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Добірка наукової літератури з теми "Glioblastome – Génétique"
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Статті в журналах з теми "Glioblastome – Génétique"
Luquain, A., S. Magnin, G. Viennet, C. Mougin, J. L. Prétet, and S. Valmary-Degano. "Mise en place de l’étude de la méthylation du gène MGMT dans le glioblastome sur la plateforme de génétique moléculaire des cancers à Besançon." Annales de Pathologie 33, no. 6 (December 2013): 434. http://dx.doi.org/10.1016/j.annpat.2013.10.010.
Повний текст джерелаAlmairac, F., M. Frenay, and P. Paquis. "Maladies génétiques et glioblastomes." Neurochirurgie 56, no. 6 (December 2010): 455–58. http://dx.doi.org/10.1016/j.neuchi.2010.07.007.
Повний текст джерелаLarsen, C. "Anomalies génétiques et moléculaires des glioblastomes (GBM)." Bulletin du Cancer 97, no. 11 (November 2010): 1389–407. http://dx.doi.org/10.1684/bdc.2010.1215.
Повний текст джерелаBurel-Vandenbos, F., F. Pedeutour, V. Paquis, P. Paquis, N. Cardot-Leccia, J. Haudebourg, M. C. Saint-Paul, and J. F. Michiels. "Association de deux anomalies génétiques rares dans un glioblastome à cellules géantes : un caryotype tumoral haploïde et une instabilité des microsatellites." Annales de Pathologie 26, no. 3 (June 2006): 239. http://dx.doi.org/10.1016/s0242-6498(06)77316-3.
Повний текст джерелаДисертації з теми "Glioblastome – Génétique"
Mercier, Marie-Cécile. "Les cellules initiatrices de tumeurs à l'origine de l'hétérogénéité d'expression de l'intégrine α5β1 dans les glioblastomes". Thesis, Strasbourg, 2018. http://www.theses.fr/2018STRAJ100/document.
Повний текст джерелаGlioblastoma (GBM) is the most aggressive primary brain tumor. Treatment failure is explained by inter and intratumoral heterogeneity. Our previous results showed that the α5β1 integrin, the fibronectin receptor, is implicated in GBM aggressiveness. We observed that its expression was heterogeneous between patients' tumors but also between different areas in a given tumor. We hypothesized that this heterogeneity may be linked to different glioma stem cells (GSC). We confirmed that α5 expression is induced after differentiation in about half of the cell lines supporting the notion of inter-tumoral heterogeneity. We also observed with single cell-derived clone analysis that intra-tumoral GICs heterogeneity exists. We noticed that when GICs are programmed to express α5 integrin, differentiated cells become more aggressive. Our data support that differentiated cells expressing the integrin have an increased capacity of proliferation and acquire a fibronectin-dependent motility and a resistance phenotype. This work provides a better understanding of the origin of more aggressive foci and highlights the interest of α5β1 integrin as a therapeutic target for a subpopulation of patients
Yaghi, Layale. "Hypoxie et régulation de l'expression de la molécule HLA-G dans le glioblastome." Paris 7, 2012. http://www.theses.fr/2013PA077060.
Повний текст джерелаHLA-G is a non classical MHC class I molecule involved in immune tolerance processes. Its expression has been described in various cancers favoring their immune escape. We analyzed HLA-G expression in glioblastoma biopsies, and found that HLA-G is expressed in 60% of the samples and is associated with reduced long term survival rate. The mechanisms underlying HLA-G gene expression were investigated in glioma cell lines U251MG, D247MG and U138MG. HLA-G expression is induced by 5-aza-2'-deoxycytidine demethylating treatment and enhanced by IFN-y and the hypoxic microenvironment. It is also dependent on the permissive state of the chromatin at the promoter and on the variation of expression of several antigen presenting machinery components. Under hypoxia mimicking conditions, we demonstrate that HLA-G expression is regulated by HIF-1 via a HRE (Hypoxia Responsive Element) located at +274 bp in exon 2. We also describe the role of HLA-G polymorphism in the 5'UTR (SNP -966 A/G located in a HRE) and 3'UTR (expression more repressed by endogenous miRNAs with haplotypes UTR-5 and -7) in the regulation of its expression. Moreover, we observe by microarray analysis that the expression of HLA-G putative miRNAs is modulated in hypoxia. HLA-G should thus be taken into account in the development of new anti-tumor therapies considering that its expression is a result of the chromatin state at the HLA-G locus, the tumor microenvironment, the endogenous miRNA expression and the polymorphism of both 5' and 3'UTR
Cosset, Erika. "Implication de la cavéoline-1 dans le phénotype des glioblastomes." Strasbourg, 2010. http://www.theses.fr/2010STRA6132.
