Academic literature on the topic 'Gliomas'
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Journal articles on the topic "Gliomas"
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Soukup, Jiri, Lucie Gerykova, Anjali Rachelkar, et al. "Diagnostic Utility of Immunohistochemical Detection of MEOX2, SOX11, INSM1 and EGFR in Gliomas." Diagnostics 13, no. 15 (2023): 2546. http://dx.doi.org/10.3390/diagnostics13152546.
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Histological identification of dispersed glioma cells in small biopsies can be challenging, especially in tumours lacking the IDH1 R132H mutation or alterations in TP53. We postulated that immunohistochemical detection of proteins expressed preferentially in gliomas (EGFR, MEOX2, CD34) or during embryonal development (SOX11, INSM1) can be used to distinguish reactive gliosis from glioma. Tissue microarrays of 46 reactive glioses, 81 glioblastomas, 34 IDH1-mutant diffuse gliomas, and 23 gliomas of other types were analysed. Glial neoplasms were significantly more often (p < 0.001, χ2) positive for EGFR (34.1% vs. 0%), MEOX2 (49.3% vs. 2.3%), SOX11 (70.5% vs. 20.4%), and INSM1 (65.4% vs. 2.3%). In 94.3% (66/70) of the glioblastomas, the expression of at least two markers was observed, while no reactive gliosis showed coexpression of any of the proteins. Compared to IDH1-mutant tumours, glioblastomas showed significantly higher expression of EGFR, MEOX2, and CD34 and significantly lower positivity for SOX11. Non-diffuse gliomas were only rarely positive for any of the five markers tested. Our results indicate that immunohistochemical detection of EGFR, MEOX2, SOX11, and INSM1 can be useful for detection of glioblastoma cells in limited histological samples, especially when used in combination.
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Olaofe, O. O., B. A. Adewara, C. C. Okongwu, and E. E. Ewoye. "Case report: A case report of optic nerve glioma in a 5-year-old African girl." Research Journal of Health Sciences 12, no. 1 (2024): 82–87. http://dx.doi.org/10.4314/rejhs.v12i1.10.
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Background: Optic nerve gliomas are rare tumors that constitute less than 5% of all pediatric central nervous system tumors.
 Case Presentation: We present the case of a 5-year-old girl with complaints of progressive protrusion of the right eye and poor vision of 3 years duration who was referred to the ophthalmologist. Ophthalmological evaluation of the right eye revealed tearing, no perception of light, inferior dystopia, severe proptosis, and a firm non-tender orbital mass palpable posterior to the eyeball. The cranial CT-scan was suggestive of a right optic nerve glioma. Histology showed Optic Glioma with extensive proliferation of meningothelial cells.
 Conclusion: Optic gliomas can be associated with extensive proliferation of meningothelial cells that can histologically mimic a meningioma. It is important to be cautious about making a diagnosis of meningioma for tumors in locations that are also characteristic of optic nerve gliomas especially in appropriate clinical settings. 
 
 
 French title: Rapport de cas : Un rapport de cas de gliome du nerf optique chez une fillette africaine de 5 ans Titre en cours - Gliome optique chez une fillette africaineContexte de l'étude : Les gliomes du nerf optique sont des tumeurs rares qui constituent moins de 5 % de toutes les tumeurs pédiatriques du système nerveux central.
 Présentation de cas : Nous présentons le cas d'une fillette de 5 ans présentant des plaintes de protrusion progressive de l'œil droit et une mauvaise vision depuis 3 ans qui a été référée à l'ophtalmologiste. L'évaluation ophtalmologique de l'œil droit a révélé un larmoiement, une absence de perception de la lumière, une dystopie inférieure, une exophtalmie sévère et une masse orbitaire ferme et non douloureuse, palpable en arrière du globe oculaire. Le scanner crânien était évocateur d'un gliome du nerf optique droit. L'histologie montrait un gliome optique avec une prolifération étendue de cellules méningothéliales.
 Conclusion : Les gliomes optiques peuvent être associés à une prolifération étendue de cellules méningothéliales pouvant mimer histologiquement un méningiome. Il est important d'être prudent avant de poser un diagnostic de méningiome pour des tumeurs situées dans des localisations également caractéristiques des gliomes du nerf optique, en particulier dans des contextes cliniques appropriés.
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Hewer, Ekkehard, Jaison Phour, Marielena Gutt-Will, Philippe Schucht, Matthias S. Dettmer, and Erik Vassella. "TERT Promoter Mutation Analysis to Distinguish Glioma From Gliosis." Journal of Neuropathology & Experimental Neurology 79, no. 4 (2020): 430–36. http://dx.doi.org/10.1093/jnen/nlaa004.
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Abstract Among the most challenging diagnostic issues in surgical neuropathology is the distinction between scant infiltration by diffuse gliomas and reactive gliosis. The best documented ancillary marker to establish a definitive diagnosis of glioma in this setting is the identification of hotspot mutations in the isocitrate dehydrogenase 1 and 2 (IDH1/IDH2) genes, which is limited, however, by the low prevalence of these mutations in gliomas of elderly adults. Since telomerase reverse transcriptase (TERT) promoter mutations are present in the vast majority of IDH-wildtype diffuse gliomas, we hypothesized that combined analysis of IDH and TERT might overcome these limitations. For this purpose, we analyzed a series of non-neoplastic and neoplastic CNS samples for the prevalence of TERT hotspot mutations. TERT mutations were identified in none out of 58 (0%) reactive gliosis samples, and in 91 out of 117 (78%) IDH-wildtype gliomas. Based on a series of 200 consecutive diffuse gliomas, we found that IDH mutation analysis alone had a sensitivity of 28% (63% and 12%, respectively, in patients below and above age of 50) for detection of gliomas, whereas a combined analysis of IDH and TERT was 85% sensitive (87% and 84%, respectively, below and above age of 50). In sum, our findings suggest that TERT promoter mutation analysis contributes favorably to a molecular panel in cases equivocal for glioma versus gliosis on morphological grounds, especially in patients above age of 50, in which IDH analysis alone performs poorly.
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Park, Jong-Whi. "Metabolic Rewiring in Adult-Type Diffuse Gliomas." International Journal of Molecular Sciences 24, no. 8 (2023): 7348. http://dx.doi.org/10.3390/ijms24087348.
