Auswahl der wissenschaftlichen Literatur zum Thema „Cancer papillaire de la thyroïde (PTC)“
Geben Sie eine Quelle nach APA, MLA, Chicago, Harvard und anderen Zitierweisen an
Inhaltsverzeichnis
Machen Sie sich mit den Listen der aktuellen Artikel, Bücher, Dissertationen, Berichten und anderer wissenschaftlichen Quellen zum Thema "Cancer papillaire de la thyroïde (PTC)" bekannt.
Neben jedem Werk im Literaturverzeichnis ist die Option "Zur Bibliographie hinzufügen" verfügbar. Nutzen Sie sie, wird Ihre bibliographische Angabe des gewählten Werkes nach der nötigen Zitierweise (APA, MLA, Harvard, Chicago, Vancouver usw.) automatisch gestaltet.
Sie können auch den vollen Text der wissenschaftlichen Publikation im PDF-Format herunterladen und eine Online-Annotation der Arbeit lesen, wenn die relevanten Parameter in den Metadaten verfügbar sind.
Zeitschriftenartikel zum Thema "Cancer papillaire de la thyroïde (PTC)"
Nezzar, Adlen. „Molecular biology and thyroid cancer“. Batna Journal of Medical Sciences (BJMS) 2, Nr. 1 (30.06.2015): 60–65. http://dx.doi.org/10.48087/bjmstf.2015.2114.
Der volle Inhalt der QuelleShrestha, Rupendra T., Darin Ruanpeng und James V. Hennessey. „Cytomorphology of Noninvasive Follicular Thyroid Neoplasm with Papillary-Like Nuclear Features and the Impact of New Nomenclature on Molecular Testing“. Medical Sciences 7, Nr. 2 (22.01.2019): 15. http://dx.doi.org/10.3390/medsci7020015.
Der volle Inhalt der QuelleLiu, Xiaoli, Justin Bishop, Yuan Shan, Sara Pai, Dingxie Liu, Avaniyapuram Kannan Murugan, Hui Sun, Adel K. El-Naggar und Mingzhao Xing. „Highly prevalent TERT promoter mutations in aggressive thyroid cancers“. Endocrine-Related Cancer 20, Nr. 4 (13.06.2013): 603–10. http://dx.doi.org/10.1530/erc-13-0210.
Der volle Inhalt der QuelleKrause, Kerstin, Stefan Karger, Oliver Gimm, Sien-Yi Sheu, Henning Dralle, Andrea Tannapfel, Kurt Werner Schmid, Corinne Dupuy und Dagmar Fuhrer. „Characterisation of DEHAL1 expression in thyroid pathologies“. European Journal of Endocrinology 156, Nr. 3 (März 2007): 295–301. http://dx.doi.org/10.1530/eje-06-0596.
Der volle Inhalt der QuelleOzmen, Hilal Kiziltunc, Seda Askin, Eda Simsek, Ayse Carlioglu, Şenay Arikan und Mustafa Utlu. „Mean Platelet Volume and Red Cell Distribution Width in Differentiated Thyroid Cancer Patients“. Open Medicine Journal 6, Nr. 1 (20.12.2019): 94–100. http://dx.doi.org/10.2174/1874220301603010094.
Der volle Inhalt der QuelleLanda, Iñigo. „Advances in Thyroid Carcinoma“. Cancers 14, Nr. 12 (13.06.2022): 2908. http://dx.doi.org/10.3390/cancers14122908.
Der volle Inhalt der QuelleSoni, H., J. Batra, S. Dhandayuthapani, A. Mishra und J. Aggarwal. „Genetic Polymorphism in Papillary Thyroid Cancerm j in North Indian Population – A review“. CARDIOMETRY, Nr. 25 (14.02.2023): 1188–91. http://dx.doi.org/10.18137/cardiometry.2022.25.11881191.
