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Готові списки джерел за темами / Natrium Iodide Symporter (NIS)

Добірка наукової літератури з теми "Natrium Iodide Symporter (NIS)"

Автор: Grafiati

Опубліковано: 7 липня 2024

Оновлено: 7 липня 2024

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Статті в журналах з теми "Natrium Iodide Symporter (NIS)":

1

Elliyanti, Aisyah, Rony Rustam, Tofrizal Tofrizal, Yenita Yenita, and Yayi D. Billianti Susanto. "Evaluating the Natrium Iodide Symporter Expressions in Thyroid Tumors." Open Access Macedonian Journal of Medical Sciences 9, B (January 5, 2021): 18–23. http://dx.doi.org/10.3889/oamjms.2021.5534.

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BACKGROUND: Decreased Natrium iodide symporter (NIS) expression levels or diminished NIS targeting thyroid cancer cells’ plasma membrane leads to radioiodine-refractory disease. AIM: The aim of this study was to analyze the NIS expression in thyroid tumors. MATERIALS AND METHODS: The samples were thyroid tissues of patients who underwent surgery for a thyroid tumor. The tissues were processed for NIS protein expressions by immunohistochemistry (IHC) and Western blot (WB). Graves’ disease samples were used as positive controls. The samples were incubated without the primary antibody, and they were used as negative controls for IHC examination. Na+/K+ ATPase was a plasma membrane protein marker in the WB procedure. RESULTS: Twenty-nine samples were assessed for NIS protein. All of them showed the expression in the cytoplasm with intensity 1+ to 3+ with Allred score 3-8. Fourteen out of 29 cases (48.2%) showed NIS cytoplasm staining intensity ≥2+ consist of 10 papillary thyroid cancer (PTC), three follicular thyroid cancer, and one adenoma. Membrane staining was found in 2 samples of PTC (6.9%). Six samples (adenoma 1 sample, PTC 5 samples) showed NIS expression at membrane very weak (1+); they were considered as negative. NIS protein has several bands of ~ 80 kDa, ~ 62 kDa, and ~ 49 kDa. CONCLUSION: NIS expression in thyroid cancer mostly expresses in the cytoplasm instead of the membrane. NIS will play a functional role in the membrane to bring iodine across the membrane against the concentration. It can be the main reason for the lack of response of radioiodine in some differentiated thyroid cancers.

2

Elliyanti, Aisyah, Tenny Putri Wikayani, Noormartany, Johan S. Masjhur, and Tri Hanggono Achmad. "Deteksi Natrium/Iodide Symporter (NIS) pada Galur Sel Kanker Payudara SKBR3 dengan Imunositofluoresens." Majalah Kedokteran Bandung 48, no. 1 (2016): 15–18. http://dx.doi.org/10.15395/mkb.v48n1.728.

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Elliyanti, Aisyah. "Deteksi Natrium/Iodide Symporter (NIS) pada Galur Sel Kanker Payudara SKBR3 dengan Imunositofluoresens." Majalah Kedokteran Bandung 48, no. 1 (2016): 15–18. http://dx.doi.org/10.15395/mkb.v48n1.728.1.

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Elliyanti, Aisyah, Tenny Putri Wikayani, Noormartany, Johan S. Masjhur, and Tri Hanggono Achmad. "Deteksi Natrium/Iodide Symporter (NIS) pada Galur Sel Kanker Payudara SKBR3 dengan Imunositofluoresens." Majalah Kedokteran Bandung 48, no. 1 (March 2016): 15–18. http://dx.doi.org/10.15395/mkb.v48n1.729.

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Elliyanti, Aisyah, Andani Eka Putra, Yunia Sribudiani, Noormartany Noormartany, Johan S. Masjhur, Tri Hanggono Achmad, and Dachriyanus Dachriyanus. "Epidermal Growth Factor and Adenosine Triphosphate Induce Natrium Iodide Symporter Expression in Breast Cancer Cell Lines." Open Access Macedonian Journal of Medical Sciences 7, no. 13 (August 6, 2019): 2088–92. http://dx.doi.org/10.3889/oamjms.2019.620.

