Добірка наукової літератури з теми "Gliomes de haut grade"
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Статті в журналах з теми "Gliomes de haut grade":
Chatel, M., M. Frenay, C. Lebrun, V. Bourg, and F. Fauchon. "Gliomes de haut grade : astrocytomes anaplasiques et glioblastomes." EMC - Neurologie 2, no. 3 (January 2005): 1–15. http://dx.doi.org/10.1016/s0246-0378(05)09101-3.
Chatel, M., M. Frenay, C. Lebrun, V. Bourg, and F. Fauchon. "Gliomes de haut grade : astrocytomes anaplasiques et glioblastomes." EMC - Neurologie 2, no. 3 (August 2005): 257–78. http://dx.doi.org/10.1016/j.emcn.2004.12.002.
Bailleul, Quentin, Andria Rakotomalala, Isabelle Ferry, Pierre Leblond, Samuel Meignan, and Alessandro Furlan. "L’art de la guerre appliqué aux DIPG." médecine/sciences 37, no. 2 (February 2021): 159–66. http://dx.doi.org/10.1051/medsci/2020279.
Delmas, J. M., M. Lahutte, L. Dulou, A. Dagain, O. Goasguen, and R. Dulou. "Gliomes de haut grade du sujet âgé : place de la chirurgie." NPG Neurologie - Psychiatrie - Gériatrie 12, no. 68 (April 2012): 57–61. http://dx.doi.org/10.1016/j.npg.2011.12.002.
Tetard, M. C., M. Vermandel, S. Mordon, J. P. Lejeune, and N. Reyns. "Modulation de la lumière dans la PDT des gliomes de haut grade." Neurochirurgie 59, no. 6 (December 2013): 239. http://dx.doi.org/10.1016/j.neuchi.2013.10.047.
Clavier, J. B., J. Voirin, P. Kehrli, and G. Noël. "Radiothérapie en conditions stéréotaxiques des gliomes de haut grade : une revue de la littérature." Cancer/Radiothérapie 14, no. 8 (December 2010): 739–54. http://dx.doi.org/10.1016/j.canrad.2010.03.021.
Lafon, M., A. Huchet, C. Bronnimann, S. Adgie, M. Martin, R. Trouette, V. Jecko, T. Wavasseur, C. Dupin, and V. Vendrely. "Réirradiation des rechutes de gliomes de haut grade après un premier radiothérapie et témozolomide." Cancer/Radiothérapie 22, no. 6-7 (October 2018): 707. http://dx.doi.org/10.1016/j.canrad.2018.07.041.
Lubrano, V., E. Uro-Coste, P. Bousquet, C. Pierroux, M. B. Delisle, and J. Lagarrigue. "Étude histo-moléculaire de 26 gliomes de haut grade : impact sur la classification et le pronostic." Neurochirurgie 52, no. 5 (November 2006): 478. http://dx.doi.org/10.1016/s0028-3770(06)71277-2.
Lebrun-Frenay, C. "Le bévacizumab dans le traitement des gliomes de haut grade : une réponse et beaucoup de questions." Revue Neurologique 170, no. 4 (April 2014): 235–36. http://dx.doi.org/10.1016/j.neurol.2014.04.001.
Wachter, T., J. P. Pignol, B. Courtois, R. Sabattier, G. Blondiaux, and N. Breteau. "Neutrons rapides et potentialisation par capture de neutrons thermiques pour le traitement des gliomes de haut grade." Neurochirurgie 51, no. 1 (February 2005): 53. http://dx.doi.org/10.1016/s0028-3770(05)83432-0.
Дисертації з теми "Gliomes de haut grade":
Dumont-Girard, Philippe. "Chimiothérapies intra-veineuses des tumeurs astrocytaires de haut grade : revue de la littérature et évaluation d'un protocole associant fotémustine, platine et VP16." Montpellier 1, 1998. http://www.theses.fr/1998MON11064.
Laprie, Anne. "Imagerie métabolique par spectrométrie de résonnance magnétique des tumeurs gliales de haut-grade irradiées de l'adulte et de l'enfant." Toulouse 3, 2007. http://www.theses.fr/2007TOU30332.
Leventoux, Nicolas. "Etude des foyers d’hétérogénéité tumorale dans les gliomes diffus de bas grade de l’adulte mutés IDH1." Thesis, Montpellier, 2018. http://www.theses.fr/2018MONTT037.
