Open AccessAutonomously functioning thyroid nodules in a former iodine-deficient area commonly harbor gain-of-function mutations in the thyrotropin signaling pathway
Author(s) -
NA Georgopoulos,
Gerasimos P. Sykiotis,
Argyro Sgourou,
Adamandia Papachatzopoulou,
KB Markou,
Venetsana Kyriazopoulou,
Athanasios G. Papavassiliou,
A. G. Vagenakis
Publication year - 2003
Publication title -
european journal of endocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.897
H-Index - 148
eISSN - 1479-683X
pISSN - 0804-4643
DOI - 10.1530/eje.0.1490287
Subject(s) - thyroid nodules , thyrotropin receptor , thyroid , endocrinology , medicine , pathogenesis , mutation , somatic cell , germline mutation , population , hormone , biology , cancer research , genetics , graves' disease , gene , environmental health
Somatic activating mutations of the thyrotropin (thyroid-stimulating hormone (TSH)) receptor (TSHR) and G(alphas) protein have been detected in solitary toxic adenomas and toxic multinodular goiters, but their role in the pathogenesis of autonomous nodules is debated. The frequency of mutations is highly variable among populations and is inversely proportional to iodine intake.
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