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Multiple metabolic pathways are utilized to maintain cellular homeostasis. Given the evidence that altered cell metabolism significantly contributes to glioma biology, the current research efforts aim to improve our understanding of metabolic rewiring between glioma’s complex genotype and tissue context. In addition, extensive molecular profiling has revealed activated oncogenes and inactivated tumor suppressors that directly or indirectly impact the cellular metabolism that is associated with the pathogenesis of gliomas. The mutation status of isocitrate dehydrogenases (IDHs) is one of the most important prognostic factors in adult-type diffuse gliomas. This review presents an overview of the metabolic alterations in IDH-mutant gliomas and IDH-wildtype glioblastoma (GBM). A particular focus is placed on targeting metabolic vulnerabilities to identify new therapeutic strategies for glioma.
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Xia, He-chun, Zhan-feng Niu, Hui Ma, et al. "Deregulated Expression of the Per1 and Per2 in Human Gliomas." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 37, no. 3 (2010): 365–70. http://dx.doi.org/10.1017/s031716710001026x.
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Background:Growing evidence shows that the deregulation of the circadian clock plays an important role in the development of malignant tumors, including gliomas. However, the molecular mechanisms of genes controlling circadian rhythm in glioma cells have not been explored.Methods:Using reverse transcription polymerase chain reaction and immunohistochemistry techniques, we examined the expression of two important clock genes, Per1 and Per2, in 33 gliomas.Results:In this study, out of 33 gliomas, 28 were Per1-positive, and 23 were Per2-positive. The expression levels of Per1 and Per2 in glioma cells were significantly different from the surrounding non-glioma cells (P<0.01). The difference in the expression rate of Per1 and Per2 in high-grade (grade III and IV) and low-grade (grade 1 and II) gliomas was insignificant (P>0.05). While there was no difference in the intensity of immunoactivity for Per2 between high-grade gliomas and low-grade gliomas (r=-0.330, P=0.061), the expression level of Per1 in highgrade gliomas was significantly lower than that in low-grade gliomas(r=-0.433, P=0.012).Conclusions:In this study, we found that the expression of Per1 and Per2 in glioma cells was much lower than in the surrounding non-glioma cells. Therefore, we suggest that disturbances in Per1 and Per2 expression may result in the disruption of the control of normal circadian rhythm, thus benefiting the survival of glioma cells. Differential expression of circadian clock genes in glioma and non-glioma cells may provide a molecular basis for the chemotherapy of gliomas.
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Sánchez, Manuel Lisardo, Arturo Mangas, and Rafael Coveñas. "Glioma and Peptidergic Systems: Oncogenic and Anticancer Peptides." International Journal of Molecular Sciences 25, no. 14 (2024): 7990. http://dx.doi.org/10.3390/ijms25147990.
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Glioma cells overexpress different peptide receptors that are useful for research, diagnosis, management, and treatment of the disease. Oncogenic peptides favor the proliferation, migration, and invasion of glioma cells, as well as angiogenesis, whereas anticancer peptides exert antiproliferative, antimigration, and anti-angiogenic effects against gliomas. Other peptides exert a dual effect on gliomas, that is, both proliferative and antiproliferative actions. Peptidergic systems are therapeutic targets, as peptide receptor antagonists/peptides or peptide receptor agonists can be administered to treat gliomas. Other anticancer strategies exerting beneficial effects against gliomas are discussed herein, and future research lines to be developed for gliomas are also suggested. Despite the large amount of data supporting the involvement of peptides in glioma progression, no anticancer drugs targeting peptidergic systems are currently available in clinical practice to treat gliomas.
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Kim, Junhyung, Min Woo Park, Young Joon Park, et al. "miR-542-3p Contributes to the HK2-Mediated High Glycolytic Phenotype in Human Glioma Cells." Genes 12, no. 5 (2021): 633. http://dx.doi.org/10.3390/genes12050633.
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(1) Background: The elevation of glucose metabolism is linked to high-grade gliomas such as glioblastoma multiforme (GBM). The high glycolytic phenotype is associated with cellular proliferation and resistance to treatment with chemotherapeutic agents in GBM. MicroRNA-542-3p (miR-542-3p) has been implicated in several tumors including gliomas. However, the role of miR-542-3p in glucose metabolism in human gliomas remains unclear; (2) Methods: We measured the levels of cellular proliferation in human glioma cells. We measured the glycolytic activity in miR-542-3p knockdown and over-expressed human glioma cells. We measured the levels of miR-542-3p and HK2 in glioma tissues from patients with low- and high-grade gliomas using imaging analysis; (3) Results: We show that knockdown of miR-542-3p significantly suppressed cellular proliferation in human glioma cells. Knockdown of miR-542-3p suppressed HK2-induced glycolytic activity in human glioma cells. Consistently, over-expression of miR-542-3p increased HK2-induced glycolytic activity in human glioma cells. The levels of miR-542-3p and HK2 were significantly elevated in glioma tissues of patients with high-grade gliomas relative to that in low-grade gliomas. The elevation of HK2 levels in patients with high-grade gliomas were positively correlated with the high levels of miR-542-3p in GBM and low-grade gliomas (LGG) based on the datasets from the Cancer Genome Atlas (TCGA) database. Moreover, the high levels of miR-542-3p were associated with poor survival rate in the TCGA database; (4) Conclusions: miR-542-3p contributes to the HK2-mediated high glycolytic phenotype in human glioma cells.
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Kim, Junhyung, Min Woo Park, Ju Won Ahn, et al. "TAMI-47. MIR-542-3P CONTRIBUTES TO THE HK2-MEDIATED HIGH GLYCOLYTIC PHENOTYPE IN HUMAN GLIOMA CELLS." Neuro-Oncology 23, Supplement_6 (2021): vi208. http://dx.doi.org/10.1093/neuonc/noab196.830.