Gliomas are the main primary brain tumours affecting around 4000 new patients in France each year. Half of gliomas are detected in the advanced stage of glioblastoma (grade IV) while 15% of tumours are diagnosed in stage II (diffuse low-grade gliomas-DLGG). These tumors affect young patients and bear characteristic mutations, including a mutation for the enzyme IDH1 commonly found in secondary glioblastomas. These low-grade tumours are treated by surgery, ideally in awake condition but due to their diffuse nature, the residual part will progress inexorably to stage III or IV with overall survival between 5 and 15 years after diagnosis. Tumor progression is highly variable and unpredictable from one patient to another. Foci of tumor progression have been identified in 20% of patients with DLGG. These foci show a higher cell density and an increased Ki67. My thesis work consisted in studying the cellular and molecular changes associated with tumor progression. From the RNA profile of the foci and adjacent territories, I was able to highlight through high-throughput techniques significant decrease in gene expression in the foci, particularly of AGXT2L1/ETNPPL, carboxypeptidase E, EDNRB, SFRP2. I hypothesized that SFRP2 and ETNPLL could oppose cell proliferation and that their decrease would pave the way for tumor transformation. An inverse correlation between the amount of ETNPPL and the survival of patients with hepatocarcinoma has been published. By limiting the amount of phospholipid precursors in the cell, ETNPPL could act as a brake against proliferation and indeed, its decrease in glioma transformation foci could remove this inhibition. My PhD work will have been innovative in the comparative approach of the different tumors’ compartments for each patient studied and will have revealed ETNPPL as correlated to gliomagenesis and as potential therapeutic target
Ngwabyt, Bikeye Sandra-Nadia. "Etude par ARN interférence de l’expression du gène ASPM dans les cellules souches tumorales des gliomes de haut grade." Thesis, Paris 11, 2011. http://www.theses.fr/2011PA11T030/document.
Glioblastoma (GBM) is the most frequent and aggressive form of primary brain tumors in adults; it is characterized by its resistance to current treatments (surgery, chemotherapy and radiotherapy). The prognosis is grim with a median survival of only 15 months underlining the importance to develop new therapeutic strategies. The recent development of the “tumor stem cell” (TSC) concept in hemopathies has been secondarily applied to gliomas with the identification of subpopulations of GBM cells which express neural stem cell markers and fulfill the criteria for stemness. Some evidences also suggest that this subpopulation could play a primary role in resistance to radio- and chemotherapy.ASPM (Abnormal Spindle Like Microcephaly Associated) is a protein regulating the proliferation of neuroblasts, highly expressed in the embryonic stage but weakly expressed in the adult brain. Preliminary reports suggesting that it could be involved in the development of gliomas (Horvath et al., 2007, Hagemann et al., 2008) prompted us to analyze further the role of this protein, focusing on its potential as a relevant candidate therapeutic target. In a series of 175 gliomas samples of various grades, we found that ASPM mRNA expression was strongly correlated with increasing tumor grade. We also found that ASPM expression increased at recurrence when compared to the initial lesion. Subsequently, we could demonstrate in vitro and in vivo that ASPM expression also increased over serial passages in gliomaspheres and in a mouse glioma xenograft model. In a therapeutic perspective, the effect of lentivirus-mediated shRNA post-transcriptional silencing of ASPM was evaluated in two different gliomasphere models and a dramatic proliferation arrest and cell death was observed. Taken together, these data suggest that ASPM is involved in the malignant progression of gliomas, possibly through expansion of a cancer stem cell compartment, and could be an attractive therapeutic target in glioblastoma multiforme.Another potential candidate tumor stem cell target in glioma is the sonic hedgehog pathway (hedgehog-Gli) which is required for GBM growth and stem cell expansion. In a collaborative study, it was found that NANOG, a transcription factor critically involved with self-renewal of undifferentiated embryonic stem cells, modulates gliomasphere clonogenicity, CD133+ stem cell behavior and proliferation. NANOG was regulated by hedgehog-Gli signalling and was essential for GBM tumourigenicity in orthotopic xenografts suggesting that it could also be a useful potential therapeutic target.Conclusions: Accumulating evidences suggest that tumor stem cells play an important role in the oncogenesis of gliomas and in their resistance to treatment. Our data support this concept and suggest that specific stemness markers may become useful targets to improve treatment of this devastating disease
Dembélé, Kléouforo-Paul. "Etude du rôle de protéines G dans les gliomes de haut grade : Implication dans la migration et le phénotype mésenchymateux." Thesis, Normandie, 2019. http://www.theses.fr/2019NORMR077.