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AIM: This study aims to investigate the effect of ATP, EGF and combination of those two to the Natrium Iodide Symporter (NIS) expression in MCF7, SKBR3 and HaCaT cell lines. METHODS: MCF7, SKBR3 and HaCaT cell lines were treated with ATP, EGF and combination of those two for 6, 12 and 24 hours. The expression of NIS mRNA was measured through quantitative-reverse transcription-polymerase chain reaction (qRT-PCR). The NIS protein expression was confirmed by immunocytofluorescence. RESULTS: NIS mRNA was expressed in SKBR3 and HaCaT cell lines but not in MCF7. The levels of NIS mRNA expression, after treatment by epidermal growth factor (EGF), adenosine Tri-Phosphate (ATP) or the combination of both for 6 and 12 hours were not significantly different from those of untreated cells. However, the treatment by a combination of ATP and EGF for 24 hours increases the level of NIS mRNA expression by 1.6 fold higher than that of the untreated cells (1.6241 ± 0.3, p < 0.05) and protein NIS expression increase significantly by the treatment than untreated cells (P < 0.05). CONCLUSION: The level of NIS expression varies among the different subtypes of breast cancer cell lines. MCF7 cell line is representing the luminal A subtype of breast cancer does not express NIS. Only SKBR3 cell line express NIS and this subtype might be suitable to receive radioiodine therapy as those cells expressing NIS. A combination treatment of EGF and ATP increases the expression of NIS mRNA and protein at the membrane in SKBR3 cells.

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Spitzweg, C. "Der Natrium-Iodid-Symporter (NIS): Bedeutung für die Bildgebung und therapeutische Optionen." Der Nuklearmediziner 30, no. 1 (March 2007): 19–30. http://dx.doi.org/10.1055/s-2006-955219.

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Lisco, Giuseppe, Anna De Tullio, Vito Angelo Giagulli, Giovanni De Pergola, and Vincenzo Triggiani. "Interference on Iodine Uptake and Human Thyroid Function by Perchlorate-Contaminated Water and Food." Nutrients 12, no. 6 (June 4, 2020): 1669. http://dx.doi.org/10.3390/nu12061669.

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Background: Perchlorate-induced natrium-iodide symporter (NIS) interference is a well-recognized thyroid disrupting mechanism. It is unclear, however, whether a chronic low-dose exposure to perchlorate delivered by food and drinks may cause thyroid dysfunction in the long term. Thus, the aim of this review was to overview and summarize literature results in order to clarify this issue. Methods: Authors searched PubMed/MEDLINE, Scopus, Web of Science, institutional websites and Google until April 2020 for relevant information about the fundamental mechanism of the thyroid NIS interference induced by orally consumed perchlorate compounds and its clinical consequences. Results: Food and drinking water should be considered relevant sources of perchlorate. Despite some controversies, cross-sectional studies demonstrated that perchlorate exposure affects thyroid hormone synthesis in infants, adolescents and adults, particularly in the case of underlying thyroid diseases and iodine insufficiency. An exaggerated exposure to perchlorate during pregnancy leads to a worse neurocognitive and behavioral development outcome in infants, regardless of maternal thyroid hormone levels. Discussion and conclusion: The effects of a chronic low-dose perchlorate exposure on thyroid homeostasis remain still unclear, leading to concerns especially for highly sensitive patients. Specific studies are needed to clarify this issue, aiming to better define strategies of detection and prevention.

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Perone, Denise, Silvânia S. Teixeira, Sueli A. Clara, Daniela C. dos Santos, and Célia R. Nogueira. "Aspectos genéticos do hipotireoidismo congênito." Arquivos Brasileiros de Endocrinologia & Metabologia 48, no. 1 (February 2004): 62–69. http://dx.doi.org/10.1590/s0004-27302004000100008.

