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Статті в журналах з теми "Cancer papillaire de la thyroïde (PTC)":
1
Nezzar, Adlen. "Molecular biology and thyroid cancer." Batna Journal of Medical Sciences (BJMS) 2, no. 1 (June 30, 2015): 60–65. http://dx.doi.org/10.48087/bjmstf.2015.2114.
Анотація:
Pendant les 20 dernières années, la compréhension de la biologie moléculaire des cancers de la thyroïde a progressé, le développement des analyses moléculaires laisse entrevoir des implications importantes pour une aide au diagnostic en pathologie thyroïdienne ; ces analyses moléculaires peuvent aussi potentiellement permettre de mieux apprécier le pronostic de certaines lésions thyroïdiennes. Quatre types de mutation représentent la grande majorité des mutations somatiques actuellement connues, ayant le plus grand impact pour le diagnostic et le pronostic des carcinomes folliculaires et papillaires de la thyroïde : il s’agit des mutations ponctuelles de BRAF et de RAS et des réarrangements de RET/PTC et de PAX8/ PPARγ. Les mutations constitutionnelles de RET permettent de distinguer les formes familiales et les formes sporadiques des carcinomes médullaires de la thyroïde. La mutation activatrice V600E du gène BRAF est l’évènement oncogénique le plus fréquent et le plus spécifique des carcinomes papillaires (CP). Les miARN devraient rapidement avoir un intérêt diagnostique des tumeurs folliculaires sur cytoponction, grâce aux travaux récents explorant un plus grand nombre de classes tumorales et notamment des groupes de tumeurs histologiquement atypiques.
2
Shrestha, Rupendra T., Darin Ruanpeng, and 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, no. 2 (January 22, 2019): 15. http://dx.doi.org/10.3390/medsci7020015.
Анотація:
The re-naming of noninvasive follicular variant papillary thyroid cancer to the apparently non-malignant, noninvasive follicular thyroid neoplasm with papillary-like nuclear features (NIFTP) impacts the prevalence of malignancy rates, thereby affecting mutation frequency in papillary thyroid cancer. Preoperative assessment of such nodules could affect management in the future. The original publications following the designation of the new nomenclature have been extensively reviewed. With the adoption of NIFTP terminology, a reduction in the follicular variant of papillary thyroid cancer (FVPTC) prevalence is anticipated, as is a modest reduction of papillary thyroid cancer (PTC) prevalence that would be distributed mainly across indeterminate thyroid nodules. Identifying NIFTP preoperatively remains challenging. RAS mutations are predominant but the presence of BRAF V600E mutation has been observed and could indicate inclusion of the classical PTC. The histological diagnosis of NIFTP to designate low-risk encapsulated follicular variant papillary thyroid cancers (EFVPTCs) would impact malignancy rates, thereby altering the mutation prevalence. The histopathologic criteria have recently been refined with an exclusion of well-formed papillae. The preoperative identification of NIFTP using cytomorphology and gene testing remains challenging.
3
Liu, Xiaoli, Justin Bishop, Yuan Shan, Sara Pai, Dingxie Liu, Avaniyapuram Kannan Murugan, Hui Sun, Adel K. El-Naggar, and Mingzhao Xing. "Highly prevalent TERT promoter mutations in aggressive thyroid cancers." Endocrine-Related Cancer 20, no. 4 (June 13, 2013): 603–10. http://dx.doi.org/10.1530/erc-13-0210.
