Growth activation alone is not sufficient to cause metastatic thyroid cancer in a mouse model of follicular thyroid carcinoma.

ABSTRACT: TSH is the major stimulator of thyrocyte proliferation, but its role in thyroid carcinogenesis remains unclear. To address this question, we used a mouse model of follicular thyroid carcinoma (FTC) (TRbeta(PV/PV) mice). These mice, harboring a dominantly negative mutation (PV) of the thyroid hormone-beta receptor (TRbeta), exhibit increased serum thyroid hormone and elevated TSH. To eliminate TSH growth-stimulating effect, TRbeta(PV/PV) mice were crossed with TSH receptor gene knockout (TSHR(-/-)) mice. Wild-type siblings of TRbeta(PV/PV) mice were treated with an antithyroid agent, propylthiouracil, to elevate serum TSH for evaluating long-term TSH effect (WT-PTU mice). Thyroids from TRbeta(PV/PV)TSHR(-/-) showed impaired growth with no occurrence of FTC. Both WT-PTU and TRbeta(PV/PV) mic

SUBMITTER: Lu C 

PROVIDER: S-EPMC2851190 | biostudies-literature | 2010 Apr

REPOSITORIES: biostudies-literature