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Hipotireoidismo congênito (HC) afeta cerca de 1:3000 a 1:4000 recém-nascidos (RN). Numerosos genes são essenciais, tanto para o desenvolvimento normal do eixo hipotálamo-hipófise-tireóide quanto para a produção hormonal, e estão associados ao HC. Cerca de 85% do hipotireoidismo primário é denominado disgenesia tireoidiana e evidências sugerem que mutações nos fatores de transcrição (TTF2, TTF1 e PAX-8) e no gene do receptor de TSH podem ser responsáveis pela doença. Os defeitos hereditários da síntese hormonal podem ser devidos a mutações nos genes NIS (natrium-iodide symporter), pendrina, tireoglobulina (TG), peroxidase (TPO). Mais recentemente, mutações no gene THOX-2 têm sido descritas para defeitos na organificacão. O hipotireoidismo central afeta cerca de 1:20.000 RN e tem sido associado com mutações nos fatores transcricionais hipofisários (POUIF1, PROP1, LHX3, HESX1). A síndrome de resistência periférica ao hormônio tireoidiano é uma doença rara que cursa com hipotireoidismo em alguns tecidos e, freqüentemente, está associada a mutações autossômicas dominantes no receptor beta (TRß).

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Spitzweg, C. "Der Natrium-Jodid-Symporter (NIS)." Der Internist 44, no. 4 (March 4, 2003): 396–411. http://dx.doi.org/10.1007/s00108-003-0877-9.

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Van Sande, J., C. Massart, R. Beauwens, A. Schoutens, S. Costagliola, J. E. Dumont, and J. Wolff. "Anion Selectivity by the Sodium Iodide Symporter." Endocrinology 144, no. 1 (January 1, 2003): 247–52. http://dx.doi.org/10.1210/en.2002-220744.

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Abstract The iodide transporter of the thyroid (NIS) has been cloned by the group of Carrasco. The NIS-mediated transport was studied by electrophysiological methods in NIS-expressing Xenopus oocytes. Using this method, the anion selectivity of NIS was different from that previously reported for thyroid cells, whereas perchlorate and perrhenate were found not transported. In this study we compared the properties of human NIS, stably transfected in COS-7 cells to those of the transport in a thyroid cell line, the FRTL5 cells, by measuring the transport directly. We measured the uptake of 125I−, 186ReO4−, and 99mTcO4− and studied the effect on it of known competing anions, i.e. ClO4−, SCN−, ClO3−, ReO4−, and Br−. We conclude that the properties of the NIS transporter account by themselves for the properties of the thyroid iodide transporter as described previously in thyroid slices. The order of affinity was: ClO4− > ReO4− > I− ≥ SCN− > ClO3− > Br−. NIS is also inhibited by dysidenin (as in dog thyroid).

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Дисертації з теми "Natrium Iodide Symporter (NIS)":

1

Farnedi, Anna <1973&gt. "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.

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Farnedi, Anna <1973&gt. "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/.

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3

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.

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Le symporteur sodium iodure (NIS), une glycoprotéine membranaire, connue pour son rôle dans la biosynthèse des hormones thyroïdiennes, catalyse le transport actif de l’iodure dans la thyroïde. Cette activité de transport lui confère des propriétés à la base du diagnostic, du suivi par imagerie radio-isotopique et du traitement par radiothérapie à l’iode 131 des cancers thyroïdiens. Plusieurs études ont montré une expression de NIS dans un grand nombre de cancers non-thyroïdiens, où il présente en général un défaut d’adressage membranaire. Nous avons identifié une nouvelle fonction biologique de NIS, indépendante de sa fonction de transport, dans la migration et l’invasion cellulaires via une activation de la GTPase RhoA connue pour son implication dans l’oncogenèse. Nous montrons également que NIS est une protéine associée aux jonctions serrées qui transite rapidement dans le cytoplasme ou au front de migration des cellules motiles. Cette étude révèle un nouveau rôle de NIS dans la carcinogenèse et dévoile certains facteurs qui gouvernent le trafic intracellulaire de NIS
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

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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.

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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.

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6

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.

