Дисертації з теми "Natrium Iodide Symporter (NIS)"
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Farnedi, Anna <1973>. "Caratterizzazione genetico-funzionale del carcinoma mammario. Valutazione dell’espressione di NIS (Natrium/Iodide Symporter)." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2008. http://amsdottorato.unibo.it/991/1/Tesi_Farnedi_Anna.pdf.
Farnedi, Anna <1973>. "Caratterizzazione genetico-funzionale del carcinoma mammario. Valutazione dell’espressione di NIS (Natrium/Iodide Symporter)." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2008. http://amsdottorato.unibo.it/991/.
Lacoste, Claire. "Le transporteur d’iode NIS dans la carcinogenèse non thyroïdienne : nouvelles fonctions, nouveaux enjeux." Thesis, Paris 11, 2011. http://www.theses.fr/2011PA11T043.
The Natrium iodide symporter (NIS) is a transmembrane glycoprotein known for its role in thyroid hormones biosynthesis, catalyzes active iodide transport in the thyroid. The iodide transport activity of NIS allows its clinical applications for diagnosis, follow-up using radio-isotopic imaging and treatment by 131I radiotherapy of thyroid cancers. Several studies described NIS expression in non thyroidal tumour tissues frequently displaying a cytoplasmic localization. In the current study, we reveal that, independently to its transport activity, NIS habors new biological functions in migration and invasion through RhoGTPase signalling pathway, a pathway involved in carcinogenesis. In addition, we establish that NIS is a tight junction-associated protein, which dynamically shuttles between tight junctions and cytoplasm during cell migration, and localizes at the leading edge of the metastatic cancer cells. Overall, these findings offer a novel appraisal of the potential role of NIS in carcinogenesis, and of the factors governing NIS intracellular trafficking
Kessel, Anne-Liese. "Der Natrium-Iodid-Symporter (NIS) als neues therapeutisches Gen zur Behandlung des Malignen Melanoms." Diss., lmu, 2010. http://nbn-resolving.de/urn:nbn:de:bvb:19-118310.
Kolokythas, Marie-Christine [Verfasser], and Christine [Akademischer Betreuer] Spitzweg. "Molekulare Bildgebung und gezielte Radionuklidtherapie extrathyreoidaler Tumore nach Stammzell-basiertem Natrium/Iodid-Symporter (NIS) - Gentransfer / Marie-Christine Kolokythas ; Betreuer: Christine Spitzweg." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2019. http://d-nb.info/1190563576/34.
Fenniche, Salma. "Rôle de la NADPH OXYDASE NOX4 dans la régulation de l'expression et de l'activité de CHD4 dans les tumeurs thyroïdiennes porteuses de la mutation BRAFV600E." Electronic Thesis or Diss., université Paris-Saclay, 2024. http://www.theses.fr/2024UPASL022.
Metabolic radiotherapy with radioiodine is the cornerstone of the treatment of distant metastases of differentiated thyroid cancers. This therapy depends on the expression at the basal membrane of thyrocytes of the Natrium Iodide Symporter 'NIS'. BRAFV600E mutation is present in 45 to 60% of papillary thyroid carcinomas, which represent 80% of thyroid cancers. The presence of this mutation is associated with the most aggressive thyroid tumors with low levels or absence of NIS expression. The loss of radioactive iodine uptake translates into resistance to metabolic radiotherapy, constituting a major issue for the treatment of patients with this cancer. One approach for treating patients refractory to metabolic radiotherapy is to increase iodine uptake.At the transcriptional level, our team has already shown, through a comparative analysis concerning approximately 500 PTCs from the TCGA database, that NOX4 was strongly expressed in PTCs-BRAFV600E compared to PTCs-BRAFwt. However, at the protein level, no link has been established between the BRAFV600E mutation and NOX4 in malignant and non-malignant tumors (BRAFV600E/BRAFwt). In my thesis project, we illustrate for the first time a positive correlation between the presence of BRAFV600E mutation and the overexpression of NOX4 protein in PTC tumor tissues. The overexpression of NOX4 was associated with an aggressive nature of tumors. Furthermore, we showed that 60% of infiltrating C-PTCs overexpress NOX4 independently of BRAF mutational status, suggesting that NOX4 could be considered as a potential co-marker of PTC aggressiveness. Interestingly, NOX4 protein was also overexpressed in non-malignant thyroid diseases (Basedow, goiters, and hyperplasias), with different subcellular localizations, suggesting a role for NOX4 in progression to thyroid malignancy.Furthermore, on a mechanistic