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Abstract BACKGROUND The elevation of glucose metabolism is linked to high-grade gliomas such as glioblastoma multiforme (GBM). The high glycolytic phenotype is associated with cellular proliferation and resistance to treatment with chemotherapeutic agents in GBM. MicroRNA-542-3p (miR-542-3p) has been implicated in several tumors including gliomas. However, the role of miR-542-3p in glucose metabolism in human gliomas remains unclear. METHODS We measured the levels of cellular proliferation in human glioma cells. We measured the glycolytic activity in miR-542-3p knockdown and over-expressed human glioma cells. We measured the levels of miR-542-3p and HK2 in glioma tissues from patients with low- and high-grade gliomas using imaging analysis. RESULTS We show that knockdown of miR-542-3p significantly suppressed cellular proliferation in human glioma cells. Knockdown of miR-542-3p suppressed HK2-induced glycolytic activity in human glioma cells. Consistently, over-expression of miR-542-3p increased HK2-induced glycolytic activity in human glioma cells. The levels of miR-542-3p and HK2 were significantly elevated in glioma tissues of patients with high-grade gliomas relative to that in low-grade gliomas. The elevation of HK2 levels in patients with high-grade gliomas were positively correlated with the high levels of miR-542-3p in GBM and low-grade gliomas (LGG) based on the datasets from the Cancer Genome Atlas (TCGA) database. Moreover, the high levels of miR-542-3p were associated with poor survival rate in the TCGA database. CONCLUSIONS miR-542-3p contributes to the HK2-mediated high glycolytic phenotype in human glioma cells.
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Amin, Samirkumar, Kevin Anderson, Beth Bourdreau, et al. "GENE-57. COMPARATIVE MOLECULAR LIFE HISTORY OF SPONTANEOUS CANINE AND HUMAN GLIOMA." Neuro-Oncology 21, Supplement_6 (2019): vi110. http://dx.doi.org/10.1093/neuonc/noz175.459.
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Abstract Diffuse gliomas are the commonest of malignant brain tumors with high-grade tumors carrying dismal prognosis. Preclinical models have proven themselves as poor predictors of clinical efficacy, attributed to the lack of a comparable tumor microenvironment. Comparative genomics of canine and human gliomas provide an attractive alternative modality to identify conserved drivers and underlying mutational processes of glioma as well as evaluate life history tradeoffs related to tissue context and aging that can shape type and relative timing of drivers in gliomagenesis. We performed a comparative genomics analysis between whole genome-, exome-, transcriptome- and methylation-sequencing of 77 canine gliomas, and human pediatric (n=217) and adult gliomas (n=822). We found alterations in common with those in human pediatric and adult gliomas in the Tp53 and cell cycle pathways, receptor tyrosine kinase and Idh1 R132 mutations. Canine gliomas showed similarity to human pediatric gliomas in terms of lower mutational rates (0.2–0.29 per megabase), hotspot mutations and amplifications of Pdgfrα, and robust aneuploidy constrained within the syntenic regions of Pdgfrα and Myc, but also in the known pediatric drivers, Hist1 and Acvr1 genes. A mutational signature reflecting homologous repair defect was detected in canine and pediatric but not adult gliomas, potentially resulting in the observed higher rates of genomic instability. Canine gliomas in majority classified as pediatric tumors using a commonly used human brain methylation classifier (Capper et al. 2018) and cell-of-origin analysis by deconvoluting canine transcriptome using lineage-specific gene signatures. By providing a large canine glioma genomic-sequencing dataset and comparing it with human glioma, our study provides unique insights into glioma etiology and the chronology of glioma-causing somatic alterations. Further, our results effectively position preclinical models of spontaneous canine glioma for use in understanding glioma drivers, and evaluate novel therapies targeting aneuploidy, especially for pediatric brain tumors.
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Wirth, Thomas, Farizan Ahmad, Agnieszka Pacholska, Haritha Samaranayake, and Seppo Ylä-Herttuala. "The Syngeneic BT4C Rat Malignant Glioma is a Valuable Model to study Myelomonocytic cells in Tumors." Cancer Growth and Metastasis 5 (January 2012): CGM.S9314. http://dx.doi.org/10.4137/cgm.s9314.
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Background The impact of infiltrating macrophages on tumor progression in malignant gliomas has been studied extensively. However, there is a lack of animal models for studying the role of infiltrating macrophages in malignant gliomas. Material and methods: The BT4C rat malignant glioma model was characterized by immunohistochemical analysis of inflammatory cell types associated with the tumors. Results BT4C malignant gliomas are highly vascularized tumors with an infiltrative behavior. BT4C gliomas demonstrated a high infiltration rate of macrophages. Particularly, a CD68/VEGFR-1 positive subtype of macrophages was detected at the edges of malignant gliomas. Also, CD133 positive cells were located mainly at the infiltrative edges of gliomas, whereas VEGFR-2 was highly expressed throughout the malignant glioma. Conclusion The immunocompetent BT4C rat malignant glioma model shows features similar to its human counterpart, which makes it a valuable model to study the impact of tumor associated macrophages in the pathology of malignant gliomas.
Dissertations / Theses on the topic "Gliomas"
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Lilja, Åsa. "Psychoneurooncology psychological dynamics in glioma patients /." Lund : Dept. of Psychology, Lund University, 1992. http://books.google.com/books?id=SnZrAAAAMAAJ.
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Sadeghi-Meibodi, Niloufar. "Image-based biomarkers for the invivo evaluation of human brain gliomas." Doctoral thesis, Universite Libre de Bruxelles, 2010. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/209991.