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La radiothérapie métabolique à l'iode radioactif est la pierre angulaire du traitement des métastases à distance des cancers différenciés de la thyroïde. Cette thérapie est basée sur l'expression à la membrane basale des thyrocytes du transporteur de l'iode appelé NIS pour « Natrium Iodide Symporter ». La mutation BRAFV600E est présente dans 45 à 60 % des cancers papillaires de la thyroïde qui représentent 80% des cancers thyroïdiens. La présence de cette mutation est associée aux tumeurs thyroïdiennes les plus agressives avec un faible niveau ou une absence d'expression du NIS. La perte de la captation d'iode radioactif se traduit par la résistance à la radiothérapie métabolique constituant un enjeu majeur pour le traitement des patients atteints de ce cancer. L'une des approches pour le traitement des patients réfractaires à la radiothérapie métabolique consiste à augmenter l'absorption de l'iode.Au niveau transcriptionnel, notre équipe a déjà montré, à travers une analyse comparative qui porte sur environ 500 PTCs de la base de données TCGA, que NOX4 est fortement exprimée dans les PTCs-BRAFV600E comparativement aux PTCs-BRAFwt. Néanmoins, au niveau protéique, aucun lien n'a été établie entre la mutation BRAFV600E et NOX4 dans les tumeurs malignes et non malignes (BRAFV600E/BRAFwt). Dans mon projet de thèse, nous illustrons pour la première fois une corrélation positive entre la présence de la mutation BRAFV600E et la surexpression de la protéine NOX4 dans les tissus tumoraux PTCs. La surexpression de NOX4 est associée au caractère agressif des tumeurs. De plus, nous avons montré que 60% des C-PTCs infiltrant surexpriment NOX4 indépendamment du statut mutationnel de BRAF, ce qui suggère que NOX4 pourrait être considérée comme un co-marqueur potentiel de l'agressivité des PTCs. De manière intéressante la protéine NOX4 était également surexprimée dans les maladies thyroïdiennes non malignes (les Basedow, goitres et hyperplasies) avec différentes localisations subcellulaires, suggérant un rôle de NOX4 dans la progression vers la malignité thyroïdienne.Par ailleurs, sur le plan mécanistique, notre équipe a précédemment montré que BRAFV600E contrôle l'expression de NOX4 sous l'effet de TGF-β /SMAD3 et que les ERO dérivées de NOX4 contribuent à la répression du NIS. L'inhibition de NOX4 favorise la réactivation du NIS. Cette réversibilité suggère une contribution à un mécanisme épigénétique. CHD4, une sous-unité du complexe du remodelage NuRD, joue un rôle important dans la répression des gènes. Elle est fortement exprimée dans les PTCs dans lequel elle est associée à un mauvais pronostic. Dans cette étude, nous avons montré que la voie TGF-β/SMAD3 régule l'expression de la protéine CHD4. Cette dernière coopère avec les DNMTs dans la répression du NIS dans plusieurs lignées thyroïdiennes tumorales mutées pour BRAFV600E. Par ailleurs, nous montrons que CHD4 répond aux dommages oxydatifs à l'ADN induites par les ERO dérivés de NOX4. En effet, l'inhibition de NOX4 ou de son partenaire fonctionnel p22phox, induit une diminution du recrutement de CHD4 à la chromatine. Ce recrutement est dépendant d'OGG1 et MSH6, deux protéines impliquées dans la réparation des dommages oxydatifs à l'ADN. Cette étude identifie CHD4 en tant que nouvelle cible thérapeutique dans les tumeurs thyroïdiennes réfractaires à la radiothérapie métabolique
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

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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.

