1990 Fiscal Year Final Research Report Summary
Molecular pathology of thyroid tumorigenesis
| Project/Area Number |
01570176
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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 |
Human pathology
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| Research Institution | Yamanashi Medical College |
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Principal Investigator |
KAWAOI Akira Yamanashi Medical College, Department of Pathology, Professor, 医学部, 教授 (30059224)
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| Co-Investigator(Kenkyū-buntansha) |
TASAKA Kachio Yamanashi Medical College, Department of Immunology, Associate Prof., 医学部, 助教授 (40093265)
SUZUKI Kouichi Yamanashi Medical College, Department of Pathology, Assistant Teacher, 医学部, 助手 (20206478)
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| Project Period (FY) |
1989 – 1990
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| Keywords | Thyroid gland / Carcinogenesis / BrdU / Sex hormones / Androgen receptor / Oncogenes / Cell culture / Nude mice |
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| Research Abstract |
1. Three cell lines have been established from diisopropanolnitrosamine (DIPN) induced rat thyroid tumors. These cells grow in monolayer fashion and failed to demonstrate the capability of thyroglobulin synthesis in terms of its immunostaining. These tumors showed transplantable to nude mice with loered differentiation and thyroglobulin synthesis.
2. Histopathological and immunohistochemical studies were conducted on rat thyroid tumors induced by DIPN to elucidate the histogenesis of thyroid carcinoma. The data obtained supported the multistage hypothesis of tumorigenesis rater than the de novo hypothesis of tumor development under the present experimental conditions. Bromodeoxyuridine (BrdU) -labelling method proved the highest growth activity in the malignant lesions.
3. Employing DIPN induced rat thyroid tumors, the possible role of androgens in thyroid carcinogenesis was examined. The results suggested that androgens acted as a stimulatory factor to the development of tumors. The results of an autoradiographic study and a receptor binding assay supported the idea that the tumor growth is stimulated by androgens through binding with the nuclear receptor of the thyrocytes.
4. The findings of the immunohistochemical study on the localization of copper-zinc and manganese superoxide dismutases (SOD) in DIPN induced rat thyroid lesions suggested a possible correlation between alterations of SOD activities and thyroid tumorigenesis, and the existence of regulatory mechanism for SOD expression.
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