Molecular pathogenesis of nodular goiter

Abstract

Therefore, the hallmark of thyroid physiology--H(2)O(2) production during hormone synthesis--is very likely the ultimate cause for the frequent mutagenesis in the thyroid gland. Because iodine deficiency increases the oxidative burden, DNA damage and mutagenesis could provide the basis for the frequent nodular transformation of endemic goiters.

Papillary Thyroid Carcinoma: A Malignant Tumor with Increased Antioxidant Defense Capacity

“…Larger goiters that have a tendency to grow and to acquire retrosternal position are characterized by increased oxidants production, whereas the negative correlation between TAS and goiter size reveals the importance of appropriate antioxidant capacity in the prevention of goiter growth. The importance of antioxidant defense has been previously demonstrated as impaired antioxidant defense that leads to the increased growth, DNA damage and malignant transformation of benign goiters (Paschke 2011). Intraglandular PTC dissemination appears to be influenced by TAS, which was significantly lower in tumor tissue of patients with multicentric PTC.…”

Oxidative Stress in Human Thyroid Gland Under Iodine Deficiency Nodular Goiter: From Harmlessness to Hazard Depending on Copper and Iodine Subcellular Distribution

“…It is generally known that nodules develop in pathologically affected thyroid tissue [2]. We established that hyperplastic thyroid epithelium under iodine deficiency nodular colloidal goiter sacrificed its ability for iodine organification and therefore increased of level of inorganic iodine.…”

“…Determination of the key molecular markers is of considerable interest as they can be used to predict such pathologies. Iodine deficiency in thyroid pathology occurrence rate is rapidly increasing [2]. It has miscellaneous origins as a result of complex interaction of endogenous and exogenous factors and arises in the setting of high level of "nonspecific" goitrogens, among them copper, in the environment.…”

Порушення Макро- Та Мікроелементного Забезпечення У Хворих На Вузлову Патологію Щитоподібної Залози З Регіонів, Постраждалих Після Чорнобильської Аварії

“…Як на-слідок, гіперплазія формує клони змінених клітин. Деякі з них складають соматичні мутації TSHR, які призводять до виникнення автономно функціоную-чих тиреоїдних вузлів або містять мутації, що сприя-ють дедиференціації, а потім виникненню холодних тиреоїдних вузлів, або аденом [12].…”