Strict regulation observed among transcriptional activity of TGFb1 and their receptor TGFbetaRI-III genes in control tissues is disturbed in all pathological tissues - it is completely disturbed in PTC and GD, and partially in NG and TNG.
Immunohistochemical analyses of TGF-β1 were performed with 120 archived formalin-fixed and paraffin-embedded thyroid resection tissue samples that included 60 cases of thyroid cancers (papillary thyroid carcinoma, follicular thyroid carcinoma), 14 cases of nodular goiter (NG), 16 cases of thyroid adenoma, 15 cases of Graves disease, 15 cases of Hashimoto's thyroiditis.
To clarify whether the +869T/C polymorphism in the transforming growth factor-beta1 (TGF-beta1) gene, which is associated with TGF-beta1 expression, is involved in the intractability of GD and severity of HD, we genotyped the TGF-beta1 +869T/C polymorphism by polymerase chain reaction-restriction fragment length polymorphism method in genomic DNA samples from 33 patients with HD who developed hypothyroidism before they were 50 years old (severe HD) and 30 untreated, euthyroid patients with HD who were older than 50 years (mild HD).