GBM is the most common (∼45% of all gliomas) and aggressive primary malignant brain tumor in adults. As described in this document's introduction, GBM highly heterogeneous phonotype associated with molecular signatures and gene expressions, but also with hypoxic and inflammatory microenvironmental conditions, contribute to frequent recurrence after complete resection-radio/chemotherapy, and explain the multiple therapeutic failures. Most of the current treatment options for GBM, although sometimes multimodal, the survival of GBM patients is not significantly improved, and the challenges to improve patient survival and quality of life remain enormous. Thus, the identification of differentially expressed factors that could better define the biological behavior of GBM, would provide a basis for the development of novel therapies and may be more effective. One of the characteristics of GBMs is their highly migratory and invasive properties, relayed mainly by chemotactic factors belonging to the hypoxic and inflammatory tumor microenvironment. G-protein coupled receptors (GPCRs) and their ligands, particularly the chemokines GPCRs, overexpressed in GBMs and stimulating migration, invasion and neoangiogenesis, play a key role in the development of GBM and the acquisition of an aggressive phenotype. In this context, our team demonstrated that UT, the receptor of urotensin II (UII), a pro-angiogenic and pro-inflammatory chemokine, as well as the well-known chemokine system SDF-1/CXCR4 are systematically co-expressed in GBMs particularly in vascular and perinecrotic areas and their expression are correlated with grade. We also demonstrated in vitro that UII/UT stimulate GBM cells chemotactic migration and invasion via activation of the pathways Gαi/PI3K and Gα13/Rho/ROCK, pathways that have previously been identified for the SDF-1α/CXCR4 system and other chemotactic GPCRs. In addition, a recent principal component analysis of TCGA (The Cancer Genome Atlas) database performed by Alexandre Mutel, PhD student in the team, has identified the expression signature of GPCRs in gliomas and particularly those which are overexpressed in mesenchymal GBM, among which many chemotactic GPCRs are included. Taking together, their redundant expression and signaling activity frequently associated with tumorigenesis, particularly in GBMs, raises the issue of studying signaling nodes common to all these GPCRs. These nodes, are primarily represented by heterotrimeric G proteins, composed of α, β and γ subunits, that couple these GPCRs relaying many intracellular secondary effectors, probably essentials in the regulation of GBM aggressiveness. In this context, the aim of my thesis work was to identify the main Ga, b and g subunits among the 31 G proteins expressed in human gliomas and those more specifically associated with the malignant grade, and the aggressiveness of GBMs and then to determine the role of one of these specific G proteins in GBM cells proliferation and invasion mechanisms. For that, we first analyzed the expression of the 31 subunits (15α, 5β and 11γ) of G proteins from the TCGA database and showed that the mRNA expression of Gαz, Gαi1, Gβ4, Gβ5 et Gγ3 are relatively low in GBMs while Gα12, Gα13, Gα15, Gαi2, Gαi3, Gβ2, Gγ5, Gγ11 and Gγ12 subunits, are particularly overexpressed in GBM and are associated with a poor prognosis in terms of recurrence and patient survival
Duval, Frédéric. "Etude rétrospective à propos de 67 cas d'astrocytomes de haut grade (janvier 1993 - Avril 1995 ) : de l'épidémiologie à la thérapeutique." Bordeaux 2, 1996. http://www.theses.fr/1996BOR2M027.
Ngwabyt-Bikeye, Sandra Nadia. "Etude par arn interférence de l'expression du gène aspm dans les cellules souches tumorales des gliomes de haut grade." Phd thesis, Université Paris Sud - Paris XI, 2011. http://tel.archives-ouvertes.fr/tel-00633421.
Nguyen, Aurélia. "Mécanismes de résistance à la chimiothérapie dans les gliomes de haut grade de l’enfant : implications des systèmes de réparation de l’ADN et de l’hypoxie intra-tumorale." Thesis, Strasbourg, 2014. http://www.theses.fr/2014STRAJ086/document.