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Gliomas constitute 36% of all primary brain tumors and 81% of all primary malignant brain tumors. The overall prognosis in patients with gliomas depends mainly on the location and histologic grade of the tumor.<p>The World Health Organization classification of gliomas is the primary basis for guiding therapy and assessing overall prognosis in gliomas. This classification system, based on histological features, often falls short of predicting therapeutic response of individual tumors within the same histological grade. Yet, it still remains the grading method for both research and clinical prospects.<p>Unlike any other organ the brain has multiple protective layers such as the skull that ensure a homeostatic environment. The resulting reduced access to the brain and the absence of plasmatic brain tumor markers bring neuroimaging in a central position in diagnosis and management of brain tumors. Moreover, neuroimaging has evolved from a purely morphologic investigation into a diagnostic tool that allows characterization of particular physical alterations within brain tissue. Understanding the relationship between the physical characteristics of tumor tissue, studied by MR imaging, and biological characteristics of the tumor is therefore important for the appropriate integration of neuroimaging in brain tumor management. The general objective of this work is to define the relationship between physiologybased MR imaging and biological features of glial tumors. Diffusion and perfusionweighted imaging, physiologybased MR techniques provide the data based on physical characteristics of the tissues. Diffusion weighted imaging (DWI) allows the measurement of water molecules diffusivity within the brain tissue by means of apparent diffusion coefficient (ADC) measurements. Perfusion weighted imaging (PWI) is based on changes of MR signal during the passage of contrast material through the intravascular space and allows hemodynamic measurements such as those of cerebral blood volume (CBV)within the brain tissue.<p>Highgrade diffuse gliomas are currently differentiated from low grade diffuse gliomas by increased cellularity with nuclear atypia, mitotic activity, endothelial proliferation and necrosis. Components of the extracellular matrix and angiogenesis constitute some other features of gliomas, which have established links with oncogenic processes that influence the proliferative and infiltrative potentials of these tumors. We have specifically targeted these features in our comparative studies with the working hypothesis that physiologybased MR measurements, obtained in vivo, might provide information that is pertinent in terms of tumor malignancy.<p>We chose to approach the biology of brain tumors in two ways: in vivo, by means of metabolic imaging techniques such as positron emission tomography (PET) and ex vivo, by means of histological and immunohistochemical analyses of tumor specimens.<p>Many studies have investigated the relation between ADC values and cellularity in gliomas. The underlining theory is based on the premise that water diffusivity within the 9 extracellular compartment is inversely related to the content and attenuation of the constituents of the intracellular space. Therefore when cellularity increases, intracellular space volume increases with a relative reduction of the extracellular space, leading to restricted diffusion of water molecules. However other factors may affect the value of ADC in gliomas such as the extracellular matrix which contains various amounts of hydrophilic macromolecules susceptible to change water molecules diffusivity. Hyaluronic acid is one highly hydrophilic component of the extracellular matrix of gliomas and its level of expression changes significantly during the progression to anaplasia in gliomas. Our hypothesis was that hyaluronan may influence ADC values in high and low grade gliomas.<p>We demonstrated a positive correlation between ADC values and the immunohistochemical level of hyaluronan in glial tumors.<p>Previous studies have confirmed the utility of positron emission tomography using C11 Methionine (PETMET) as a prognostic tool in patients with gliomas. Higher MET uptake is associated with greater proliferative potential and a higher level of malignancy in gliomas.<p>The increased aminoacid uptake in gliomas seems to reflect increased transport mediated by aminoacid carriers located in the endothelial cell membrane. Our hypothesis was that CBV measurements, index of tumor vascularity, may be related to tumor aminoacid metabolism.<p>We found a positive correlation between maximum CBV values and maximum MET uptake values in gliomas.<p>A limitation to these preliminary studies was lack of direct correlation between MRbased measurements and histologic and metabolic data. Indeed, glial tumors are known for their remarkable tissue heterogeneity across different grades, within the same grade, and even within a single given tumor. Therefore we used image coregistration and stereotactic biopsies to further assess the relationship between MRbased imaging data and both metabolic and histologic analysis.<p>The second part of our studies was based on measurements at the exact same localization on both MR and PET images where biopsy specimens were performed. We found a local relationship between CBV and MET uptake values. Both measurements correlated with mitotic activity and endothelial proliferation; two features of tumor aggressiveness.<p>In order to quantify tumor cellularity and tumor angiogenesis, we respectively measured cell density and vessel density using immunohistochemical markers to identify vessels. We found a regional relationship between CBV and cell density, as well as vessel density in gliomas whereas no correlation was found regionally between ADC and cell density.<p>We concluded that CBV measurements may be used locally as indices of angiogenesis and cellularity in gliomas; whereas local ADC measurements are more variable and may not be used as a marker of cellularity in heterogeneous tumors such as gliomas.<br>Doctorat en Sciences médicales<br>info:eu-repo/semantics/nonPublished
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Nanda, Dharminderkoemar. "Gene therapy for gliomas." [S.l.] : Rotterdam : [The Author] ; Erasmus University [Host], 2008. http://hdl.handle.net/1765/13140.
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Noreen, Razia. "FTIR imaging of collagens in gliomas." Thesis, Bordeaux 1, 2011. http://www.theses.fr/2011BOR14316/document.
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Le gliome est le type le plus agressif et mortel de tumeur cérébrale. Ces tumeurs se caractérisent par la présence conjointe de phénotypes solides (de bas grade, moins invasif, hautement vascularisé) et diffus (haut grade, très envahissant et diffus) des glioblastomes multiformes. Les collagènes sont des composants majeurs de la MEC des cellules tumorales des gliomes, et sont également présents dans la membrane basale des vaisseaux sanguins, mais avec une composition différente entre vasculatures saine et tumorale. L'abondance et la typologie des collagènes dans la MEC des cellules tumorales et la vasculature représentent donc un marqueur potentiel de diagnostic pour la gradation des tumeurs gliales. Nous avons développé la spectro-imagerie infrarouge à transformée de Fourier pour déterminer les modifications morphologiques et moléculaires apparaissant dans les formes solides et diffuses de gliomes, ainsi que dans les vasculatures saine et tumorale. Nous avons d'abord mis en évidence les vasculatures saine et tumorale en utilisant des nanoparticules injectées dans le système sanguin. Ensuite, nous avons appliqué des méthodes de reconstruction spectrale pour distinguer les tissus sains vs. ceux des formes solide et diffuse de tumeurs sur la base de leurs contenus en collagène de la MEC. Enfin, nous avons déterminé les changements de types du collagène au cours de la progression tumorale, validant ainsi la notion que l’analyse de ces contenus est potentiellement un marqueur diagnostic pour la gradation des gliomes<br>The glioma is the most aggressive and lethal type of brain tumor. Such tumor is characterized both by solid (low grade, less invasive, highly vascularized) and diffuse (high grade, very invasive and diffuse) phenotypes in high-grades. Collagens are major components of ECM in glioma tumor cells, and are also present in basement membrane of blood vessels in vasculature, but with different composition between healthy and tumor capillaries. The abundance and typology of collagens in tumor cell ECM and vasculature is thus a potential diagnostic marker for grading glioma tumors. We developed Fourier transform infrared (FTIR) spectro-imaging as a functional technique to determine the morphological and molecular changes occurring in solid and diffuse form of tumor tissues as well as in healthy and tumor vasculatures. We first highlighted healthy and tumor vasculatures using nanoparticles injected in blood system. Then, we applied curve-fitting methods to distinguish between healthy tissue vs. solid and diffuse tumor tissues on the basis of the collagen contents found in ECM. Finally, we determined collagen typology changes during tumor progression, thus validating that collagen contents analysis is potentially a diagnostic marker for glioma grading
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Alentorn, Agusti. "Caractérisation génomique et génétique des gliomes diffus de bas grade de l’adulte." Thesis, Paris 11, 2014. http://www.theses.fr/2014PA11T011.
