We are analyzing https://link.springer.com/article/10.1007/s00423-011-0788-5.

Title:
Molecular pathogenesis of nodular goiter | Langenbeck's Archives of Surgery
Description:
Introduction Familial clustering of goiters mostly with an autosomal dominant pattern of inheritance has repeatedly been reported. Moreover, other environmental and etiologic factors are likely to be involved in the development of euthyroid goiter. Therefore, a multifactorial etiology based on complex interactions of both genetic predisposition and the individuals’ environment is likely. Methods The line of events from early thyroid hyperplasia to multinodular goiter argues for the predominant neoplastic (i.e., originating from a single mutated cell) character of nodular structures. Etiologically, relevant somatic mutations are known in two thirds of papillary and follicular thyroid carcinomas and hot thyroid nodules. In contrast, the somatic mutations relevant for benign cold or benign isocaptant thyroid nodules which constitute the majority of thyroid nodules are unknown. Results The nodular process is triggered by the oxidative nature of thyroid hormone synthesis or additional oxidative stress caused by iodine deficiency or smoking. If the antioxidant defense is not effective, this oxidative stress will cause DNA damage followed by an increase of the spontaneous mutation rate which is a substrate for tumorogenesis. Conclusions Therefore, the hallmark of thyroid physiology—H2O2 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.
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article, google, scholar, pubmed, thyroid, cas, endocrinol, clin, goiter, metab, nodules, mutations, iodine, gene, krohn, med, growth, paschke, mutation, eur, nodular, cold, deficiency, expression, euthyroid, multinodular, cell, somatic, dna, nontoxic, symporter, iodide, receptor, van, content, familial, factors, genetic, oxidative, damage, mutagenesis, cancer, study, genes, toxic, thyrotropin, privacy, cookies, molecular, etiology,

Topics {✒️}

month download article/chapter related subjects sporadic nontoxic goiter caspase-3-dependent apoptosis induced population-based twin study gq-protein-protein kinase tgf-beta signaling cascade iodine-deficient mouse thyroid thyroid-stimulating hormone receptor multinodular goiter-1 locus na+/i- symporter gene iodide transport defect calcium-phosphoinositol signaling pathway thyroid physiology—h2o2 production thyrotropin-secreting pituitary adenoma multinodular goiter argues toxic multinodular goiter cyclic amp-dependent proliferation nontoxic goiter de la vieja full article pdf sodium/iodide symporter privacy choices/manage cookies gonzalez-navarro cj nodular goiter growth familial euthyroid goiter euthyroid familial goiter deoxyribonucleic acid damage early thyroid hyperplasia thyroid diseases tsh receptor gene nontoxic goitre multifactorial etiology based regulating thyroid growth thyrotropin receptor gene multinodular goiter goiter inhibiting action na+/i- symporter cold thyroid nodules recurrent t354p mutation homozygous missense mutation la rosa gl la porta ga hot thyroid nodules toxic thyroid nodules spontaneous mutation rate thyroid cancer cases thyroid hormone synthesis thyroid-hormone synthesis chromosomal instability

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         description:Familial clustering of goiters mostly with an autosomal dominant pattern of inheritance has repeatedly been reported. Moreover, other environmental and etiologic factors are likely to be involved in the development of euthyroid goiter. Therefore, a multifactorial etiology based on complex interactions of both genetic predisposition and the individuals’ environment is likely. The line of events from early thyroid hyperplasia to multinodular goiter argues for the predominant neoplastic (i.e., originating from a single mutated cell) character of nodular structures. Etiologically, relevant somatic mutations are known in two thirds of papillary and follicular thyroid carcinomas and hot thyroid nodules. In contrast, the somatic mutations relevant for benign cold or benign isocaptant thyroid nodules which constitute the majority of thyroid nodules are unknown. The nodular process is triggered by the oxidative nature of thyroid hormone synthesis or additional oxidative stress caused by iodine deficiency or smoking. If the antioxidant defense is not effective, this oxidative stress will cause DNA damage followed by an increase of the spontaneous mutation rate which is a substrate for tumorogenesis. Therefore, the hallmark of thyroid physiology—H2O2 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.
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