Pediatric malignant glioma (PMGs), are associated with a very dismal prognosis. They are distinct from their adult counterparts (AMGs), biologically but also clinically, with a lower response to temozolomide (the current reference alkylating chemotherapy) compared to AMGs. Temozolomide efficacy is reduced by the activity of the DNA repair enzyme, O6-methylguanine-DNA-methyltransferase (MGMT), whose expression is frequently silenced by promoter methylation. First, the development of a new methylation-specific PCR showed a lower frequency of MGMT methylation in PMGs (15%) vs AMGs (45%, p<0,001). Secondly, intra-tumor hypoxia and the upstream deregulation of mTOR-HIF-1α axis, well-known to be involved in chemo-resistance and the up-regulation of MGMT expression, were studied in a PMG cohort. The targeting of this axis was then studied in vitro using a therapy combining rapamycin and irinotecan. For this, pediatric patient-derived malignant glioma cell lines were developed
Perek-Courbon, Nathalie. "Etude des mécanismes cellulaires d'incorporation du Tc-99m-tetrofosmin dans un modèle de cellules tumorales gliales de haut grade : études comparatives avec le thallium 201 et le Tc-99m-setamibi." Saint-Etienne, 1999. http://www.theses.fr/1999STET003T.
Clement, Alexandra. "La caractérisation de la mutation IDH1R¹³²H dans un modèle de gliome humain de haut grade par imagerie multimodale, une étude translationnelle in vitro et in vivo." Thesis, Université de Lorraine, 2020. http://www.theses.fr/2020LORR0213.
The integration of molecular parameters in the classification of gliomas by the WHO in 2016, particularly IDH1R¹³²H mutational status, has significant diagnostic impact. This mutation is associated with a better prognosis but the physiopathological mechanisms underlying its expression remain poorly understood. Our work evaluates a multimodal imaging approach integrating multiparametric MRI and multiparametric multitracer PET to non-invasively characterize this mutation in gliomas. High grade human glioma cells (U87-MG) expressing or not the IDH1R¹³²H mutation (IDH1+ ; IDH1-), constructed using CRISP/Cas9 were studied in cell culture (in vitro), in a preclinical rat model after stereotactic grafting (in vivo) and after autopsy (ex vivo). In vitro, IDH1+ tumors expressed low levels of integrins αvβ3 and TSPO receptors which are considered to be biological markers of aggressiveness involving angiogenesis and tumor inflammation pathways. In vivo, MRIs (4.7T) of these IDH1+ tumors showed areas of high vascular densities which were characterized by functional neo-vascularizations, comparable to healthy cerebral vascular networks. Magnetic resonance spectra variations confirmed these results and revealed a less aggressive metabolite profile for these IDH1+ tumors. The combination of static and dynamic PET parameters with decreased uptake and a pronounced decrease in the PET slope of [⁶⁸Ga]NODAGA-(RGDyK)₂, as well as decreased PET uptake of [¹⁸F]DPA-714 in IDH1+ tumors, targeting αvβ3 integrins and TSPO receptors, yielded good diagnostic performances to discriminate the IDH1R¹³²H mutation. Ex vivo, spectroscopic analyses indicated less aggressive metabolic profile. This translational study demonstrates the benefits of multimodal and multiparametric imaging, and associates expression of the IDH1R¹³²H mutation, in high-grade human glioma cells with a less aggressive tumor profile. Validation of results from this pilot study in human primary cell cultures, may lead to a clinical multimodal imaging study to non-invasively characterize the IDH1R¹³²H mutation
Частини книг з теми "Gliomes de haut grade":
Cottier, J. P., M. Ribeiro, S. Chapet, C. Destrieux, X. Cazals, M. A. Lauvin, Y. Pointreau, and A. Raimbault. "Imagerie post-thérapeutique des gliomes de haut grade." In Imagerie Post-Thérapeutique en Oncologie, 1–20. Elsevier, 2014. http://dx.doi.org/10.1016/b978-2-294-73840-1.00001-0.
"Lymphomes non-Hodgkinien grade intermédiaire et haut grade (LNH B et T)." In Protocoles de traitement. Service d’hémato-oncologie HDQ-HDL 2020 (9e édition), 153–63. Presses de l'Université Laval, 2020. http://dx.doi.org/10.2307/j.ctv1h0p3z5.28.
Simon, Matthias, and Alexander Grote. "Glioneuronal and other epilepsy-associated tumours." In Oxford Textbook of Neurological Surgery, edited by Ramez W. Kirollos, Adel Helmy, Simon Thomson, and Peter J. A. Hutchinson, 129–40. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780198746706.003.0010.