Abstract
The etiology of thyroid autonomy and autonomously functioning thyroid nodules has been reviewed, with emphasis on histological (1, 2), molecular (3), and clinical aspects (4) as well as transgenic animal experiments that model thyroid autonomy (5). Somatic TSH receptor (TSHR) mutations have been discovered as the most prevalent molecular event in the etiology of autonomously functioning thyroid nodules (6). However, the mechanisms that induce TSHR mutations or determine their variable clinical phenotype are currently unknown. The purpose of this review is therefore to integrate new findings concerning the early molecular etiology of thyroid autonomy with previous molecular, histological, and in vitro results and to examine their possible clinical and therapeutic consequences.
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