2001 Fiscal Year Final Research Report Summary
Gene Therapy for the Childhood Brain Tumors
Project/Area Number |
12670780
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Pediatrics
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Research Institution | JIKEI UNIVERSITY SCHOOL OF MEDICINE |
Principal Investigator |
MATSUSHIMA Hiroshi Jikei University School of Medicine, Department of Pediatrics, Associate Professor, 医学部, 助教授 (70190460)
|
Co-Investigator(Kenkyū-buntansha) |
IMAI Masayuki Jikei University School of Medicine, Department of Pediatrics, Assistant, 医学部, 助手 (30203300)
HAMANO Shinichiro Jikei University School of Medicine, Department of Pediatrics, Assistant, 医学部, 助手 (80208595)
NARA Takahiro Jikei University School of Medicine, Department of Pediatrics, Assistant Professor, 医学部, 講師 (80180537)
MINAMITANI Motoyuki Jikei University School of Medicine, Department of Pediatrics, Assistant, 医学部, 助手 (00229775)
ARITA Jiro Jikei University School of Medicine, Department of Pediatrics, Assistant, 医学部, 助手 (40246369)
|
Project Period (FY) |
2000 – 2001
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Keywords | Genetherapy / Nervegrowthfactor / Nerve growth factor receptor / Tumor necrosis factor / Ik-B / IκB-2 / クロストーク |
Research Abstract |
The human trkA cDNA was transfected into the human neuroblastoma cells to investigate the possibility of the gene therapy for childhood neuronal tumors. TrkA expression in irmnature neurons was sufficient to generate a functional NGF receptors that lead to growth arrest and differentiation of immature neurons in vitro and in. vivo following NGF treatment. Hence, NGF/NGF-receptor cascade may be useful for the gene therapy to he childhood neuronal tumors that are thought to be developed from the neuronal stem cells. Furthermore, we investigated the roles of NFk-B/Ik-B in NGF/NGFR signal cascade. TNF treatment significantly enhanced NGF induced-morphological and -molecular differentiation of neuronal cells. However, expression of dominant negative Ik-B-α interfered the effects of NGF. These results suggest the presence of cross talk between NGFINGFR signal cascade and TNF /NFk-B/IkB-α cascade.
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