Анотація:
Mutations 1 295 228 C>T and 1 295 250 C>T (termed C228T and C250T respectively), corresponding to −124 C>T and −146 C>T from the translation start site in the promoter of the telomerase reverse transcriptase (TERT) gene, have recently been reported in human cancers, but not in thyroid cancers yet. We explored these mutations in thyroid cancers by genomic sequencing of a large number of primary tumor samples. We found the C228T mutation in 0 of 85 (0.0%) benign thyroid tumors, 30 of 257 (11.7%) papillary thyroid cancers (PTC), 9 of 79 (11.4%) follicular thyroid cancers (FTC), 3 of 8 (37.5%) poorly differentiated thyroid cancers (PDTC), 23 of 54 (42.6%) anaplastic thyroid cancers (ATC), and 8 of 12 (66.7%) thyroid cancer cell lines. The C250T mutation was uncommon, but mutually exclusive with the C228T mutation, and the two mutations were collectively found in 11 of 79 (13.9%) FTC, 25 of 54 (46.3%) ATC, and 11 of 12 (91.7%) thyroid cancer cell lines. Among PTC variants, the C228T mutation was found in 4 of 13 (30.8%) tall-cell PTC (TCPTC), 23 of 187 (12.3%) conventional PTC, and 2 of 56 (3.6%) follicular variant PTC samples. No TERT mutation was found in 16 medullary thyroid cancer samples. The C228T mutation was associated with the BRAF V600E mutation in PTC, being present in 19 of 104 (18.3%) BRAF mutation-positive PTC vs 11 of 153 (7.2%) the BRAF mutation-negative PTC samples (P=0.0094). Conversely, BRAF mutation was found in 19 of 30 (63.3%) C228T mutation-positive PTC vs 85 of 227 (37.4%) C228T mutation-negative PTC samples (P=0.0094). We thus for the first time, to our knowledge, demonstrate TERT promoter mutations in thyroid cancers, that are particularly prevalent in the aggressive thyroid cancers TCPTC, PDTC, ATC and BRAF mutation-positive PTC, revealing a novel genetic background for thyroid cancers.
4
Krause, Kerstin, Stefan Karger, Oliver Gimm, Sien-Yi Sheu, Henning Dralle, Andrea Tannapfel, Kurt Werner Schmid, Corinne Dupuy, and Dagmar Fuhrer. "Characterisation of DEHAL1 expression in thyroid pathologies." European Journal of Endocrinology 156, no. 3 (March 2007): 295–301. http://dx.doi.org/10.1530/eje-06-0596.
Анотація:
Iodotyrosine dehalogenase 1 (DEHAL1) is a transmembrane protein involved in the recycling of iodide in the human thyroid. The aim of the present study was (I) to investigate whether DEHAL1 expression is different in differentially functioning thyroid pathologies and (II) to evaluate DEHAL1 as a possible marker of thyroid cell differentiation. Design and methods: Real-time PCR for DEHAL1 and its isoform DEHAL1B was performed in a series of 105 thyroid specimens, including toxic thyroid nodules (TTN), Graves’ disease (GD) thyroids, benign cold thyroid nodules (CTN), normal thyroid tissues and thyroid cancers (follicular thyroid carcinomas (FTC), papillary thyroid carcinomas (PTC), partially differentiated thyroid cancers (PDTC) and anaplastic thyroid carcinomas (ATC)). In addition, DEHAL1 protein expression was studied by immunohistochemistry in 163 benign and malignant thyroid pathologies and normal thyroids. Results: (I) The highest DEHAL1 mRNA levels were found in GD thyroids, while downregulation of DEHAL1 and DEHAL1B mRNA occurred in PTC and ATC (P<0.001 and <0.05 respectively); (II) DEHAL1 protein was overexpressed in TTNs and GD thyroids with predominant apical staining in all samples; (III) a weaker and patchy staining pattern was found in CTNs and normal thyroids; (IV) in differentiated thyroid cancers (FTC and PTC), a diffuse cytoplasmic DEHAL1 expression was found; and (V) in PDTC and ATC, DEHAL1 expression was faint or absent. Conclusion: Upregulation of DEHAL1 protein expression and sublocalisation of DEHAL1 at the apical cell pole in TTNs and GD thyroids is consistent with increased thyroid hormone turnover during thyrotoxicosis. Diffuse cytoplasmatic localisation or downregulation of DEHAL1 expression in thyroid cancers suggests alteration or loss of DEHAL1 function during thyroid cell dedifferentiation.