level, our team has previously shown that BRAFV600E controls the expression of NOX4 under the effect of TGF-β/SMAD3 and that NOX4-derived ROS contribute to the repression of NIS. Inhibition of NOX4 promotes reactivation of the NIS. This reversibility suggests a contribution to an epigenetic mechanism. CHD4, a subunit of the NuRD remodeling complex, plays an essential role in gene repression. it was found to be strongly expressed in PTCs, in which it was associated with a poor prognosis. In this study, we showed that the TGF-β/SMAD3 pathway regulates the expression of CHD4 protein. The latter cooperates with DNMTs in repressing NIS in several thyroid tumor cells lines mutated for BRAFV600E. Furthermore, we showed that CHD4 responds to oxidative DNA damage induced by NOX4-derived ROS. Indeed, inhibition of NOX4 or its functional partner p22phox reduces the recruitment of CHD4 to chromatin. This recruitment depends on OGG1 and MSH6, two proteins involved in oxidative DNA damage repair. This study identifies CHD4 as a new therapeutic candidate in radioiodine-refractory thyroid cancers
Gotthardt, Inka. "Interferenzen endokrin aktiver Substanzen mit der Hypothalamus-Hypophysen-Schilddrüsenachse." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2010. http://dx.doi.org/10.18452/16145.
Endocrine active compounds (EACs) can be of natural or synthetic origin and show hormone-like effects that interfere with feedback regulation of hormonal networks. Interferences with the hypothalamic-pituitary-thyroid axis (HPT-axis) result in extensive consequences as thyroid hormones are essential for regulation of development, growth, and metabolism. In the work presented here, the active profile of potent inhibitors of the HPT-axis namely 4-methylbenzylidene-camphor (4-MBC) and genistein (GEN) was investigated. 4-MBC, a UV filter used in sunscreens and various cosmetics, was identified as a goiter causing agent using ovariectomized rats. 4-MBC acts at the level of hypothalamus and pituitary gland by modulating the expression of thyrotropin-releasing hormone (TRH) as well as thyroid-stimulating hormone (TSH) that regulate feedback on the HPT-axis. Furthermore, biosynthesis of thyroid hormones was impaired by 4-MBC secondary to the inhibition of iodide transport with concomitantly increased messenger RNA (mRNA)-levels of the sodium-iodide symporter (NIS). In parallel expression of the angiogenesis marker vascular endothelial growth factor (VEGF) was increased, indicating hypothyroidism. After the application of 4-MBC the expression of L-3,3’,5-triiodothyronine (T3)-regulated target genes was reduced in the periphery both on the mRNA and protein level. The documented species-specific effects indicate a difference in pharmacokinetics, possibly secondary to differential expression of cytochrome P450 genes. GEN is contained in soy and red clover and its mechanistic analysis was carried out in thyroid hormone receptor (TR) deficient mice (TRα0/0). The gender-dependent effects of GEN on tissue specificity did not follow an obvious pattern and warrant continuative analysis. The work presented here supports the assumption that EACs can interfere with function and regulation of the HPT-axis at levels that were previously considered safe.
Lin, Xiaoqin. "Regulation of sodium iodide symporter expression/function and tissue-targeted gene transfer of sodium iodide symporter." Connect to this title online, 2003. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1070462866.
Title from first page of PDF file. Document formatted into pages; contains xi, 123 p.; also includes graphics (some col.) Includes bibliographical references (p. 109-123). Available online via OhioLINK's ETD Center
Grünwald, Geoffrey. "Targeted delivery of the theranostic sodium iodide symporter (NIS) for cancer gene therapy." Diss., Ludwig-Maximilians-Universität München, 2013. http://nbn-resolving.de/urn:nbn:de:bvb:19-158988.
Liu, Yu-Yu. "Modulation of Sodium/Iodide Symporter Expression and Function in Thyroid." The Ohio State University, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=osu1293691026.
Flanigan, Matt. "Modulation of the sodium/iodide symporter (NIS) by MEK inhibition in MCF7 breast cancer cells." Connect to resource, 2009. http://hdl.handle.net/1811/36943.
Grünwald, Geoffrey [Verfasser], and Ernst [Akademischer Betreuer] Wagner. "Targeted delivery of the theranostic sodium iodide symporter (NIS) for cancer gene therapy / Geoffrey Grünwald. Betreuer: Ernst Wagner." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2013. http://d-nb.info/1038151805/34.
