| Project/Area Number |
08672052
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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 |
小児外科
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| Research Institution | CHIBA UNIVERSITY |
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Principal Investigator |
TANABE Masahiro Chiba University School of Medicine, Department of Pediatric Surgery, Associate Professor, 医学部, 助教授 (10207160)
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| Co-Investigator(Kenkyū-buntansha) |
KURODA Hiroaki Chiba University School of Medicine, Department of Pediatric Surgery, Senior Res, 医学部・付属病院, 医員
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| Project Period (FY) |
1996 – 1997
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| Project Status |
Completed (Fiscal Year 1997)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1997: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 1996: ¥1,000,000 (Direct Cost: ¥1,000,000)
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| Keywords | neuroblastoma / retinoic acid / ganglioneuroblastoma / MR Spectroscopy / 分化誘導 / MR Spctroscopy |
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| Research Abstract |
To induce neuroblastoma differentiation resulting in ganglioneuroblastoma, we used a human neuroblastoma cell line (SH-SY-5Y) growing in nude mice. All-trans-retinoic acid (RA) was dissolved in corn oil to concentrations of 5,10,20, and 40mM.Mice were treated with intragastric administration of 0.1mL RA for 7 consective days to investigate drug toxicity, antitumor effects and histological changes of tumors after RA treatment.
Drug toxicity : Survival of 5 mice per each group was examined on the eighth day after 7 consective days of RA treatment. All mice treated with 5mM survived but 4 with 10mM,1 with 20mM and no mice treated with 40mM of RA survived.
Effects on tumor growth : Control animals received corn oil alone. Tumor growth was assessed 3 times per week from the time when a tumor was first found. RA (5mM) treatment started when the tumor grew in volume to 300-900mm^3. Tumor growth was delayd during tretment with RA,but demonstrated the same rate of growth as contrls after sessation of treatment. Tumor growth delay after RA treatment was 2.6 days and specific growth delay was 0.49.
Histological changes : Histological examination by H&E Staining showed stromal development with neuritic processes, cell enlargement, and focal necrosis in tumors, resulting in a rosette-fibrillary type from a round cell type of neuroblastoma. Immunohistochemical staining showed that the number of NSE or Synaptofesin positive cells increased and Ki67 positive cells decreased in comparisson with the conrol group afater RA treatment. However, no S-100 prortein postive cells were recognised in the tumor after RA treatment. Electronic microscopic examination showed proliferation of neuritic processes.
Growth of neuroblastoma (SH-SY-5Y) was suppressed by in vivo RA treatment and histological examination showed development of neuritic processes, but these changes did not indicate that RA induced neuroblastoma differentiation resulting in ganglioneuroblastoma.
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