5
Ozmen, Hilal Kiziltunc, Seda Askin, Eda Simsek, Ayse Carlioglu, Şenay Arikan, and Mustafa Utlu. "Mean Platelet Volume and Red Cell Distribution Width in Differentiated Thyroid Cancer Patients." Open Medicine Journal 6, no. 1 (December 20, 2019): 94–100. http://dx.doi.org/10.2174/1874220301603010094.
Анотація:
Aim: The purpose of this study was to investigate MPV and RDW values in DTC patients. Background: Differentiated Thyroid Cancer (DTC) is subdivided into papillary, follicular and papillary micro thyroid cancers. Mean Platelet Volume (MPV) and red cell distribution width (RDW) are markers which have been investigated in many cancers, but no data are available for DTC. Objective: MPV and RDW values were assessed in 108 patients with DTC, consisting of 44 with Papillary Thyroid Cancer (PTC) (mean age 43±13.9 years), 34 with Papillary Micro Thyroid Cancer (PmTC) (mean age 43.1 ± 10.6), and 28 with Follicular Cancer (FC) (mean age 46.9±12.5), and 77 control subjects (mean age 47.5±5.9). Methods: The patient and control groups were matched in terms of age, and body mass index. All subjects were investigated using platelet and biochemical parameters. Results: Both MPV [(PTC, PmTC, and FC) (p=0.000, p=0.000 and p=0.001, respectively)] and RDW (PTC, PmTC, and FC) (p=0.02, p=0.04 and p=0.02, respectively)] values increased in patients with DTC compared to the controls. MPV values were significantly positively correlated with CRP (r=0.247; p=0.043), postoperative thyroglobulin (r=0.246; p=0.03), gamma glutamyl transferase (r=0.024; p=0.762), tumor size (r=0.209; p=0.047) and RDW (r=0.207; p=0.005). Age, gender, total cholesterol, and C-reactive protein were identified as independent predictors of MPV. Adjustment for other these factors produced no alteration in these relative risks at multiple regression analysis. Conclusion: Our results suggest that patients with DTC have higher MPV and RDW values than healthy controls. MPV may represent a good follow-up criterion in DTC patients because of its positive correlation with tumor size and thyroglobulin.
6
Landa, Iñigo. "Advances in Thyroid Carcinoma." Cancers 14, no. 12 (June 13, 2022): 2908. http://dx.doi.org/10.3390/cancers14122908.
Анотація:
“Thyroid cancer” encompasses a heterogeneous group of tumors that range from the predominant papillary thyroid cancer (PTC) subtype, which shows excellent survival rates, to the poorly differentiated (PDTC) and anaplastic thyroid cancer (ATC) forms, accounting for most of the disease-related morbidity and mortality [...]
7
Soni, H., J. Batra, S. Dhandayuthapani, A. Mishra, and J. Aggarwal. "Genetic Polymorphism in Papillary Thyroid Cancerm j in North Indian Population – A review." CARDIOMETRY, no. 25 (February 14, 2023): 1188–91. http://dx.doi.org/10.18137/cardiometry.2022.25.11881191.
Анотація:
Papillary thyroid cancer (PTC) is one of the generic types of thyroid cancer and most prevalent form of malignancy among all cancers of the thyroid. It is also one of the few cancers with a rapidly increasing incidence. PTC constitutes approximately 85% of all thyroid cancer cases. PTC is usually contained within the thyroid gland and generally biologically indolent. The present article provides an updated condensed overview of PTC, which focuses mainly on the molecular and biomarker investigations.
8
Martin, 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, no. 11 (October 22, 2021): 1959. http://dx.doi.org/10.3390/diagnostics11111959.
