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Molecular Pathogenesis of Euthyroid and Toxic Multinodular Goiter
The purpose of this review is to summarize current knowledge of the etiology of euthyroid and toxic multinodular goiter (MNG) with respect to the epidemiology, clinical characteristics, and molecular pathology. In reconstructing the line of events from early thyroid hyperplasia to MNG we will argue...
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Published in: | Endocrine reviews 2005-06, Vol.26 (4), p.504-524 |
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container_title | Endocrine reviews |
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creator | Krohn, Knut Führer, Dagmar Bayer, Yvonne Eszlinger, Markus Brauer, Volker Neumann, Susanne Paschke, Ralf |
description | The purpose of this review is to summarize current knowledge of the etiology of euthyroid and toxic multinodular goiter (MNG) with respect to the epidemiology, clinical characteristics, and molecular pathology.
In reconstructing the line of events from early thyroid hyperplasia to MNG we will argue the predominant neoplastic character of nodular structures, the nature of known somatic mutations, and the importance of mutagenesis. Furthermore, we outline direct and indirect consequences of these somatic mutations for thyroid pathophysiology and summarize information concerning a possible genetic background of euthyroid goiter.
Finally, we discuss uncertainties and open questions in differential diagnosis and therapy of euthyroid and toxic MNG. |
doi_str_mv | 10.1210/er.2004-0005 |
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In reconstructing the line of events from early thyroid hyperplasia to MNG we will argue the predominant neoplastic character of nodular structures, the nature of known somatic mutations, and the importance of mutagenesis. Furthermore, we outline direct and indirect consequences of these somatic mutations for thyroid pathophysiology and summarize information concerning a possible genetic background of euthyroid goiter.
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In reconstructing the line of events from early thyroid hyperplasia to MNG we will argue the predominant neoplastic character of nodular structures, the nature of known somatic mutations, and the importance of mutagenesis. Furthermore, we outline direct and indirect consequences of these somatic mutations for thyroid pathophysiology and summarize information concerning a possible genetic background of euthyroid goiter.
Finally, we discuss uncertainties and open questions in differential diagnosis and therapy of euthyroid and toxic MNG.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Biological Transport</subject><subject>Chromosome Aberrations</subject><subject>Differential diagnosis</subject><subject>Endocrinopathies</subject><subject>Epidemiology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Genetic Linkage</subject><subject>Goiter</subject><subject>Goiter, Nodular - genetics</subject><subject>Goiter, Nodular - pathology</subject><subject>Goiter, Nodular - physiopathology</subject><subject>Humans</subject><subject>Hyperplasia</subject><subject>Intracellular Signaling Peptides and Proteins</subject><subject>Iodides - metabolism</subject><subject>Medical sciences</subject><subject>Mutagenesis</subject><subject>Mutation</subject><subject>Non tumoral diseases. Target tissue resistance. Benign neoplasms</subject><subject>Pathogenesis</subject><subject>Protein Array Analysis</subject><subject>Receptors, Thyrotropin - genetics</subject><subject>Signal Transduction</subject><subject>Thyroid</subject><subject>Thyroid Gland - physiopathology</subject><subject>Thyroid. 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Psychology</topic><topic>Genetic Linkage</topic><topic>Goiter</topic><topic>Goiter, Nodular - genetics</topic><topic>Goiter, Nodular - pathology</topic><topic>Goiter, Nodular - physiopathology</topic><topic>Humans</topic><topic>Hyperplasia</topic><topic>Intracellular Signaling Peptides and Proteins</topic><topic>Iodides - metabolism</topic><topic>Medical sciences</topic><topic>Mutagenesis</topic><topic>Mutation</topic><topic>Non tumoral diseases. Target tissue resistance. Benign neoplasms</topic><topic>Pathogenesis</topic><topic>Protein Array Analysis</topic><topic>Receptors, Thyrotropin - genetics</topic><topic>Signal Transduction</topic><topic>Thyroid</topic><topic>Thyroid Gland - physiopathology</topic><topic>Thyroid. 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In reconstructing the line of events from early thyroid hyperplasia to MNG we will argue the predominant neoplastic character of nodular structures, the nature of known somatic mutations, and the importance of mutagenesis. Furthermore, we outline direct and indirect consequences of these somatic mutations for thyroid pathophysiology and summarize information concerning a possible genetic background of euthyroid goiter.
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subjects | Animals Biological and medical sciences Biological Transport Chromosome Aberrations Differential diagnosis Endocrinopathies Epidemiology Fundamental and applied biological sciences. Psychology Genetic Linkage Goiter Goiter, Nodular - genetics Goiter, Nodular - pathology Goiter, Nodular - physiopathology Humans Hyperplasia Intracellular Signaling Peptides and Proteins Iodides - metabolism Medical sciences Mutagenesis Mutation Non tumoral diseases. Target tissue resistance. Benign neoplasms Pathogenesis Protein Array Analysis Receptors, Thyrotropin - genetics Signal Transduction Thyroid Thyroid Gland - physiopathology Thyroid. Thyroid axis (diseases) Vertebrates: endocrinology |
title | Molecular Pathogenesis of Euthyroid and Toxic Multinodular Goiter |
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