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Endokrin aktive Substanzen (EACs) sind exogene Substanzen natürlichen oder synthetischen Ursprungs, die mit der Feedbackregulation hormoneller Netzwerke interferieren können und somit deren Homöostase beeinflussen. Störungen der Hypothalamus-Hypophysen-Schilddrüsenachse (HPT-Achse) haben weitreichende Konsequenzen, da Schilddrüsenhormone essentiell für die Regulation von Entwicklung, Wachstum und Stoffwechsel sind. In der vorliegenden Arbeit wurde das Wirkprofil potenter Inhibitoren der thyreotropen Achse am Beispiel von 4-Methylbenzyliden-campher (4-MBC) und Genistein (GEN) untersucht. Der UV-Filter 4-MBC wurde in der ovariektomierten Ratte als goitrogene Substanz identifiziert. 4-MBC interferiert auf Ebene von Hypothalamus und Hypophyse mit der Expression Feedback-assoziierter Gene und beeinflusst daher die Feedbackregulation der thyreotropen Achse. Darüber hinaus wird die Biosynthese von Schilddrüsenhormonen durch Inhibition des Iodidtransports bei gleichzeitig erhöhter messenger RNA (mRNA)-Konzentration des Natrium-Iodid-Symporters (NIS) durch 4-MBC beeinträchtigt. Parallel dazu lässt die verstärkte Expression des Angiogenesemarkers vascular endothelial growth factor (VEGF) nach subakuter Exposition auf die Entstehung einer Hypothyreose schließen. Die damit einhergehenden Veränderungen sind auch in peripheren Organen durch die Analyse 3,3‘,5-Triiod-L-thyronin (T3)-regulierter Zielgene dokumentiert. Zudem wurden diese Effekte maßgeblich durch die Expositionszeit beeinflusst, da nach chronischer Exposition vermutlich auch kompensatorische Prozesse eine wichtige Rolle spielen. Die gezeigten speziesspezifischen Effekte lassen sich möglicherweise auf Unterschiede in der Pharmakokinetik zurückführen, z.B. in Folge differentieller Expression von Cytochrom P450-Genen.
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.

8

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.

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Thesis (Ph. D.)--Ohio State University, 2003.
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

9

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.

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10

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.

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Частини книг з теми "Natrium Iodide Symporter (NIS)":

1

Kucharska, Anna M., Barbara Czarnocka, and Urszula Demkow. "Anti-natrium/Iodide Symporter Antibodies and Other Anti-thyroid Antibodies in Children with Turner’s Syndrome." In Advances in Experimental Medicine and Biology, 131–38. Dordrecht: Springer Netherlands, 2012. http://dx.doi.org/10.1007/978-94-007-4549-0_17.

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2

Grimsdell, Ben, Adeel Saleem, Alessia Volpe, and Gilbert O. Fruhwirth. "Genetic Engineering of Therapeutic Cells with the Sodium Iodide Symporter (NIS) to Enable Noninvasive In Vivo Therapy Tracking." In Methods in Molecular Biology, 303–30. New York, NY: Springer US, 2023. http://dx.doi.org/10.1007/978-1-0716-3499-8_18.

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3

Elliyanti, Aisyah. "Radioiodine for Graves’ Disease Therapy." In Graves' Disease [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.96949.

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Radioiodine-131 (RAI) is an isotope of the chemical element iodine and is commonly used for hyperthyroidism, including Graves’ disease. It is given orally, and its concentration in the thyroid gland. The RAI transport involves a natrium iodide symporter (NIS) role that brings two cations sodium (Na+) and one anion of iodide (I-) across the membrane. The process is facilitated by the enzyme Na+/K+ ATPase. RAI is a beta (β) and gamma (γ) particles emitter. β particle is used for therapy and γ particle for imaging (theranostic). β particle inhibits cell growth by inducing cell death through apoptosis or necrosis of some of the sufficient thyroid cells. The aim of RAI therapy in Graves’ disease is to control hyperthyroidism and render the patient hypothyroidism. It is easier to manage patients with hypothyroidism with levothyroxine and fewer complications. This review will focus on RAI’s therapeutic approach in Graves’ disease, including patient preparation, selecting activity dose, adverse events, contraindication, controversies issues such as malignancy and fertility, the follow-up to ensuring the patient remains euthyroid or need a replacement therapy if they become hypothyroidism. RAI therapy is safe as definitive therapy and cost-effective for Graves’ disease therapy.

4

Carrasco, Nancy, and Rachel R. Kaspari. "Sodium/Iodide Symporter (NIS)." In Encyclopedia of Endocrine Diseases, 429–32. Elsevier, 2018. http://dx.doi.org/10.1016/b978-0-12-801238-3.96015-x.