Анотація:
Background: The primary endpoint was to analyze the preoperatory inflammatory markers and platelet indices in papillary thyroid cancer (PTC) patients compared with patients with benign thyroid pathology. The secondary endpoints were to analyze the relationship between these markers and the pathological features of PTC and to compare their pre- and postoperative levels in PTC patients. Methods: In this retrospective case-control study, we analyzed the files of 1183 patients submitted to thyroidectomy between January 2012 and December 2018. A total of 234 patients with PTC (mean age 51.54 ± 13.10 years, 84.6% females) were compared with an age-, gender- and BMI-matched control group of 108 patients with histologic benign thyroid disorders. Results: PTC patients had higher platelet count (PLT) (p = 0.011), plateletcrit (PCT) (p = 0.006), neutrophil (p = 0.022) and fibrinogen (p = 0.005) levels. Subgroup analysis showed that PTC females had higher PLT (p = 0.006), PCT (p < 0.001) and erythrocyte sedimentation rate (ESR) (p = 0.005), while males had higher neutrophil (p = 0.040) levels. Papillary thyroid cancer patients under 55 years had higher PLT (p < 0.001) and PCT (p = 0.010), while patients over 55 years had higher mean platelet volume (p = 0.032), neutrophil-to-lymphocyte ratio (p = 0.013), ESR (p = 0.005) and fibrinogen (p = 0.019) levels. Preoperative values for platelet indices and inflammatory markers were similar to the postoperative determinations in PTC patients. Fibrinogen (AUROC = 0.602, p = 0.02; cut-off = 327.5 mg/dL, Se = 53.8%, Sp = 62.9%) and PLT (AUROC = 0.584, p = 0.012; cut-off = 223.5 × 103/mm3, Se = 73.1%, Sp = 42.6%) were independent predictors of the presence of PTC. Conclusions: Our data show that fibrinogen and platelet count could be promising, inexpensive, independent predictors for the presence of PTC when compared with benign thyroid disorders.
9
Arican, Cigdem D., Tulin Ozturk, Muhammet Sait Sager, Ipek Sertbudak, Serkan Teksoz, Cansu Turker Saricoban, and Abdulkerim Uygur. "Incidental Papillary Microcarcinoma and Papillary Thyroid Carcinoma in Multinodular Goiter." Analytical Cellular Pathology 2023 (January 14, 2023): 1–7. http://dx.doi.org/10.1155/2023/2768344.
Анотація:
Introduction. This study aimed to examine the incidence of incidental papillary microcarcinoma (PMC) and papillary thyroid carcinoma (PTC) in patients with benign multinodular goiter (MNG) and to compare their relationship with some prognostic factors from a new perspective. Methods. Bilateral total thyroidectomy (BTT) was used to evaluate the data of 716 patients who underwent a surgery for MNG. The prognostic data for these tumors and the relationship between patients with bilateral and multifocal tumors were evaluated using statistical tests. Results. Papillary carcinomas were detected in 201 patients, PMC in 134 of them, and PTCs in 67. Bilaterality was more common in patients with PTCs than in those with PMC. The incidence of bilaterality in male patients with PTC was statistically more common. The presence of intra-tumoral lymphocytes was higher in multifocal PTC cases than in unifocal PTC cases. Conclusion. The results revealed that the number of PMC s was high in incidental tumors, and patients with PTC with male sex, bilaterality, multifocality, and tumor capsule invasion were associated with poor prognosis.
10
Tao, Ling, Li Yang, Ping Tian, Xiangyang Guo, and Yanping Chen. "Knockdown of circPVT1 inhibits progression of papillary thyroid carcinoma by sponging miR-126." RSC Advances 9, no. 23 (2019): 13316–24. http://dx.doi.org/10.1039/c9ra01820d.
Дисертації з теми "Cancer papillaire de la thyroïde (PTC)":
1
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.
