This study aimed to investigate iodide uptake and the expressions of thyroid-specific molecules after the transfection of human thyrotropin receptor (hTSHR) gene in poorly differentiated follicular thyroid cancer cell line (FTC-133).
The activating TSHR mutation could promote in vivo FTC development in PAX8-PPARgamma-positive thyrocytes under poor blood supply with deprivation of growth factors but restraint the tumor growth when growth factors are supplied.
Therefore, expression analyses for Tg, TSH-R, cytokeratin 19 (CK 19), human telomerase reverse transcriptase (hTERT) and oncofoetal fibronectin (onfFN) were carried out using cDNAs derived from (1) leukocyte fractions, (2) 18 follicular thyroid carcinomas (FTCs) and 48 papillary thyroid carcinomas (PTCs), and (3) leukocytes of two thyrocyte-depleted individuals treated for C-cell carcinoma of the thyroid.
This is the first case report of a patient with toxic follicular thyroid carcinoma harbouring two different TSHR mutations and presenting with non-functional lung metastases.
This mutation, which was previously reported to activate both cyclic adenosine monophosphate and the inositol phosphate-diacylglycerol cascades, may have been responsible for the constitutive activation of the thyrotropin receptor and resulting hyperfunction of this follicular carcinoma.
Only 2 of 30 had somatic mutations of the TSH-R (codon 632: ACC to GCC, Thr to Ala; and ACC to ATC, Thr to Ile, respectively), the latter in a patient with a thyroid hormone-producting follicular carcinoma.