Der volle Inhalt der QuelleMartin, Sorina, Theodor Mustata, Oana Enache, Oana Ion, Andreea Chifulescu, Anca Sirbu, Carmen Barbu et al. „Platelet Activation and Inflammation in Patients with Papillary Thyroid Cancer“. Diagnostics 11, Nr. 11 (22.10.2021): 1959. http://dx.doi.org/10.3390/diagnostics11111959.
Der volle Inhalt der QuelleArican, Cigdem D., Tulin Ozturk, Muhammet Sait Sager, Ipek Sertbudak, Serkan Teksoz, Cansu Turker Saricoban und Abdulkerim Uygur. „Incidental Papillary Microcarcinoma and Papillary Thyroid Carcinoma in Multinodular Goiter“. Analytical Cellular Pathology 2023 (14.01.2023): 1–7. http://dx.doi.org/10.1155/2023/2768344.
Der volle Inhalt der QuelleTao, Ling, Li Yang, Ping Tian, Xiangyang Guo und Yanping Chen. „Knockdown of circPVT1 inhibits progression of papillary thyroid carcinoma by sponging miR-126“. RSC Advances 9, Nr. 23 (2019): 13316–24. http://dx.doi.org/10.1039/c9ra01820d.
Der volle Inhalt der QuelleDissertationen zum Thema "Cancer papillaire de la thyroïde (PTC)"
Azouzi, Naima. „Etude de l’implication de la NADPH oxydase NOX4 et du stress oxydatif dans la radiorésistance des cancers papillaires de la thyroïde exprimant l’oncogène BRAFV600E“. Thesis, Université Paris-Saclay (ComUE), 2016. http://www.theses.fr/2016SACLS416.
Der volle Inhalt der QuelleOne of the major properties of the thyroid is iodine uptake from the bloodstream through an iodide transporter (NIS for Natrium Iodide Symporter). This capacity plays a key role in the thyroid hormones synthesis, but also in both diagnosis and treatment of thyroid cancer. However, due to a decrease or absence of the NIS expression in some tumors and metastases, patients become refractory to the metabolic radiotherapy and present a radioresistance, which cause a public health problem.The BRAFV600E oncogene, a potent activator of the MAP kinase pathway, is detected in 40-60% of papillary thyroid cancer (PTC), which represent 80% of total thyroid cancers. The BRAFV600E mutation is associated with the more aggressive thyroid tumors. However, the pharmacological inhibition of the MAP kinase pathway, constitutively induced by the BRAFV600E oncogene, is not able to restore alone the expression of NIS in patients with BRAFV600E mutated thyroid cancer. This suggests that other compensatory mechanisms may contribute to the radioresistance. A recent study in a mouse model demonstrated that downregulation of NIS by BRAFV600E oncogene is mediated through the TGF beta activation. An other showed that the expression of NIS is dependent on the redox status of the cell, suggesting a role for the reactive oxygen species (ROS). In cells, ROS can be produced by the NADPH oxidases (NOX/DUOX). The Thyroid gland expresses three of them: DUOX2, which is necessary for the thyroid hormones synthesis, but also DUOX1 and NOX4 whose the physiological role remains unknown. NOX4, which is overexpressed in the PTCs, has been shown to be a new key effector of the TGF beta pathway.In my thesis project, I was interested in studying the role of NOX4 in the negative regulation of NIS in BRAFV600E mutated CPT. The study of the mechanism, made from two human cell lines derived from BRAF-mutated papillary thyroid cancers (BCPAP and 8505C), has revealed that the oncogene BRAFV600E controls the expression of NOX4 at the transcriptional level via the TGF-beta/Smad3 pathway. These results were validated on both a rat thyroid cell line conditionnaly expressing BRAFV600E and on human thyrocytes in primary culture. Importantly, the use of antioxidants such as N-acetyl cysteine (NAC) or specific inhibition of NOX4 expression by RNA interference allow reinduction of NIS expression. These results, which show that ROS produced by NOX4 inhibit the expression of iodine transporter (NIS), establish a link between the oncogene BRAFV600E and NOX4. A comparative analysis of the NOX4 expression, made from 500 papillary thyroid cancers mutated or not for BRAF (TCGA data), confirms that NOX4 is significantly increased in BRAF-mutated cancers and that this is correlated with a decrease of NIS mRNA. Furthermore, the level of NOX4 is inversely related to thyroid differentiation score, suggesting that NOX4 might be involved in the dedifferentiation process. This study opens a new opportunity for optimizing the use of metabolic radiotherapy in the treatment of thyroid cancers refractory to radioiodine I131and makes NOX4 as a potential therapeutic target
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.
