| Project/Area Number |
10671118
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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 |
General surgery
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| Research Institution | The University of Tokushima |
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Principal Investigator |
MIKI Hitoshi Second Department of Surgery, School of Medicine, The University of Tokushima, MD, Ph.D. Assistant Professor, 医学部, 講師 (40219605)
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| Co-Investigator(Kenkyū-buntansha) |
MASUDA Eitaro Second Department of Surgery, School of Medicine, The University of Tokushima, MD, Ph.D. Instructor, 医学部, 助手 (50314860)
KOMAKI Kansei Second Department of Surgery, School of Medicine, The University of Tokushima, MD, Ph.D. Assistant Professor, 医学部・附属病院, 講師 (60215382)
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| Project Period (FY) |
1998 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥3,200,000 (Direct Cost: ¥3,200,000)
Fiscal Year 1999: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 1998: ¥1,900,000 (Direct Cost: ¥1,900,000)
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| Keywords | thyroid anaplastic carcinoma / VEGF / metastasis / undifferentiated carcinoma / 血管内皮細胞増殖因子 / 血管新生 |
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| Research Abstract |
Proliferation and metastasis of undifferentiated human thyroid carcinoma cell line (ACT-1) was studied. The doubling time of ACT-1 was 48 hours. Transplantation of ACT-1 (2.5 x 10ィイD15ィエD1 cells) into subcutaneous tissues of severe combined immunodeficient (SCID) mice resulted in growing tumor, and pulmonary metastasis occurred three months after transplantation. Moreover, 3.0 x 10ィイD15ィエD1 cells of ACT-1 formed lung nodules three months after injection into the tail vein of SCID mice.
ACT-1 cells secreted IL-6, IL-8, M-CSF, GM-CSF and vascular endothelial growth factor (VEGF) in high concentration into culture medium. Expression of VEGF mRNA in ACT-1 was confirmed by RT-PCR. Expression of VEGF protein in surgically resected tissue from the patient from whom ACT-1 was derived was also confirmed by immunohistochemical method.
The effect of IL-6 and IL-8 on VEGF secretion from ACT-1 was studied. IL-8 did not make any influence on secretion of VEGF. However, IL-6 (100 ng/ml) stimulated secretion of VEGF from ACT-1, and this effect of IL-6 on VEGF secretion was neutralized by anti IL-6 antibody. Therefore, IL-6 produced by ACT-1 itself seems to stimulate the secretion from ACT-1 of VEGF, which develops the host vessels to support growth of carcinoma.
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