Анотація:
Une des propriétés majeures de la thyroïde est de capter l’iode de la circulation sanguine grâce à la présence d’un transporteur d’iodure (NIS pour Natrium Iodide Symporter). Cette capacité d’accumulation d’iode par les thyrocytes joue un rôle clé dans la synthèse des hormones thyroïdiennes ainsi dans le diagnostic et le traitement des cancers de la thyroïde. Cependant, en raison d’une diminution ou de l’absence de l’expression du NIS dans certaines tumeurs et métastases, des patients deviennent réfractaires à la radiothérapie métabolique et présentent une radiorésistance, causant ainsi un problème de santé publique.L’oncogène BRAFV600E, un puissant activateur de La voie MAP kinase, est détecté dans 40 - 60% des cancers thyroïdiens de type papillaires (CPT) qui représentent 80% de la totalité des cancers thyroïdiens. La mutation BRAFV600E est associée aux tumeurs thyroïdiennes les plus agressives. Cependant l’inhibition pharmacologique de la voie MAP kinase induite constitutivement par l’oncogène BRAFV600E ne permet pas, à elle seule, de rétablir l’expression du NIS chez des patients atteints d’un cancer de la thyroïde muté BRAFV600E. Ceci suggère que d’autres mécanismes compensatoires peuvent contribuer à la radiorésistance. Une étude récente menée sur un modèle murin a montré que la régulation négative du NIS par l’oncogène BRAFV600E est médiée par la voie du TGF beta. Une autre a montré que l’expression du NIS serait dépendante de l’état redox de la cellule, suggérant un rôle des espèces réactives de l’oxygène (ROS). Dans les cellules les ROS peuvent être produites par les NADPH oxydases (NOX/DUOX). La thyroïde en exprime trois : DUOX2 nécessaire à la synthèse des hormones thyroïdiennes ainsi que DUOX1 et NOX4 dont le rôle physiologique reste inconnu. NOX4, surexprimé dans les CPTs, a été montré être un nouvel effecteur clé de la voie du TGF beta dans d’autres cancers.Dans mon projet de thèse, je me suis intéressée à l’étude du rôle de NOX4 dans la régulation négative du NIS dans les CPT mutés BRAFV600E. L’étude du mécanisme, réalisée à partir de deux lignées humaines issues de cancers papillaires mutés pour BRAF (BCPAP et 8505C), a permis d’établir que l’oncogène BRAFV600E contrôle l’expression de NOX4 au niveau transcriptionnel via la voie TGF-beta/Smad3. Ces résultats ont été validés sur une lignée de rat exprimant de manière conditionnelle BRAFV600E ainsi que sur des thyrocytes humains en culture primaire. De manière importante, l’utilisation d’antioxydants tels que le N-acetyl cystéine (NAC) ou l’inhibition spécifique de l’expression de NOX4 par ARN interférence permet de réinduire l’expression du NIS. Ces résultats qui montrent que les ROS produites par NOX4 inhibent l’expression du transporteur de l’iode (NIS) établissent un lien entre l’oncogène BRAFV600E et NOX4. Une analyse comparative de l'expression de NOX4 effectuée à partir de 500 cancers papillaires de la thyroïdes mutés ou non pour BRAF (données TCGA) confirme que NOX4 est significativement augmenté dans les cancers porteurs de la mutation BRAF et que ceci est corrélé à une diminution de l’ARNm du NIS. Par ailleurs, le niveau de NOX4 est inversement corrélé au score de différenciation thyroïdien, suggérant que NOX4 pourrait être impliqué dans le processus de dédifférenciation. Cette étude ouvre une nouvelle opportunité pour l’optimisation de l’utilisation de la radiothérapie métabolique dans le traitement des cancers thyroïdiens réfractaires à l’iode I131 et présente NOX4 comme une cible thérapeutique potentielleOne 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
2
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.
Анотація:
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 métaboliqueMetabolic 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
3
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.