Der volle Inhalt der QuelleMetabolic 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
Ali, Hafiz Muhammad. „Effects of siRNA-squalene nanoparticles on RET/PTCs junction oncogenes in papillary thyroid carcinoma : from molecular and cellular studies to preclinical investigations“. Thesis, Paris 11, 2014. http://www.theses.fr/2014PA11T016/document.
Der volle Inhalt der QuellePapillary thyroid carcinoma (PTC) is the most common of thyroid cancers. PTC is characterized by chromosomal rearrangements affecting chromosome 10 and leading to RET/PTC junction oncogenes. The most frequent ones are RET/PTC1 and RET/PTC3. Because the junction oncogenes are present only in the tumour cells, they represent a good target for a specific therapy such as small interfering RNA (siRNA). Our aim is to introduce a new pharmacological approach by siRNA for PTC. To perform the experiments, human BHP10-3 SCmice cell line expressing RET/PTC1 was used. Due to absence of commercially available RET/PTC3 cell line, we established a new RP3 cell line (from NIH/3T3 mouse fibroblasts, transfected stably with the RET/PTC3 expression vector) which was found to become tumorigenic in nude mice. siRNAs were designed within the junction sequences of both RET/PTC1 and RET/PTC3. Both siRNAs were found efficient and specific against their own junction oncogenes and were not able to inhibit the expression of alternate sequences. Then, siRNAs were vectorized in the form of nanoparticles (NPs) of squalene (SQ). In vitro, both siRNA RET/PTC1-SQ NPs and siRNA RET/PTC3-SQ NPs were found to be inefficient in gene and protein inhibitions except once transfected with lipofectamine. Therefore, a peptide GALA-Chol was added in siRNA RET/PTC1-SQ NPs which rendered them efficient in vitro in gene and protein inhibitions but found to be inefficient in vivo. The nanoparticles of siRNA RET/PTC1-SQ NPs (0.5 mg/kg/mouse) and siRNA RET/PTC3-SQ NPs (2.5 mg/kg/mouse) were found to drastically reduce the tumor growth and RET/PTCs oncogene and oncoprotein expressions. Moreover, they induced cell death by cleavage of both caspase-3 and PARP-1 and partially restored differentiation (decrease of Ki67 marker). Our findings highly support the use of siRNAs-SQ NPs as a treatment for patients affected by PTC expressing RET/PTCs
Liu, Tingting, und 劉婷婷. „Thyroid transcription factor 1 gene(TITF1): apotential heritable determinant of papillary thyroid carcinoma(PTC)“. Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B39793898.
Der volle Inhalt der QuelleKrishnan, Aswini [Verfasser]. „Identification and characterization of novel targets in Papillary Thyroid Cancer (PTC) / Aswini Krishnan“. Mainz : Universitätsbibliothek Mainz, 2019. http://d-nb.info/1195196849/34.
Der volle Inhalt der QuelleIrani, Soussan. „The Endothelin Axis and Angiogenesis in Papillary Thyroid Carcinoma“. Thesis, Griffith University, 2014. http://hdl.handle.net/10072/366833.
Der volle Inhalt der QuelleThesis (PhD Doctorate)
School of Medical Science
Griffith Health
Full Text
Paulin, Christian. „Étude du cancer papillaire de la thyroïde : établissement et caractérisation de la lignée B-CPAP“. Lyon 1, 1996. http://www.theses.fr/1996LYO1T072.