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La caractérisation moléculaire multidimensionnelle des tumeurs et des tumeurs gliales en particulier est une étape importante pour l’identification de biomarqueurs (diagnostique, pronostique, théranostique et/ou de prédisposition), pour l’identification de cibles thérapeutiques et pour une meilleure compréhension de l’oncogénèse moléculaire.Nos travaux ont permis de confirmer et de consolider certaines données de la littérature comme par exemple : (i) la valeur pronostique favorable de la codélétion 1p/19q, (ii) la valeur pronostique favorable de la mutation IDH, (iii) le caractère mutuellement exclusive des mutations TP53 et de la codélétion 1p/19q et (iv) la rareté des altérations génétiques du PDGFRA dans les gliomes de bas grade (GDBG). De manière plus originale, nous avons identifié plusieurs sous-groupes génomiques de GDBG pertinents sur le plan clinico-biologique, notamment au sein des GDBG non 1p/19q codélétés : (i) 19q-délété ; (ii) 11p-délété, (iii) 7-gagné, (iv) 19-gagné et (v) inclassés. La perte du bras chromosomique 19q annule la valeur pronostique favorable de la mutation IDH dans les GDBG non 1p/19q codélétés. Nous avons également identifié des mutations géniques originales dans les GDBG (i.e. mutation TEP1 et RNF40) qui renforcent le rôle des télomères et du remodelage de la chromatine au sein des GDBG.Enfin, nous nous sommes concentrés sur la caractérisation des GDBG 11p-délétés qui sont de phénotype majoritairement astrocytaire et de moins bon pronostic. Ces GDBG surexpriment des gènes des cellules immunitaires (les GIM -Glioma infiltrating microglia-, les macrophages de type 1, les macrophages de type 2) et sont infiltrés par des cellules macrophagiques et microgliales. Ce microenvironnement dérégulé peut constituer une cible thérapeutique au sein des GDBG 11p-délétés. En conclusion, nos travaux participent à la dissection clinico-moléculaire des GDBG et à préciser la biologie d’un sous-type de GDBG caractérisé la perte du bras chromosomique 11p<br>Multildimensional molecular characterization of tumors and more specifically of gliomas is of pivotal importance to identify: (i) new biomarkers (i.e. diagnostic, prognostic, theranostic or predisposing), (ii) new therapeutic targets and (iii) to improve our understanding of molecular oncogenesis.Our work has confirmed and consolidated previous data published in the literature, for example that: (i) 1p/19q co-deletion is associated with better prognosis, (ii) IDH mutation is associated with better prognosis, (iii) TP53 mutations and 1p/19q codeletion are mutually exclusive and (iv) PDGFRA is rarely altered, at genomic level, in low-grade gliomas (LGG).More originally, we have identified several genomic groups, with clinical and biological relevances, in LGG and more specifically in LGG without 1p/19q co-deletion: (i) 19q-deleted, (ii) 11p-deleted, (iii) 7-gained, (iv) 19-gained and (v) unclassified. Interestingly, 19q deletion abrogates the positive prognostic value of IDH mutation in LGG without 1p/19q codeletion.We have also identified new recurrent somatic gene mutations in LGG (i.e. TEP1 and RNF40 mutations), supporting the critical role of telomeres and chromatin remodelling in LGG.Finally, we have characterized further 11p-deleted LGG that exhibit mostly astrocytic phenotype and poor prognosis. This subgroup includes LGG overexpressing genes of inflammatory/immune cells (GIM -Glioma infiltrating microglia-, M1 macrophages and M2 macrophages) and infiltrated by macrophagic/microglial cells. This peculiar microenvironment detected in 11p-deleted LGG might be used as a therapeutic target. In conclusion, our work participates to characterize clinico-biological portrait of LGG and to describe a singular genomic subgroup of LGG characterized by 11p loss
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Fu, Peng. "Membrane Hsp70 expression in gliomas." Diss., lmu, 2012. http://nbn-resolving.de/urn:nbn:de:bvb:19-149571.
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Horst, Maarten ter. "Gene therapy of malignant gliomas." [S.l.] : Rotterdam : [The Author] ; Erasmus University [Host], 2008. http://hdl.handle.net/1765/10864.
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Lau, Cara Jean. "Gene therapy for malignant gliomas." Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=18478.
