| Project/Area Number |
21591875
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Cerebral neurosurgery
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| Research Institution | Kagoshima University |
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Principal Investigator |
ARITA Kazunori 鹿児島大学, 医歯学総合研究科, 教授 (90212646)
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| Co-Investigator(Kenkyū-buntansha) |
YUNOUE Syunji 鹿児島大学, 医学部・歯学部附属病院, 助教 (20404478)
HIRANO Hirofumi 鹿児島大学, 医学部・歯学部附属病院, 講師 (00264416)
TAKANO Kouji 東京大学, 大学病院, 助教 (20236243)
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| Project Period (FY) |
2009 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2011: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2010: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2009: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | pituitary adenoma / CD133 / endothelial progenitor / angiogenesis / tumor stem cell / 下垂体腺腫 / 腫瘍幹細胞 / CD133陽性細胞 / endothelial progenitor cell |
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| Research Abstract |
Stem-like cells in tumors are capable of self-renewal and pluri-differentiation ; they are thought to play important roles in tumor initiation and maintenance. Stem-like cells in malignant glioma express CD133. We examined samples from human pituitary adenoma, a generally benign neoplasm, for CD133 expression using routine immunohistochemical and biochemical methods.
Our study of 70 pituitary adenomas(clinically nonfunctioning adenomas and growth hormone-, prolactin-, adrenocorticotropic hormone-, and thyroid stimulating hormone producing adenomas) showed that 18(25. 7%) expressed CD133. This rate was higher in clinically non-functioning(33.3%) than functioning adenomas(12.0%)(p=0.085). Real-time PCR assay revealed the expression of CD133 mRNA in samples immunohistochemically positive for CD133. Neither the patient age and gender, nor the tumor size or postoperative recurrence rate correlated with CD133 positivity. CD133^+cells ubiquitously coexpressed CD34, nestin, and VEGFR2(KDL1). S-100 and GFAP were not coexpressed with CD133. Chromogranin A, Pit-1, SF-1, and NeuroD1 were immune-negative, indicating that CD133^+cells did not have the potential to differentiate into functional endocrine cells.
Our data suggest that the expression of CD133 in pituitary adenomas is related to immature endothelial progenitor cells that may play a role in the neovascularization of pituitary adenomas. Further studies are needed to elucidate the significance of CD133^+ cells with respect to neovascularization and their sustainable growth in pituitary adenomas.
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