Der volle Inhalt der QuelleBonnin, Christian. „Evolution de 111 microcarcinomes papillaires thyroi͏̈diens : étude rétrospective de 1953 à 1994, expérience de l'Institut Bergonié“. Bordeaux 2, 1996. http://www.theses.fr/1996BOR23091.
Der volle Inhalt der QuelleSeignovert, Béatrice Coste. „Exploitation d'une enquête internationale sur le diagnostic et le traitement du nodule thyroi͏̈dien et des cancers différenciés de la thyroi͏̈de“. Montpellier 1, 1988. http://www.theses.fr/1988MON11228.
Der volle Inhalt der QuelleMartinez, Alfaro Minerva. „Réarrangements du proto-oncogène RET dans le cancer papillaire de la thyroi͏̈de : prévalence dans les carcinomes sporadiques (microcarcinomes) et familiaux, et effets des radiations ionisantes sur RET“. Lyon 1, 2002. http://www.theses.fr/2002LYO1T181.
Der volle Inhalt der QuelleBücher zum Thema "Cancer papillaire de la thyroïde (PTC)"
Kitahara, Cari M., Arthur B. Schneider und Alina V. Brenner. Thyroid Cancer. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190238667.003.0044.
Der volle Inhalt der QuelleBuchteile zum Thema "Cancer papillaire de la thyroïde (PTC)"
Khan, Dr Amena. „WELL DIFFERENTIATED THYROID CANCERS“. In Futuristic Trends in Medical Sciences Volume 3 Book 12, 353–63. Iterative International Publisher, Selfypage Developers Pvt Ltd, 2024. http://dx.doi.org/10.58532/v3bfms12p1ch31.
Der volle Inhalt der QuelleSarquis, Marta MS, Juliana Brito Brandao, Adauto Versiani Ramos, Marcio Lauria Weissheimer und Eduardo Pimentel Dias. „Surgical Strategy's Impact on the Papillary Thyroid Carcinoma (PTC) Postoperative Staging“. In CLINICAL - Thyroid Cancer, P3–655—P3–655. The Endocrine Society, 2011. http://dx.doi.org/10.1210/endo-meetings.2011.part4.p11.p3-655.
Der volle Inhalt der QuelleGharwan, H., ML Pratt und HG Fein. „Papillary Thyroid Cancer (PTC) Presenting as Extensive Radioiodine-Resistant Bone Metastases in a Young Woman a Decade after Neck Irradiation for Hodgkin's Lymphoma.“ In The Endocrine Society's 92nd Annual Meeting, June 19–22, 2010 - San Diego, P1–585—P1–585. Endocrine Society, 2010. http://dx.doi.org/10.1210/endo-meetings.2010.part1.p12.p1-585.
Der volle Inhalt der QuelleKonferenzberichte zum Thema "Cancer papillaire de la thyroïde (PTC)"
Ahmed, Elham, Abdul Khan, Kirti S. Prabhu, Kodappully Siveen, Zafar Nawaz, Hatem Zayed und Shahab Uddin. „Sanguinarine Mediated Anti-Tumor activity Via Targeting JAK/STAT3 Pathway in Thyroid Cancer“. In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0155.
Der volle Inhalt der QuelleSiraj, Abdul K., Rong Bu, Sandeep K. Parvathareddy, Yan Kong, Padmanaban Annaiyappanaidu, Saeeda O. Ahmed, Maha Al-Rasheed und Khawla S. Al-Kuraya. „Abstract 2425: Prevalence of NTRK fusions and clinico-pathological characteristics of Middle Eastern papillary thyroid cancer revealed enrichment in BRAF wild-type PTC“. In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-2425.
Der volle Inhalt der QuelleDanysh, Brian P., Maria E. Cabanillas und Marie-Claude Hofmann. „Abstract 2933: Long-term BRAF(V600E) inhibition results in a spontaneous KRAS(G12D) mutation and increased epithelial to mesenchymal transition (EMT) in papillary thyroid cancer cells (PTC)“. In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-2933.
Der volle Inhalt der Quelle