Derwahl M, Manole D, Sobke A, Broecker M
University Clinic of Internal Medicine, Bergmannsheil, Ruhr-University of Bochum, Germany.
Exp Clin Endocrinol Diabetes. 1998;106 Suppl 4:S6-9. doi: 10.1055/s-0029-1212048.
In iodine deficiency areas, activating mutations in the TSH receptor and Gs-alpha gene are found in the majority of toxic thyroid adenomas and in some toxic goiter nodules. Since TSH receptor and Gs-alpha gene mutations are very rare in areas with high iodine supply, iodine deficiency has been suspected to favor the occurrence of these mutations by yet unknown pathways. However, TSH receptor and Gs-alpha gene mutations alone are not sufficient to cause toxic adenomas and nodules. There is compelling evidence that other secondary and cAMP-independent mechanisms, including enhanced expression of various growth factors, their corresponding receptors and of signaling proteins, may affect the mutated cell and thus promote cell proliferation and in turn generation of the tumor.
在碘缺乏地区，大多数毒性甲状腺腺瘤和一些毒性甲状腺肿结节中发现促甲状腺激素（TSH）受体及Gs-α基因的激活突变。由于在碘供应充足地区TSH受体和Gs-α基因突变非常罕见，因此怀疑碘缺乏通过尚不明的途径促使这些突变的发生。然而，单独的TSH受体和Gs-α基因突变不足以导致毒性腺瘤和结节。有确凿证据表明，其他继发性且不依赖环磷酸腺苷（cAMP）的机制，包括各种生长因子、其相应受体及信号蛋白表达增强，可能影响突变细胞，从而促进细胞增殖，进而导致肿瘤的产生。
