Overexpression of epidermal growth factor and epidermal growth factor-receptor mRNAs in dyshormonogenetic goiters

Thyroid malignancy has been induced by long-term endogenous thyrotropin (TS H) stimulation in experimental animals, leading to local and distant metast asis. It has been postulated that constant and prolonged endogenous TSH sti mulation in dyshormonogenetic thyroid tissues could result in thyroid neopl asia. The possible role of growth factors and oncogenes in goitrogenesis an d favoring neoplasia has also been mentioned. Overexpression of certain gro wth factors and/or their receptors, and of oncogenes implicated in growth p romotion may play a significant role in the relatively frequent finding of thyroid malignancy in congenital goiters. In this study the expression of e pidermal growth factor (EGF), epidermal growth factor receptor (EGF-R), tra nsforming growth factor-beta (TGF-beta), c-myc, and p53 mRNAs was determine d in 14 thyroid tissue samples: 6 from patients with thyroid peroxidase (TP O) gene mutations, 4 with thyroglobulin (Tg) gene defects and 4 normal thyr oid tissues. EGF mRNA overexpression was seen in 7 of 10 dyshormonogenetic tissues (3.5 to 12.0 arbitrary optical densitometry units [AODU]) and consi dered significantly higher (p < 0.01) when compared to normal thyroid tissu es (0.25 to 0.32 AODU). Moreover, overexpression of EGF-R mRNA was present in 6 of 10 dyshormonogenetic tissues (2.23 to 13.03 AODU) and considered si gnificantly higher (p ( 0.01) when compared to normal thyroid tissues (0.42 to 0.65 AODU). There was no difference in c-myc, p53, and TGF-<beta> mRNAs expression between dyshormonogenetic and normal tissues. The overexpressio n of EGF and EGF-R mRNAs found in dyshormonogenetic tissues may suggest tha t this growth factor may play a role in cellular proliferation and contribu te to goiter formation.