1994 Fiscal Year Final Research Report Summary
Experimental research for childhood brain tumor
| Project/Area Number |
04670620
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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 |
Pediatrics
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| Research Institution | THE JIKEI UNIVERSITY SCHOOL OF MEDICINE |
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Principal Investigator |
MATSUSHIMA Hiroshi The Jikei University School of Medicine, Senior Investigator, 医学部, 講師 (70190460)
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| Co-Investigator(Kenkyū-buntansha) |
佐久間 秀哉 東京慈恵会医科大学, 医学部, 助手 (00246406)
中江 陽一郎 東京慈恵会医科大学, 医学部, 助手 (40188876)
奥野 章 東京慈恵会医科大学, 医学部, 講師 (70147289)
前川 喜平 東京慈恵会医科大学, 医学部, 教授 (80056613)
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| Project Period (FY) |
1992 – 1994
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| Keywords | brain tumor / gene therapy / nerve growth factor / differentiation / nerve growth factor receptor / シグナル伝達 |
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| Research Abstract |
The human trkA cDNA was transfected into the primitive neuroblasts to investigatethe roles of neuronal growth and differentiation. The cells lack expression of functional nerve growth factor (NGF) receptor (NGFR) genes. Trnasfectants expressing the trkA trnascriptionall activate immediate-early genes following NGF stimulation. NGFtratment results in growth arrest as well as down- regulation of the amlified N-myc oncogene. TrkA expressing neuroblasts are induced morphologicval and molecular differentiation. Thus, introduction of the trkA into the malignant neuroblasts generates a functional NGF receptor on the cell surface that leads the malignant cells to growth-arrest and differentiation in vitro and in vivo. Hence, NGF/NGFR signal cascade may be useful for the treatment of childhood brain tumor originated from primitive neuroblasts.
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