Повний текст джерелаCaveolin-1 (cav1) plays a crucial role in cancer development and progression. Although caveolin-1 expression is increased in glioma, cav1 negative (cav1low) and positive (cav1high) cells coexist in glioblastoma (GBM). We reported that cav1low GBM cells display a more aggressive phenotype than cav1high GBM cells, suggesting that cav1 is a tumor suppressor in brain tumors. Transcriptomic analysis showed that cav1 represses α5β1 integrin so that cav1 and α5β1 integrin expressions were inversely correlated. We identified α5β1 integrin as the mediator of cav1’s effect in GBM. Moreover, cav1 affects the TGFβR/Smad2 pathway: silencing cav1 increased the secretion of TGF-β1, the expression of TGFβ receptor and the activity of its downstream effector Smad2. Conversely, forced expression of cav1 repressed the TGFβR/Smad2 pathway so that cav1 expression and TGFβR/Smad2 activity are inversely correlated. Using selective inhibitors, we showed that the TGFβR/Smad2 pathway was involved in the regulation of α5β1 integrin expression by cav1. Two Smad2-dependent signaling pathways were involved; one independent and one dependent of the TGFβRI. The reverse correlation between cav1 and α5β1/TGFβR/Smad2 was confirmed in different GBM cell lines. We showed that cav1low/α5β1/TGFβR/Smadhigh cells are highly sensitive to SB431542 (TGFβRI inhibitor) and K34c (selective antagonist of α5β1 integrin). Finally, subpopulations of patients suffering glioma were uncovered by performing the molecular profiling of the three interconnected genes in human biopsies. The status of cav1/α5β1/TGFβ/Smad2 might be a useful marker of the tumor behavior and a predictor of anti-TGFβR or anti-α5β1 integrin therapies
Labit-Bouvier, Corinne. "Marqueurs moléculaires diagnostiques et pronostiques des tumeurs neuroépithéliales." Aix-Marseille 2, 2003. http://www.theses.fr/2003AIX20691.
Повний текст джерелаTempé, Denis. "Régulation des protéines Gli, effecteurs transcriptionnels de la voie de signalisation Hedgehog, par le système Ubiquitine-Protéasome." Paris, Muséum national d'histoire naturelle, 2004. http://www.theses.fr/2004MNHN0009.
Повний текст джерелаIn vertebrates, Sonic hedgehog (Shh) morphogenetic activities are mediated by Gli transcription factors. My PhD work has focused on Gli3 and Gli1 regulation by the Ubiquitin-Proteasome pathway. Upon PKA phosphorylation, the deletion of Gli3 carboxyterminal transactivation domain generates transcriptional repressor. The SCF-type E3 Ubiquitin-ligase component ßTrCP is required for Gli3 proteolytic processing, binds to Gli3 and promotes its poly-ubiquitination. Gli1 binds ßTrCP and can be ubiquitinated, without any proteolytic processing. Shh and Gli1-dependant transactivation can be blocked by a Proteasome inhibitor as well as by downregulating ßTrCP expression by RNA interference. This work could establish that the SCFßTrCP complex participates in Shh signaling both in a negative and a positive manner. Further studies should unravel the unusual mechanisms likely involved in controlling Gli proteins by SCFßTrCP and PKA/GSK3ß activities
Merle, Patrick. "Etude de ligands de l'ADN G-quadruplexe télomérique dans le traitement du glioblastome et cancer bronchique : approches combinatoires." Thesis, Clermont-Ferrand 1, 2011. http://www.theses.fr/2011CLF1MM14.
Повний текст джерелаMontagne, Audrey. "Etude de l'expression d'une transposase domestiquée : SETMAR." Thesis, Tours, 2015. http://www.theses.fr/2015TOUR4017/document.