Cazarin, de Menezes Juliana. "Role of NADPH Oxidase 4 in the Redox Regulation of the Sodium (Na+)/ iodide (I-) Symporter in Papillary Thyroid Cancer." Thesis, Université Paris-Saclay (ComUE), 2018. http://www.theses.fr/2018SACLS068.
The co-transporter Na+/ I- (NIS) mediates iodide uptake in thyroid gland which is a key step in hormonal biosynthesis. Iodide accumulation by thyrocytes is the basis of radioiodine therapy (RAI) which is the standard post-surgery therapeutic approach to efficiently eliminate remaining cancer lesions and metastasis of differentiated thyroid cancer (DTC). However, 5-10% of DTC patients become RAI-refractory which is indicative of poor prognosis. Reduced NIS expression and NIS internalization are in this process. BRAFV600E mutation is the most common genetic event in papillary thyroid cancers (PTCs), the most prevalent type of DTC. In rat thyrocytes, BRAFV600E induces secretion of TGFβ that activates Smad pathway resulting in NIS downregulation and overexpression of TGFβ is associated with NIS repression in patients. NADPH oxidase NOX4, a professional reactive oxygen species (ROS) generating enzyme, is a key mediator of TGFβ signaling in many cell types and has been previously demonstrated to be overexpressed thyroid cancers. To better understand the molecular mechanisms involved in PTC loss of iodine avidity, the aim of this work is to evaluate whether NOX4 is a key player of BRAFV600E-mediated NIS repression in thyroid cell lines. Using a normal rat thyroid cell line (PC-BRAF) we demonstrated that TGF-β administration or expression of BRAFV600E resulted in reduced NIS mRNA, reduced iodine uptake and increased NOX4 mRNA expression. NOX4 silencing or treatment with SIS3 an inhibitor of Smad pathway partially inhibited NIS repression indicating the implication of both Smad pathway and NOX4. To confirm this results we used a human thyroid cancer cell lines that harbors BRAFV600E mutation (BCPAP and 8505c) and observed an increase in NIS expression followed by BRAFV600E or NOX4 downregulation. Exogenous H2O2 induced DNA methyl-transferase 1 (DNMT1) enrichment in tight-chromatin protein fraction which was decreased by antioxidants or NOX4 silencing in BCPAP cells. TGF increased DNMT1 protein levels in chromatin-enriched cell fraction which was reversed by NADPH oxidase inhibitor, Diphenyleneiodonium (DPI). TGF-mediated DNA methylation and histone H3K9/K14 hypoacetylation were detected in NIS promoter, which is a repressive transcriptional mark. The data obtained suggest that NOX4 is a mediator of BRAFV600-TGF signaling and has a repressive role over NIS expression probably through epigenetic mechanisms. These results should lead to a better understanding of NIS expression regulation in thyroid cancer, bringing functional data for the development of new therapeutic tools
Gärtner, Florian. "Untersuchungen über die endogene Expression und Regulation des Natrium-Iodid-Symporters (NIS) in extrathyreoidalen Tumoren in vitro und in vivo." Diss., lmu, 2009. http://nbn-resolving.de/urn:nbn:de:bvb:19-95931.
Knoop, Kerstin. "Molecular imaging and radionuclide therapy in non-thyroidal tumors after mesenchymal stem cell- mediated sodium/iodide symporter (NIS) gene transfer." Diss., Ludwig-Maximilians-Universität München, 2014. http://nbn-resolving.de/urn:nbn:de:bvb:19-178550.
Klutz, Kathrin. "Molecularly targeted imaging and radionuclide therapy of non-thyroidal tumors following viral and non-viral sodium iodide symporter (NIS) gene delivery." Diss., lmu, 2010. http://nbn-resolving.de/urn:nbn:de:bvb:19-136957.
Losch, Agnieszka [Verfasser]. "Untersuchung der Effektivität der Radioiodtherapie in vivo nach Stimulation der Expression des Natrium-Iodid-Symporters (NIS) in humanen extrathyreoidalen Tumorzellen / Agnieszka Losch." Hamburg : Staats- und Universitätsbibliothek Hamburg Carl von Ossietzky, 2020. http://d-nb.info/122938734X/34.
Rauer, Christine [Verfasser]. "Untersuchungen zur Regulation des Natrium-Iodid-Symporters (NIS)und der Thyreoperoxidase (TPO) durch die sterol regulatory element-binding proteins (SREBPs) / Christine Rauer." Gießen : Universitätsbibliothek, 2014. http://d-nb.info/1068589639/34.
