| Project/Area Number |
05671163
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Cerebral neurosurgery
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| Research Institution | Kobe University School of Medicine |
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Principal Investigator |
KOKUNAI Takashi Kobe University School of Medicine, Instructor of Attached Hospital, 医学部・附属病院, 講師 (30178248)
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| Co-Investigator(Kenkyū-buntansha) |
TAMAKI Norihiko Kobe University School of Medicine, Professor, 医学部, 教授 (10030941)
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| Project Period (FY) |
1993 – 1995
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| Project Status |
Completed (Fiscal Year 1995)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1995: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1994: ¥400,000 (Direct Cost: ¥400,000)
Fiscal Year 1993: ¥1,200,000 (Direct Cost: ¥1,200,000)
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| Keywords | Brain tumor / Tumor-suppressor gene / p53 gene / Nerve growth factor receptor / Differentiation / Medulloblastoma |
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| Research Abstract |
The expression of mutant p53 gene product was found in 34% mudulloblastoma, 22% ependymoma, and 47% other gliomas in various pediatric brain tumors, although it was not found in normal brain tissues including cerebellum. And also, the localization of mRNA of mutan p53 gene analyzed by in situ hybridization was the almost same localization of mutant p53 gene product. And also, the tissues with high MIB1 index were shown the high expression of mutant p53 gene product. It was correlated between the growth potential and the expression of mutant p53 gene product.
In primitive neuroectodermal tumors, nerve growth factor receptor (NGF-R) was expressed in immature neurogenic tumors, such as medulloblastoma.. We selected the subclones of tropomyosin receptor kinase (trk) -positive cells and low-affinity NGF-R-positive cells from human medullobrastoma cell line (MED-3) and examine the responsibility against NGF.Trk-positive subclone showed the induction of differentiation and the inhibition of cell growth inducd by NGF.It was suggested the role of trk gene protooncogene in differentiation of medulloblastoma. Furthermore, the prognosis in trk-positive medulloblastoma was better than that in trk-negative medulloblastoma. On the otherhand, there was no correlation between the prognosis, the period of recurrence and the responsibility against treatment and the expression of mutant p53 gene product. From the above results, it was suggested that trk protooncogene is the target gene in differentiation of medulloblastoma.
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