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Molecular pathology of thyroid tumorigenesis

甲状腺肿瘤发生的分子病理学

基本信息

批准号：
01570176
负责人：
KAWAOI Akira
金额：
$ 1.41万
依托单位：
Yamanashi Medical College
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (C)
财政年份：
1989
资助国家：
日本
起止时间：
1989 至 1990
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-01570176/
关键词：
Thyroid gland Carcinogenesis BrdU Sex hormones Androgen receptor Oncogenes Cell culture Nude mice

项目摘要

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.

1.用二异丙醇亚硝胺（DIPN）诱发大鼠甲状腺肿瘤，建立了三种细胞系。这些细胞生长在单层的方式，并未能证明甲状腺球蛋白合成的能力，在其免疫染色。结果：1.该肿瘤可移植于裸鼠体内，分化不良，甲状腺球蛋白合成异常.本文对DIPN诱发的大鼠甲状腺肿瘤进行了组织学和免疫组化研究，以探讨甲状腺癌的组织发生。在目前的实验条件下，所获得的数据支持肿瘤发生率的多阶段假说，而不是肿瘤发展的从头假说。溴脱氧尿苷（BrdU）标记法证实恶性病变中生长活性最高.采用DIPN诱发的大鼠甲状腺肿瘤，研究了雄激素在甲状腺癌发生中的可能作用。结果提示，雄激素对肿瘤的发生、发展起刺激作用。放射自显影研究和受体结合试验的结果支持了雄激素通过与甲状腺细胞核受体结合来刺激肿瘤生长的观点.用免疫组化法对DIPN诱发的大鼠甲状腺病变组织中铜锌锰超氧化物歧化酶（SOD）的定位研究表明，SOD活性的改变与甲状腺肿瘤的发生可能存在相关性，并存在SOD表达的调控机制。