / aggrecanase / Ets-1 / microarray / peripheral nerve tumor / 12q22-23 LOH / Ets transcription factor / MMP |
Research Abstract |
Our main purpose is to analyze interaction between proteinase and extracellular matrix on glioma invasion. In the year of 2003, we published a review on relationship between matrix metalloproteinase and glioma invasion. We had cloned N-Tes (Patented in 2001), which belongs Testican family and inhibits glioma invasion previously. In addition to this, we found other Testican family (Testican-1 and 3) also suppress invasion of glioma, while Testican-2 contributes invasive activity. Then, we reported that phosphorylation of an adapter protein of Crk I is related to glioma invasion. We also reported that low expression level of Apaf-1 which is an apoptosis inducing protein is related to loss of heterozygosity on chromosome 12 in glioblastoma. In the year of 2004, we reported that almost all the glioblastoma originated from basal ganglia has mutation in TP53 gene. In the year of 2005, we reported that ADAMTS-5,which belongs to ADAMTS family metalloproteinase, is highly expressed in glioblastoma. We also found ADAMTS-5 can degrade brevican which is the most abundant extracellular matrix in brain. In addition to this, we reported that cyclin D1 is related to good prognosis in medulloblastoma and that cyclin D1 is also highly expressed in atypical teratoid/rhabdoid tumor. Then, we edited a book titled, "Brain Tumor Surgery- new strategy based on biological behavior of brain tumors", containing 47 articles of current knowledge on brain tumor therapy. These results are quite fruitful, since we have added some important knowledge on mechanism of invasive process and genetic mutation in glioblastoma, which is the most lethal of brain tumor.
|