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Gliomas are the most common primary brain tumours found in adults. The median survival of patients diagnosed with the most malignant form, glioblastoma multiforme (GBM), is 9-12 months and has changed little over the years despite advances in medical technology. Gene therapy may offer new solutions to treat this resistant disease. Hence, we tested three different gene therapy strategies. In our first study, we tested the efficacy of targeted therapy to correct common aberrations found in gliomas including amplification/mutation of receptor tyrosine kinases (RTK) and loss of PTEN, which result in an overactive PI3K/Akt pathway. Without PTEN, FOXO transcription factors are inactivated, and the cell becomes resistant to apoptosis and cell cycle arrest. By using an adenoviral vector (AdV) expressing an activated FOXO1 mutant (AdFOXO1;AAA), we restored apoptosis and cell cycle arrest, reduced tumour volume and prolonged survival in an intracerebral xenograft model. Secondly, we examined the therapeutic capacity of a novel replicating/non-disseminating AdV expressing the fusion protein of cytosine deaminase and uracil phosphoribosyltransferase (CU). CU can convert the non-toxic pro-drug, 5-fluorocytosine (5-FC) to the tissue diffusible chemotherapeutic drug, 5-fluorouracil (5-FU) to target dividing cells. In vitro, the replicating vectors were superior to the non-replicating vectors, but the fully replicating/disseminating vector did not perform considerably better than the replicating/non-disseminating vector suggesting that dissemination may not be advantageous. In vivo, the replicating/non-disseminating vector administered in conjunction with 5-FC prolonged survival in both an athymic and an immunocompetent mouse model. Moreover, an immune bystander effect in vivo was mediated by macrophages and T cells. Lastly, we investigated a method to harness a tool of the immune system, IFN-ß; this cytokine is known to have anti-angiogenic, anti-proliferative, and immunomo<br>Les gliomes sont des tumeurs primaires de cerveau les plus communes retrouvées dans les adultes. La survie médiane des patients diagnostiqués avec la forme la plus maligne, le glioblastome multiforme (GBM), est de 9 à 12 mois et a peu changé au cours des années en dépit des avances en technologie médicale. La thérapie génique peut offrir de nouvelles solutions pour traiter cette maladie résistante. Durant nos travaux, nous avons examiné trois stratégies différentes de thérapie génique Dans notre première étude, nous avons examiné l'efficacité de la thérapie visée à corriger des anomalies communes retrouvées dans les gliomes, comprenant l'amplification/mutation de récepteurs de type tyrosine kinase (RTK) et la perte de PTEN, qui mènent en conséquence à une voie activée de PI3K/Akt. Sans PTEN, les facteurs de transcription FOXO sont inactivés, et la cellule devient résistante à l'arrêt du cycle cellulaire et à l'apoptose. En utilisant un vecteur adénoviral (AdV) exprimant une protéine activée du mutant FOXO1 (AdFOXO1;AAA.), nous avons reconstitué les signaux pour l'arrêt du cycle cellulaire et l'apoptose in vitro ainsi que in vivo. Deuxièmement, nous avons examiné la capacité thérapeutique d'un nouveau vecteur adénovirale qui a la capacité de se répliquer sans provoquer de lyse cellulaire et qui exprime en plus la protéine de fusion uracile phosphoribosyltransférase/cytosine déaminase (CU). La protéine CU peut convertir le promédicament non-toxique, le 5-fluorocytosine (5-FC) à la drogue chimiothérapeutique diffusible, le 5-fluorouracile (5-FU) qui a comme cible des cellules en division cellulaire. In vitro, les vecteurs à capacité de répliquation étaient meilleurs que ceux qui ne pouvaient pas se répliquer. In vivo, le vecteur en présence du 5-FC a prolongé la survie de deux modès animaux (avec et sans sytèmes immunitaires). Dans un dernier temps, nous avons étudié une méthode pour exprimer l'IF
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Bergthold, Guillaume. "Genomic Profiling of Pediatric Low-Grade Gliomas." Thesis, Paris 11, 2015. http://www.theses.fr/2015PA11T053/document.
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Les gliomes de bas-grade représentent la tumeur cérébrale la plus fréquente chez l’enfant. Elles sont caractérisées par un large spectre de sous-types tumoraux, très hétérogènes. Leur définition actuelle est principalement basée sur des critères histologiques ce qui représente une limite importante car ces classifications souffrent d’un manque de précision. Les progrès récents de la génomique nous permettent d’approfondir considérablement les connaissances sur la biologie de ces tumeurs afin d’enrichir leur classification actuelle. Ce travail présente une analyse approfondie des altérations génomiques de l’ADN et l’ARN des gliomes de bas-grade pédiatriques. Le premier niveau d’analyse se base sur l’analyse du séquençage à haut débit de 169 gliomes de bas-grade de l’enfant. Bien que les mutations des gènes BRAF et FGFR1 sont les plus fréquemment décrites dans ces tumeurs, nous avons identifié pour la première fois le réarrangement chromosomique MYB-QKI majoritairement associé aux gliomes angiocentriques. Dans un deuxième temps ce travail décrit l’analyse du transcriptome de 151 gliomes de bas grade extraits à partir de tissu conservé en paraffine. Nous avons observé des différences moléculaires en fonction de leur sous-type histologique, de la localisation tumorale et de leur statut BRAF. Dans le dernier volet de ce travail, nous avons testé la faisabilité d’isoler par cytométrie en flux une cellule unique en les distinguant selon un marqueur de différenciation glial (A2B5+ et A2B5-) et d’effectuer une analyse transcriptomique à haut-débit en séquençant l’ARN à l’échelle d’une cellule unique. Cette technique nous a permis de décrire des différences moléculaires intéressantes entre des cellules A2B5+ et A2B5-. Ces résultats soulignent l’intérêt d’exploiter des nouvelles technologies de pointe pour servir de base à l’étude des caractéristiques biologiques des cellules tumorales<br>Low-grade gliomas represent the most frequent brain tumor arising during childhood. They are characterized by a broad spectrum of tumor types.The definition of low-grade gliomas has been mainly based on morphology. This histological classification of pediatric low-grade gliomas (PLGG), suffers from the lack of reproducibility. The recent progress in molecular biology and genetics has brought new insights in the biology of those tumors and allows better understanding of their biology. This work provides a comprehensive analysis of two different genetic approaches in PLGGs. The first part is based on the description of somatic genetic alterations of the DNA. Using a large PLGG cohort, we have dissect the genome of those tumors and draw the landscape of their genetic alteration. Although BRAF and FGFR1 alterations are predominantly altered, we have discovered a new translocation, MYB-QKI, that is almost exclusively present in a specific histological subgroup; angiocentric gliomasThe second part of the thesis describes transcriptomic analysis of bulk PLGGs. This work describes molecular differences between PLGGs from distinct histologies and arising from different locations in the brain as well as different BRAF mutation status.We were also able to test single-cell expression analyses in three pilocytic astrocytomas (PAs) using RNA-sequencing. In this experimental work we have successfully tested the hypothesis that we can isolate single-cells from fresh PLGG tumors in order to analyze the trasncriptome at a large scale. We observed that single-cells expressing A2B5, a glial progenitor marker, isolated in pediatric PAs are characterized as a distinct biological population. These results underline the importance to improve the precision of the transcriptomic studies to capture the molecular signal of tumor cells and further understand the different pattern between normal cells and tumor cells
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Gulati, Sasha. "Surgical Resection of High-Grade Gliomas." Doctoral thesis, Norges teknisk-naturvitenskapelige universitet, Institutt for laboratoriemedisin, barne- og kvinnesykdommer, 2012. http://urn.kb.se/resolve?urn=urn:nbn:no:ntnu:diva-16444.