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5

Spitzweg, Christine, and John C. Morris. "The Sodium–Iodide Symporter (NIS)." In Comprehensive Handbook of Iodine, 979–89. Elsevier, 2009. http://dx.doi.org/10.1016/b978-0-12-374135-6.00101-1.

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6

"NIS (sodium [Na]-iodide symporter)." In Encyclopedia of Genetics, Genomics, Proteomics and Informatics, 1348. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6754-9_11428.

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7

Josefsson, Malin, and Eva Ekblad. "Sodium Iodide Symporter (NIS) in Gastric Mucosa." In Comprehensive Handbook of Iodine, 215–20. Elsevier, 2009. http://dx.doi.org/10.1016/b978-0-12-374135-6.00022-4.

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8

Hernán Carro, Gerardo, and Juan Pablo Nicola. "The Molecular Basis for Radioiodine Therapy." In Thyroid Cancer - The Road From Genes to Successful Treatment [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.108073.

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Radioactive iodine (radioiodine) therapy is a standard and effective therapeutic approach for high-risk differentiated thyroid carcinomas, based on the unique ability of the thyroid follicular cell to accumulate iodide through the sodium/iodide symporter (NIS). However, a recurrent limitation of radioiodine therapy is the development of radioiodine-refractory differentiated thyroid carcinomas, which are associated with a worse prognosis. Loss of radioiodine accumulation in thyroid carcinomas has been attributed to cell dedifferentiation, resulting in reduced NIS expression and NIS intracellular retention involving transcriptional and posttranscriptional or posttranslational mechanisms, respectively. Emerging therapies targeting the oncogene-activated signal pathways potentially involved in thyroid carcinogenesis have been able to recover radioiodine accumulation in radioiodine-refractory tumors, which constitutes the rationale of redifferentiation therapies. Here, we will comprehensively discuss the molecular mechanisms underlying radioiodine therapy, refractoriness to radioiodine therapy in differentiated thyroid carcinomas, and novel strategies for restoring radioiodine accumulation in radioiodine-refractory thyroid carcinomas.

9

"Correlation between natrium iodide symporter and c-fos expressions in breast cancer cell lines." In Advances in Biomolecular Medicine, edited by A. Elliyanti, N. Noormartany, J. S. Masjhur, Y. Sribudiani, A. M. Maskoen, and T. H. Achmad, 19–22. CRC Press, 2017. http://dx.doi.org/10.1201/9781315208619-5.

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10

Knoop, Kerstin, Marie Kolokythas, Kathrin Klutz, Michael J. Willhauck, Nathalie Wunderlich, Dan Draganovici, Christian Zach, et al. "Therapeutic Potential of Stem Cell-Mediated Sodium Iodide Symporter (NIS) Gene Delivery in Liver Cancer." In BASIC/TRANSLATIONAL - Thyroid Cancer, P2–679—P2–679. The Endocrine Society, 2011. http://dx.doi.org/10.1210/endo-meetings.2011.part3.p12.p2-679.

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Тези доповідей конференцій з теми "Natrium Iodide Symporter (NIS)":

1

Fletcher, Alice, Rebecca Thompson, Martin Read, Andrew Turnell, Vicki Smith, and Chris J. McCabe. "Abstract LB-327: Identification of novel sodium iodide symporter (NIS) interactors which modulate iodide uptake." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-lb-327.

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2

Karaca, Turan. "Pendrin and sodium / iodide symporter (NIS) protein expression in testicular tissue of diabetic rat*." In 15th International Congress of Histochemistry and Cytochemistry. Istanbul: LookUs Scientific, 2017. http://dx.doi.org/10.5505/2017ichc.pp-167.

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3

Dwyer, Roisin M., James Ryan, Ronan Havelin, John C. Morris, Cathal O'Flatharta, Brian Miller, Zhonglin Liu, et al. "Abstract 5392: Mesenchymal stem cell (MSC) mediated delivery of the sodium iodide symporter (NIS) supports radionuclide imaging and treatment of breast cancer." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-5392.

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