Повний текст джерелаSETMAR is a chimeric gene consisting of a SET domain (encoding methylase histone functions) and a MAR domain (having retained some of the of the HsMAR1 transposase functions). Studies have shown that the two domains are biologically active and are involved in the stability and / or in the regulation of the human genome expression. The literature suggests that SETMAR expression is higher in cancer cells than in normal cells. Our working hypothesis is that SETMAR protein is overexpressed in pathological conditions, allowing cells to overcome the cellular cycle checkpoints, helping to increase the genetic instability. Our goal is to study the regulation of the SETMAR expression and its involvement in oncogenesis, glial in particular
Tabouret, Emeline. "Glioblastome et angiogenèse : profils évolutifs, interaction avec l'invasivité et implications thérapeutiques." Thesis, Aix-Marseille, 2015. http://www.theses.fr/2015AIXM5012/document.
Повний текст джерелаGlioblastomas are the most frequent and aggressive primary brain tumors for adult. They are characterized by a high angiogenesis leading to the evaluation of the bevacizumab. Our aim was to identify potential predictive biomarkers of bevacizumab activity and to analyze the evolutive profile of the angiogenic factors during the disease. If no clinical factor allows the identification of patient subgroup benefiting of bevacizumab, MMP2 and MMP9 plasma level at baseline were correlated to response, progression-free survival and overall survival of patients with recurrent high grade glioma treated by bevacizumab. Moreover, plasma levels of these markers change during treatment and significantly varied at the time of progression. We observed similar results for patients with inflammatory breast cancer treated with neoadjuvant bevacizumab, reinforcing the potential value of these prebiomarkers. In tumor tissue, while we did not observed changes in MMP2/MMP9 expression between the initial diagnosis and the recurrence post radio-chemotherapy, we observed a modification of the expression of angiogenic factors with a potential switch from the VEGFR2-HIF1α to the CXCL12-CXCR4 pathway. These results lead to new perspectives in angiogenic modulation and glioblastoma treatment
Khalil, Najat. "L'activation des récepteurs activés par les proliférateurs de peroxysomes beta/delta, stimule l'expression de Siah-1L et entraîne la prolifération et la migration de cellules de glioblastomes." Thesis, Université de Lorraine, 2013. http://www.theses.fr/2013LORR0286/document.
Повний текст джерелаGlioblastoma represent the most frequent primary brain tumor in adults. We highlighted the role of PPARß/delta in glioblastoma tumorigenesis. We have shown that activation of this receptor stimulates proliferation and migration of glioblastoma cells T98G. We also showed that activation of PPARß/delta induces the expression of Siah-1L gene and that overexpression of Siah-1L stimulates cell proliferation and migration of glioblastoma cells. We also studied the regulation of Siah-1L gene and showed that its expression is induced by PPARß/delta. Cloning of Siah-1L gene promoter sequence and the study of its regulation showed that the induction of the expression of Siah-1L by PPARß/delta is mediated by a response element located at the promoter sequence
Ferrandon, Sylvain. "Évaluation du Statut télomérique : vers une thérapeutique personnalisée du glioblastome : application en Hadronthérapie par ions carbone." Thesis, Lyon 1, 2013. http://www.theses.fr/2013LYO10005.
Повний текст джерелаGlioblastoma, high grade tumor of neuroepithelial tissue, is poor prognosis cancer. Despite an invasive standard treatment (surgery, radiochemotherapy), the overall survival of patients does not exceed 15 months, largely due to aggressive recurrence (radioresistance of residual cells). Hadrontherapy with Carbon ion beam have strong radiobiological arguments: i) high ballistic precision (save healthy tissues), ii) Relative Biological Efficiency (RBE) above conventional radiotherapy (dose escalation), iii) independent response of oxygen enhancement ratio (hypoxic tumors). Hadrontherapy have shown promising preliminary results in treatment of brain tumors. However, the rareness of health centers which purposed Handrontheray necessitates the use of predictive markers of resistance to conventional radiotherapy to address bad responder patient. Telomere homeostasis is also known to modulate radiosensitivity of different types of cancer. Thus, this work has two arms. On the one hand, we have shown that telomere length and POT1 (Protection Of Telomere1) level (RNA and protein) can be used by clinicians to diagnose bad responder of standard treatment and towards the hadrontherapy. On the other hand, we have shown that pharmacological treatment inhibitory of telomerase (GRN163L, Geron Corp) can improve the radiationinduced responses to conventional radiotherapy on human glioblastoma mice model