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Reseksjon av høygradige gliomer Høygradige gliomer er den vanligste formen for primær hjernesvulst. Glioblastomer (Verdens Helseorganisasjon grad IV) og anaplastiske astrocytomer (Verdens Helseorganisasjon grad III) utgjør mellom 70 og 85 % av høygradige gliomer. Høygradige gliomer er assosiert med både høy morbiditet og mortalitet. Nærmest alle pasienter med høygradige gliomer opplever tilbakefall og dør som følge av sykdommen. Til tross for kirurgi, strålebehandling og cellegift, er median overlevelse for pasienter med glioblastom fremdeles under 12 måneder. For pasienter med anaplastisk astrocytom er median overlevelse 2 til 3 år. Høygradige gliomer infiltrerer omkringliggende hjernevev, og hensikten med kirurgi er, foruten å histopatologisk verifisere diagnosen, å fjerne så mye av svulsten som mulig uten å påføre pasienten nye eller økte nevrologiske utfall. I vår avdeling benytter vi et navigasjonssystem under operasjonene som nyttiggjør tredimensjonale preoperative MR-bilder og tredimensjonal ultralydavbildning under operasjonen. Dette navigasjonssystemet gjør at kirurgen til en hver tid kan se posisjonen til sine instrumenter i forhold til hjernen og svulsten. Ved hjelp av funksjonell MR (eller mer presist blood-oxygenation-level-dependent functional magnetic resonance imaging) og diffusjon tensor traktografi (DTT) kan en henholdsvis kartlegge viktige områder i hjernens grå og hvite substans før operasjonen. Disse undersøkelsene utføres som regel når svulster ligger i nær relasjon til ekstra følsomme områder av hjernen (for eksempel språkområder og viktige områder for bevegelse). Informasjon fra disse undersøkelsene kan også importeres i navigasjonssystemet som benyttes under operasjonen. I de to første studiene i denne avhandlingen ønsket vi å undersøke hvordan funksjonell MR og DTT ble brukt i preoperative vurderinger. Vi evaluerte om funksjonell MR og DTT i kombinasjon med tredimensjonal ultralydavbildning under operasjonen la forholdene til rette for skånsom fjerning av høygradige gliomer beliggende i ekstra følsomme områder av hjernen. I den tredje studien undersøkte vi konsekvensene av kirurgiske komplikasjoner og nevrologiske utfall som følge av kirurgi på glioblastompasienters funksjonsnivå og overlevelse. Videre gjorde vi volumetriske analyser for å beregne hvor mye svulstvev vi klarte å fjerne hos pasienter med primære glioblastomer behandlet i vår avdeling. I den fjerde studien undersøkte vi om det var noen sammenheng mellom overlevelse og fall i selvrapportert livskvalitet kort tid etter kirurgi hos pasienter med glioblastomer. Den femte studien var basert på data fra Kreftregisteret og undersøkte overlevelse og behandling blant eldre pasienter (≥66 år) med glioblastomer over en tyve års periode. Hovedfunnene i denne avhandlingen er: - Kombinasjonen av funksjonell MR, DTT og tredimensjonal ultralydavbildning kan være nyttig når en utfører kirurgisk reseksjon av høygradige gliomer beliggende i ekstra følsomme områder av hjernen. - Pasienter som opplevde komplikasjoner og nevrologiske utfall som følge av kirurgi hadde lavere sannsynlighet for å motta strålebehandling og kjemoterapi. - Tidlig fall i helserelatert livskvalitet etter kirurgi synes å være en sterk og uavhengig negativ prognostisk faktor for pasienter med glioblastom. - Økende alder er en sterk og uavhengig negativ prognostisk faktor for pasienter med glioblastom. Selv om det har vært en intensivering av behandling over tid, har gevinsten i den eldste aldersgruppen vært begrenset. Prognosen for de eldste er fremdeles svært dårlig til tross for multimodal behandling<br>High-grade gliomas are the most common primary brain tumour. Glioblastomas (World Health Organization Grade IV) and anaplastic astrocytomas (World Health Organization Grade III) account for 70-85% of high-grade gliomas. High-grade gliomas are associated with high morbidity and mortality. Virtually all patients with high-grade glioma will experience recurrence and will eventually die from progressing disease. Despite surgery, radiotherapy, and chemotherapy, median survival in patients with glioblastoma still does not exceed 12 months. The median survival for patients with anaplastic astrocytoma (AA) has been reported to be between 2 and 3 years. According to current guidelines, surgery is warranted to establish a histopathologic diagnosis and to achieve safe, maximal, and feasible resection. However, these aggressive tumours cannot be cured and overly aggressive resection is not recommended due to the risk of new neurological deficits. High-grade glioma surgery is a delicate balance between achieving maximal tumour resection and inducing new deficits. In our department a neuronavigation system based on preoperative 3D magnetic resonance imaging (MRI) and intraoperative 3D ultrasound is utilised when resecting high-grade gliomas. Blood-oxygenation-level-dependent functional magnetic resonance imaging (BOLD fMRI) and diffusion tensor tractography (DTT) are specialized MRI techniques for imaging eloquent cortices and neural tracts in grey and white matter, respectively. The neuronavigation system allows the integration of BOLD fMRI and DTT data if the tumours are located in eloquent regions. In the two first studies of this thesis we sought to investigate the use of BOLD fMRI and DTT for preoperative assessments and determine whether using these data together with 3D intraoperative ultrasound enabled safe resection of high-grade gliomas situated in eloquent regions. In the third study we wanted to explore the impact of surgical morbidity on functional outcome and survival in GBM patients. Further, we sought to determine extent of tumour resection achieved in a consecutive sample of primary GBM from our own department. In the fourth study we wanted to determine if changes in health related quality of life early after surgery could be a predictor for survival in patients with glioblastoma. The aims of the fifth study were to explore survival and the treatment provided to elderly patients (≥66 years) diagnosed with glioblastoma during a 20-year time period in a population-based cohort using the Norwegian Cancer Registry. This thesis investigated the role of surgical resection in the treatment of high-grade gliomas and the following conclusions can be drawn: - The combination of BOLD fMRI, DTT, and 3D intraoperative ultrasound may facilitate resection of high-grade gliomas harboured in eloquent areas while preserving motor and language function. - Functional neuronavigation combined with intraoperative 3D ultrasound can, in most patients, enable resection of brain lesions with general anaesthesia without jeopardizing neurological function. - Patients with perioperative complications and surgically acquired deficits were less likely to receive adjuvant therapy. - Early deterioration in HRQL after surgery was independently and markedly associated with impaired survival in patients with glioblastoma. - Advancing age remains a very strong and independent negative prognostic factor in glioblastoma. Although there has been an increase in the aggressiveness of treatment provided to elderly with glioblastoma, the gain for the oldest age group seems at best very modest. The prognosis of the oldest age group remains very poor, despite multimodal treatment.