Schug, Christina [Verfasser], and Ernst [Akademischer Betreuer] Wagner. "Advanced mesenchymal stem cell-mediated gene delivery of the theranostic sodium iodide symporter (NIS) in non-thyroidal tumors / Christina Schug ; Betreuer: Ernst Wagner." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2019. http://d-nb.info/1188564315/34.
Schug, Christina [Verfasser], and Ernst [Akademischer Betreuer] Wagner. "Advanced mesenchymal stem cell-mediated gene delivery of the theranostic sodium iodide symporter (NIS) in non-thyroidal tumors / Christina Schug ; Betreuer: Ernst Wagner." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2018. http://d-nb.info/1173616195/34.
Knoop, Kerstin [Verfasser], and Ernst [Akademischer Betreuer] Wagner. "Molecular imaging and radionuclide therapy in non-thyroidal tumors after mesenchymal stem cell- mediated sodium/iodide symporter (NIS) gene transfer / Kerstin Knoop. Betreuer: Ernst Wagner." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2014. http://d-nb.info/1065180403/34.
Klutz, Kathrin [Verfasser], and Ernst [Akademischer Betreuer] Wagner. "Molecularly targeted imaging and radionuclide therapy of non-thyroidal tumors following viral and non-viral sodium iodide symporter (NIS) gene delivery / Kathrin Klutz. Betreuer: Ernst Wagner." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2010. http://d-nb.info/1017688311/34.
Urnauer, Sarah [Verfasser], and Ernst [Akademischer Betreuer] Wagner. "Improved synthetic gene delivery vehicles for advanced bioimaging-guided tumor-targeted application of the sodium iodide symporter (NIS) as theranostic gene / Sarah Urnauer ; Betreuer: Ernst Wagner." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2017. http://d-nb.info/1148941177/34.
Bou, Nader Myriam. "Rôle du Symporteur Sodium Iodure dans la carcinogenèse non thyroïdienne." Thesis, Paris 11, 2014. http://www.theses.fr/2014PA11T084/document.
The sodium iodide symporter (NIS) is a glycosylated protein that mediates the active transport of iodide for thyroid hormone biosynthesis. The ability of the thyroid to accumulate iodide via NIS has provided the basis for diagnostic imaging and served as effective treatment by radioiodine to target and destroy thyroid cancers. This propriety makes NIS a real marker of clinical interest for potential use in non-thyroid cancers which express it, however, the mechanisms of regulation and membrane targeting of NIS remain unknown. We identify a new function of NIS in cell migration and invasion independently of its transport activity. This function is facilitated by the activation of RhoA after the protein-protein interaction of NIS and LARG (Leukemia-Associated RhoA Guanine Exchange Factor). Our work has shown that this accumulation of NIS in intracellular compartments of cancer cells was also observed in primary and metastatic liver cancers. Our results pointed out the importance of TGF-β signaling pathway, frequently activated in human cancers, in NIS default targeting. Our work suggests that a therapy based on pharmacological inhibitors of TGF-β could be able to correct this targeting defect, making metabolic radiotherapy possible
Kessel, Anne-Liese [Verfasser]. "Der Natrium-Iodid-Symporter (NIS) als neues therapeutisches Gen zur Behandlung des Malignen Melanoms / vorgelegt von Anne-Liese Kessel." 2010. http://d-nb.info/1006234659/34.
Tavares, Ana Catarina Marques Gomes. "The pathogenic role of mTOR pathway in papillary thyroid carcinoma and its impact on sodium iodide symporter (NIS) expression." Doctoral thesis, 2017. https://hdl.handle.net/10216/107286.
Tavares, Ana Catarina Marques Gomes. "The pathogenic role of mTOR pathway in papillary thyroid carcinoma and its impact on sodium iodide symporter (NIS) expression." Tese, 2017. https://repositorio-aberto.up.pt/handle/10216/107286.
Gärtner, Florian C. [Verfasser]. "Untersuchungen über die endogene Expression und Regulation des Natrium-Iodid-Symporters (NIS) in extrathyreoidalen Tumoren in vitro und in vivo / vorgelegt von Florian C. Gärtner." 2009. http://d-nb.info/992654130/34.
Paixão, Francisca Ventura. "Deciphering the pathways leading to the enhancement of NIS transcription in thyroid tissue." Master's thesis, 2019. http://hdl.handle.net/10362/69909.