Анотація:
Le cancer papillaire de la thyroïde (PTC) est celui le plus fréquent de la thyroïde. Il est caractérisé par des réarrangements chromosomique affectant le gène RET, dont les plus fréquemment observés sont RET/PTC1 et RET/PTC3. Les oncogène de jonction sont spécifiques à la tumeur et représentent une cible privilégiée pour une thérapie ciblée par des petits ARN interférents (siRNA). Notre but est d’introduire une nouvelle approche pharmacologique par siRNA pour les PTC. Pour réaliser nos expériences, la lignée cellulaire humaine PTC, BHP10-3 SCmice exprimant l’oncogène RET/PTC1 a été utilisé. En absence de lignée RET/PTC3 commercialisée nous avons établi la lignée cellulaire RP3 (stablement transfecté la lignée NIH/3T3 issue de fibroblastes de souris par un vecteur d’expression RET/PTC3) qui s’est avérée tumorigène chez la souris. Ensuite, des siRNAs dirigés contre la jonction ont été dessinés. Les siRNAs ont été trouvés efficaces et spécifiques contre leurs propres oncogènes de jonction et ne sont pas capables d'inhiber l'expression de séquences alternées. Les siRNAs ont été vectorisés sous forme de nanoparticules (NPs) de squalène (SQ). In vitro, les NPs siRNA RET/PTC1-SQ et NPs siRNA RET/PTC3-SQ sont incapables d’inhiber l’expression de l’oncogène et l’oncoprotéine sauf transfectés par lipofectamine. Pour cela, un peptide, le GALA-Chol a été combiné aux NPs siRNA RET/PTC1-SQ ce qui les a rendu efficace in vitro dans l’inhibition de l’oncogène et de l’oncoprotéine mais inefficace sur la croissance tumorale in vivo probablement par agrégation des NPs siRNA RET/PTC1-SQ GALA-Chol dans la circulation sanguine. En revanche les NPs siRNA RET/PTC1-SQ (0.5mg/kg/souris) et NPs siRNA RET/PTC3-SQ (2.5mg/kg/souris) sont efficaces in vivo, ils inhibent considérablement la croissance tumorale, réduisent l’expression des oncogènes et des oncoprotéines RET/PTCs, induisent la mort cellulaire par clivage de la caspase-3 et de PARP-1 et restaurent partiellement la différenciation (diminution de marqueur Ki67). Ces résultats suggèrent l'utilisation des NPs siRNAs-SQ en tant que traitement pour les patients atteints de PTC exprimant les oncogènes de jonctions RET/PTCsPapillary 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
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Liu, Tingting, and 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.
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Krishnan, 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.
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Irani, Soussan. "The Endothelin Axis and Angiogenesis in Papillary Thyroid Carcinoma." Thesis, Griffith University, 2014. http://hdl.handle.net/10072/366833.
Анотація:
Papillary Thyroid Cancer (PTC) is the most common thyroid cancer accounting for 80% of all cases. The prognosis is good, with 5-year survival rates of 95%, but in some cases the tumour behaves in an aggressive manner characterized by local recurrence and/or metastasis, processes contributed to by angiogenesis.
Angiogenesis is an essential physiologic activity involved in normal tissue biology and several pathologic conditions such as cardiac failure, and cancer. During carcinogenesis, tumour cells secrete pro-angiogenic factors to initiate angiogenesis. Angiogenesis also causes the migration of endothelial cells from pre-existing vessels to improve nutrient and oxygen delivery to tumours, angiogenesis has a key role in tumour growth and metastasis.
Vascular endothelial growth factor (VEGF) has a pivotal role in the control of angiogenesis, aggressiveness in thyroid cancers. The endothelins (ETs) are a family of genes inducing DNA synthesis and cellular growth in different cells, affecting vascular tone and angiogenesis. ET-1 has a direct effect on neoplastic cells by inducing cellular proliferation, migration as well as invasion and inhibition of apoptosis. ET-1 induces VEGF expression by increasing hypoxia-inducible factor-1α (HIF-1α) stimulation.Thesis (PhD Doctorate)
School of Medical Science
Griffith Health
Full Text
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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.
