Pathogenesis and Treatment of Multinodular Goiter

Derwahl, Michael; Studer, H

doi:10.1007/978-1-4615-4945-1_7

Cited by 16 publications

(14 citation statements)

References 90 publications

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“…However, this straightforward interpretation neglects some findings that point to an intricate complexity of TSH-dependent and -independent mechanisms within a network of interacting positive and negative signals. 12 TSH is not only involved in the control of differentiated functions, it also regulates the expression of growth factors and their receptors. 12,13 This has been demonstrated, for example, for the expression of epidermal growth factor (EGF) receptors, 14 and for insulinlike growth factor I (IGF-I)-dependent signaling.…”

Section: Discussionmentioning

confidence: 99%

Metformin Treatment for Small Benign Thyroid Nodules in Patients with Insulin Resistance

Rezzónico

Pusiol

et al. 2011

Metabolic Syndrome and Related Disorders

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Section: Discussionmentioning

confidence: 99%

Metformin Treatment for Small Benign Thyroid Nodules in Patients with Insulin Resistance

Rezzónico

Pusiol

et al. 2011

Metabolic Syndrome and Related Disorders

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“…Cell proliferation, a hallmark of goitre development, results from increased thyrotropin (TSH) secretion associated with the release of growth factors acting as paracrine or autocrine agents (for review see Derwahl & Studer 1998). Cell death plays a central role in regulating the thyroid cell mass, especially during the goitre involution induced by iodine or by thyroid hormones (Wollman et al 1968, Denef et al 1981, Rognoni et al 1987.…”

Section: Introductionmentioning

confidence: 99%

Cell necrosis and apoptosis are differentially regulated during goitre development and iodine-induced involution

Mutaku

Poma²,

Many

et al. 2002

Journal of Endocrinology

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Necrosis and apoptosis coexist in the thyroid during goitre development and involution, but little is known about their respective causes. To test the possible role of free radicals, we analysed separately necrosis and apoptosis in male Wistar rats with depressed or normal antioxidant protection. Vitamin E-deficient and -sufficient rats were made goitrous with perchlorate in drinking water; involution was induced by repeated injection of NaI, without or with methimazole. Increase of thyroid malondialdehyde concentration and decrease of glutathione peroxidase activity confirmed the depressed antioxidant protection in vitamin E-deficient rats. Plasma thyroxine and TSH levels were not modified. Necrosis (swollen cells) and apoptosis (pyknotic cells) were quantified on histological sections. In vitamin E-sufficient rats, dead cells were very rare in control thyroids, increased 3-fold in goitre and still further during involution.Necrotic epithelial cells predominated in the goitre and their number declined after iodide supplementation, without or with methimazole. In contrast, the number of apoptotic cells and the caspase-3 activity were increased in goitre and further increased after involution, with twothirds of pyknotic cells being observed in the interstitium. Apoptosis was prevented by methimazole. Vitamin E deficiency significantly increased total cell death and epithelial cell necrosis and induced the occurrence of much cell debris in the follicular lumen during involution, with no modification of the apoptotic reaction. These results show that the type of cell death is differentially regulated during goitre development and involution: necrosis is related to the oxidative status of the cells, while apoptosis comes with iodine-induced involution.

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“…Apenas 3 pacientes dos 35 avaliados apresentaram aumento concomitante da expressão dos 2 genes. O BMN é uma patologia comum, que é caracterizado pela heterogeneidade na função e crescimento das células foliculares (2). O bócio esporádico e o endêmico, definido quando a prevalência de bócio visível ou palpável é maior que 5% na população de escolares, são fundamentalmente a mesma patologia da glândula tireóide.…”

Section: Discussionunclassified

“…Em conseqüência, a característica do bócio multinodular é a heterogeneidade no crescimento e função das células foliculares. O nódulo bem delimitado, com estrutura claramente distinta do tecido circundante e definido como clonal através da análise genética, é, no presente, a melhor definição de neoplasia, benigna ou maligna (2). A maioria dos nódulos solitários de tireóide são neoplasias clonais, indicando que originam-se de uma única célula precursora (3).…”

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“…O crescimento das células tireoideanas é regulado pelo hormônio hipofisário TSH e por outros fatores de crescimento, como epidermal growth factor (EGF) e insulin-like growth factor-I (IGF-I), embora a seqüência de eventos ainda não seja inteiramente esclarecida (2,6). Desde a elucidação do receptor do TSH e dos seus mecanismos intracelulares via proteína G e cAMP/IP3, é consensual a participação do TSH no desenvolvimento do bócio.…”

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Aumento da expressão do proto-oncogene ras no bócio multinodular: possível envolvimento na patogênese

Golbert

Kolling

Leitão

et al. 2003

Arq Bras Endocrinol Metab

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RESUMOA transformação neoplásica resulta de uma série de alterações genéti-cas, envolvendo ativação de proto-oncogenes e inativação de genes supressores tumorais. Ativação do proto-oncogene ras por mutações em ponto é a alteração genética mais freqüente em tumores espontâ-neos da tireóide. Avaliamos a expressão do gene ras no bócio nodular. Fragmentos de tecido tireoidiano normal e neoplásico foram coletados durante o ato cirúrgico, sendo que 79 pacientes tiveram diagnóstico histopatológico de bócio colóide e foram incluídos no estudo. O RNA total foi extraído pelo método de Trizol e o cDNA sintetizado através do Reverse Trancriptidase. Os genes H-ras e K-ras foram amplificados através de PCR com primers específicos. Do total da amostra, 62% apresentaram aumento da expressão de um dos genes ras estudados. Evidenciou-se aumento da expressão do H-ras em 9 dos 29 (31%) casos e do K-ras em 12 dos 32 (37,5%) tumores estudados. Os resultados demonstraram aumento da expressão do ras na doença nodular da tireóide e sugerem um papel importante desses genes na transformação neoplásica da tireóide. Neoplastic transformation results from a series of genetic alterations involving activation of protooncogenes and inactivation of tumor suppressor genes. Activation of ras protooncogenes by point mutation is the most frequent genetic alteration in spontaneous thyroid neoplasias. The goal of this study was to evaluate ras gene expression in the nodular goiter. Seventy-nine patients submitted to thyroidectomy and with a histological diagnosis of nodular goiter were included in the study. Tissues were obtained from both tumor and normal thyroid during surgery and frozen in liquid N 2 . Total RNA was isolated using TRIzol reagent and the cDNA was synthesized by reverse transcription. Twenty-one of the 34 (62%) nodules showed elevated expression of at least one of the ras genes studied. H-ras exhibited overexpression in 9 of 29 (31%) and K-ras in 12 of 32 (37.5%) tumor samples examined. Our results showed ras over expression in nodular disease, with different pattern of expression between H and K-ras genes, suggesting that control of these proto-oncogenes expression might play an important role on neoplastic transformation in thyroid cells. OBÓCIO MULTINODULAR (BMN) é definido como aumento da glându-la tireóide devido à proliferação multifocal de tireócitos, resultando em estruturas foliculares heterogêneas. É uma patologia comum, clinicamente detectada em 2-6% dos indivíduos em regiões com dieta suficiente de iodo (1).

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Pathogenesis and Treatment of Multinodular Goiter

Cited by 16 publications

References 90 publications

Metformin Treatment for Small Benign Thyroid Nodules in Patients with Insulin Resistance

Metformin Treatment for Small Benign Thyroid Nodules in Patients with Insulin Resistance

Cell necrosis and apoptosis are differentially regulated during goitre development and iodine-induced involution

Aumento da expressão do proto-oncogene ras no bócio multinodular: possível envolvimento na patogênese

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