Growth Factor Expression in Cold and Hot Thyroid Nodules

Eszlinger, Markus; Krohn, Knut; Kratzsch, Jürgen; Voigt, Carsten; Paschke, Ralf

doi:10.1089/105072501300042767

Cited by 20 publications

(13 citation statements)

References 36 publications

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“…The values were similar regardless of whether the nodules were hot or cold (72). In other studies TGF-b1 was detected by immunohistochemistry and was found not only in thyrocytes but also in endothelial and connective tissue cells.…”

Section: Goiter and Benign Thyroid Tumorssupporting

confidence: 67%

Role of Transforming Growth Factor Beta in the Regulation of Thyroid Function and Growth

Pisarev

Thomasz

Juvenal

2009

Thyroid

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Transforming growth factor beta (TGF-beta) exists in nature as three isoforms. They exert their effects by binding to a type II receptor located at the cell membrane. The TGF-beta-type II receptor complex then recruits type I receptor, and this new complex stimulates the phosphorylation of Smads 2 and 3, which are subsequently transferred to the nucleus, where they regulate gene transcription. The thyroid gland expresses the TGF-beta1 gene mRNA and synthesizes the protein, which under physiologic conditions regulates thyroid growth and function. Different studies have demonstrated that TGF-beta1 inhibits cell proliferation and a number of functional parameters. These include cyclic adenosine monophosphate (AMP) formation, iodine uptake and organification, hormone secretion, and the expression of thyroglobulin, thyroid peroxidase, and Na(+)/I(-) symporter. The expression of the TGF-beta1 gene and protein may be stimulated by iodine under normal conditions. Since TGF-beta1 mimics some of the inhibitory actions of iodine, its participation in thyroid autoregulation has been proposed; however, this concept is still debated. In thyroid tumors, the inhibitory action of TGF-beta1 on cell proliferation is progressively lost as the tumor becomes more undifferentiated. The alterations in the signaling pathway of TGF-beta1 are not the same in tumors from different species. Even within the same species, such as the pig thyroid, the results may be different depending on whether monolayers or follicular suspensions are employed. The data suggest that it is not entirely possible to apply the results obtained in animal studies to normal or pathological human thyroid tissue. More studies are required to provide the information needed to develop treatments, based on targeting the signaling pathway of TGF-beta1, for undifferentiated thyroid cancer and other thyroid diseases.

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Section: Goiter and Benign Thyroid Tumorssupporting

confidence: 67%

Role of Transforming Growth Factor Beta in the Regulation of Thyroid Function and Growth

Pisarev

Thomasz

Juvenal

2009

Thyroid

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“…Eszlinger et al have found elevated IGF-1 levels in hot nodules, and suggested that this peptide may play a prominent role for selective growth advantages of hot or cold nodules (26). Our study has revealed no difference in the tissue levels of IGF-1 between hot and cold nodules.…”

Section: Discussionsupporting

confidence: 48%

The Role of Insulin-Like Growth Factor 1 in the Development of Benign and Malignant Thyroid Nodules

Baştürk¹,

Kement²,

Yavuzer³

et al. 2012

Balkan Med J

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Objective: This study aims to investigate the role of IGF-1 in the development of nodular thyroid disease. Material and Methods:A total number of 100 consecutive patients operated for nodular thyroid disease in our institution were included in this prospective study. In addition to classical pathological examinations, nodules and extranodular healthy tissues were sampled and immunochemically stained for IGF-1. The materials were independently evaluated using an Allred Scoring System ranging from 0 to 8. If the score was ≥1, the tissue was accepted as IGF-1 positive.Results: IGF-1 positivity was observed in 88% and 58% of the samples obtained from nodules and extranodular healthy tissues, respectively. Allred 8-unit scores were higher in benign nodules (n=89; 4.1±2.3) and papillary carcinomas (n=7; 6.7±1.3), than in extranodular healthy tissues in the same patients (2.3±2.3 and 3.3±1.9, respectively); and higher in papillary carcinomas than in benign nodules, when the scores were compared to each other (p<0.01 for all comparisons).Conclusions: Allred 8-unit scores for IGF-1 increase in the presence of benign thyroid nodules, papillary cancer. The results of our study support the findings of previous studies demonstrating the role of IGF-1 in the development of thyroidal nodules.

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“…Already in two former studies, we could identify differences in the expression of genes associated with the TGF-b signaling between AFTNs and their normal ST on protein-and mRNA-level. The investigation of TGF-b1 by ELISA revealed a significantly decreased TGF-b1 level in AFTNs in comparison to their STs (Eszlinger et al, 2001a) and a recent investigation of 588 genes by cDNA expression array showed a significantly decreased expression of the type III TGF-b receptor (betaglycan) in AFTNs (Eszlinger et al, 2001b). In addition, the differential expression of the type III TGF-b receptor was previously confirmed by real-time RT-PCR of 10 AFTNs and their ST (Eszlinger et al, 2001b).…”

Section: Genmapp Analysismentioning

confidence: 77%

Gene expression analysis reveals evidence for inactivation of the TGF-β signaling cascade in autonomously functioning thyroid nodules

et al. 2004

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Molecular eventsthat lead to the development of autonomously functioning thyroid nodules (AFTNs) are somatic mutations of the thyrotropin receptor (TSHR) in approximately 60% of the nodules and less frequently, somatic mutations in the G s a protein. However, AFTNs without known mutations indicate that other causes remain to be identified. Moreover, the impact of constitutively activating TSHR mutations on the signal transduction network of the thyroid epithelial cell is unknown. We therefore investigated gene expression in 15 AFTNs and their surrounding tissue using Affymetrix GeneChips. Most prominently, data analysis revealed a changed pattern of gene expression in the TGF-b signaling cascade and 25 differentially regulated genes in AFTNs, including thyroid peroxidase, type I iodothyronine deiodinase and sialyltransferase (SIAT) 1. Strikingly coexpression of SIAT 1 and TSHR in COS-7 cells increased TSH binding and cell surface expression of the TSHR. Moreover, differences in gene expression patterns for AFTNs with and without TSHR mutations indicate specific alterations of signal transduction in AFTNs without TSHR mutations. These results suggest that AFTNs with TSHR mutations harbor further mechanisms of forward stimulation. Furthermore, they give important leads to elucidate the molecular etiology of AFTNs without TSHR mutations.

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Growth Factor Expression in Cold and Hot Thyroid Nodules

Cited by 20 publications

References 36 publications

Role of Transforming Growth Factor Beta in the Regulation of Thyroid Function and Growth

Role of Transforming Growth Factor Beta in the Regulation of Thyroid Function and Growth

The Role of Insulin-Like Growth Factor 1 in the Development of Benign and Malignant Thyroid Nodules

Gene expression analysis reveals evidence for inactivation of the TGF-β signaling cascade in autonomously functioning thyroid nodules

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