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Bonnin, 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.
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Seignovert, 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.
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Martinez, 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.
Книги з теми "Cancer papillaire de la thyroïde (PTC)":
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Kitahara, Cari M., Arthur B. Schneider, and Alina V. Brenner. Thyroid Cancer. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190238667.003.0044.
Анотація:
Thyroid cancer, once considered relatively uncommon in the general population, is now the eighth most commonly diagnosed cancer among women worldwide, and the third most common cancer among women under 45 years of age. The incidence is substantially higher in women than men (3:1 ratio); this differential is highest between ages 15 and 39 and declines with age. Nearly all thyroid cancers derive from the follicular epithelium, and the most common histological type is papillary thyroid cancer (PTC). Incidence of thyroid cancer has been increasing in many countries since the early 1980s. This trend appears to be attributable to a combination of diagnostic changes, improvements in the detection and diagnosis of smaller PTCs, and changes in the prevalence of environmental factors. While less common, the incidence of larger, more advanced-stage PTCs has increased at a similar rate to that of smaller PTCs.
Частини книг з теми "Cancer papillaire de la thyroïde (PTC)":
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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.
Анотація:
Well differentiated thyroid cancers are a class of cancers that have one of the best prognosis. They include papillary and follicular cancers with a few of their subtypes. They often present as solitary thyroid nodules. Cervical lymph node metastases is more common in papillary carcinoma than follicular carcinomas. Diagnosis is made with the help of thyroid ultrasonography coupled with fine needle aspiration cytology. Surgical management can either be lobectomy for low risk, small tumors or sub total/ total thyroidectomy for larger, high risk tumors. Total thyroidectomy enables better post operative follow up via serum thyroglobulin levels and radio iodine scans. Remnant thyroid tissue is ablated with radioiodine and patients are kept on suppressive doses of thyroxine to decrease risk of recurrence. 10 year prognosis is usually >95%, especially in patients with PTC.
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Sarquis, Marta MS, Juliana Brito Brandao, Adauto Versiani Ramos, Marcio Lauria Weissheimer, and 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.
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Gharwan, H., ML Pratt, and 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.
Тези доповідей конференцій з теми "Cancer papillaire de la thyroïde (PTC)":
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Ahmed, Elham, Abdul Khan, Kirti S. Prabhu, Kodappully Siveen, Zafar Nawaz, Hatem Zayed, and 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.
Анотація:
Sanguinarine (SNG), a natural compound with an array of pharmacological activities, has promising therapeutic potential against a number of pathological conditions, including malignancies. This research aimed to investigate the antiproliferative and anti-cancer potential of SNG against two well characterized papillary thyroid cancer (PTC) cell lines, BCPAP and TPC-1 .In both cell lines , SNG was able to inhibit cell proliferation in time and dose dependent manner. Western blot analysis revealed increased expression of apoptosis and autophagy markers , caspase-3,cleaved caspase-3 , P62, and LC3. SNG modulate its anticancer effect through ROS production, because NAC was able to reverse SNG effect. Interestingly, co-treatment of PTC with SNG and cisplatin amplified anticancer activity. Finally, SNG treatment of PTC spheroid suppressed its growth with downregulation of stemness markers including ALDH2 and SOX2 markers. In conclusion, SNG enhanced the anti cancer activity against PTC cells and the effect is amplified when cisplatin is added.
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Siraj, Abdul K., Rong Bu, Sandeep K. Parvathareddy, Yan Kong, Padmanaban Annaiyappanaidu, Saeeda O. Ahmed, Maha Al-Rasheed, and 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.
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Danysh, Brian P., Maria E. Cabanillas, and 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.