Books on the topic "Gliomas"
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von Deimling, Andreas, ed. Gliomas. Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-31206-2.
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S, Berger Mitchel, and Wilson Charles B. 1929-, eds. The gliomas. W.B. Saunders, 1999.
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Schramm, J., ed. Low-Grade Gliomas. Springer Vienna, 2010. http://dx.doi.org/10.1007/978-3-211-99481-8.
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Barnett, Gene H., ed. High-Grade Gliomas. Humana Press, 2007. http://dx.doi.org/10.1007/978-1-59745-185-7.
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1924-, Suzuki Jirō, ed. Treatment of glioma: With 137 figures. Springer-Verlag, 1988.
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Scarabino, Tommaso, and Saverio Pollice, eds. Imaging Gliomas After Treatment. Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-31210-7.
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Scarabino, Tommaso, ed. Imaging Gliomas After Treatment. Springer Milan, 2012. http://dx.doi.org/10.1007/978-88-470-2370-3.
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Kurt, Piscol, Klinger M. 1943-, Brock M. 1938-, and Deutsche Gesellschaft für Neurochirurgie. Tagung, eds. Neurosurgical standards, cerebral aneurysms, malignant gliomas. Springer-Verlag, 1992.
Find full textBook chapters on the topic "Gliomas"
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Herholz, Karl. "Gliomas." In PET and SPECT in Neurology. Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-54307-4_41.
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Jenkins, Robert. "Gliomas." In Molecular Pathology in Clinical Practice: Oncology. Springer US, 2009. http://dx.doi.org/10.1007/978-0-387-87366-4_13.
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Herholz, Karl. "Gliomas." In PET and SPECT in Neurology. Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-53168-3_39.
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Jenkins, Robert. "Gliomas." In Molecular Pathology in Clinical Practice. Springer New York, 2007. http://dx.doi.org/10.1007/978-0-387-33227-7_27.
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Dolgushin, Mikhail, Valery Kornienko, and Igor Pronin. "Gliomas." In Brain Metastases. Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-57760-9_28.
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Lavi, Ehud. "Gliomas." In Molecular Pathology in Clinical Practice. Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-19674-9_38.
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Timson, David J., Richard J. Reece, James B. Thoden, et al. "Gliomas." In Encyclopedia of Molecular Mechanisms of Disease. Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_3134.
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Kim, Jonathan, Sumayya J. Almarzouqi, Michael L. Morgan, and Andrew G. Lee. "Optic Gliomas." In Encyclopedia of Ophthalmology. Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-35951-4_1216-1.
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Lin, Tiffany F., and Michael Prados. "Brainstem Gliomas." In Pediatric Oncology. Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-30789-3_3.
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Gullotta, F. "Cryptic Gliomas." In Minimal Neoplasia. Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-83245-1_18.
Full textConference papers on the topic "Gliomas"
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Aleksandrova, P. V., K. I. Zaytsev, P. V. Nikitin, et al. "OCT-based feature analysis of brain tissue ex vivo: rat gliomas 101.8, C6 and human gliomas of different grades." In 2024 International Conference Laser Optics (ICLO). IEEE, 2024. http://dx.doi.org/10.1109/iclo59702.2024.10624409.
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Dutra, Milla Giancristofaro, Bernardo Valle Zanetti, Ana Luiza Badini Tubenchlak, et al. "Management of low-grade gliomas." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.052.
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Background: Gliomas are the most aggressive and prevalent primary malignant tumors of the central nervous system. For better mapping, they are subclassified into degrees in proportion to their malignancy. Although low-grade patients have a better prognosis, they are extremely heterogeneous. Since the high variability in the outcomes of the condition, it is essential to investigate the current therapeutic strategies available. Objective: Analyze the management of low-grade gliomas. Methods: In April 2021, a literature review was conducted on MEDLINE using the descriptors: “Glioma”, “Low Grade”; “Treatment”; as well as their variations obtained in MeSH. Controlled and randomized clinical trials carried out on humans in the last five years were included. Results: 63 articles were found and 10 of them were analyzed in this review. The research has shown that total tumor resection is the therapeutic modality that causes the greatest drop in the mortality rates. Furthermore, the greater the extraction, the greater the progression-free survival. In this way, for greater safety of large-scale surgeries, several intraoperative techniques have been developed. An example is the waking approach, which presents favorable long-term functional results and low failure rates. However, the isolated surgery is often not sufficiently curative. Therefore, it is necessary to complement radiotherapy and chemotherapy with temozolomide, associated with a 5 to 10 year survival rate when combined. Conclusions: Studies have shown that total resection of the tumor is the best way to manage low-grade gliomas, but it is often combined with temozolamide chemotherapy and radiotherapy for a better prognosis.
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FELIN, CAROLLINA DANEZI, GIULLIANO DANEZI FELIN, GIANCARLLO DANEZI FELIN, FELLIPE DANEZI FELIN, and IZABELLA PAZ DANEZI FELIN. "GENÉTICA MOLECULAR DOS GLIOMAS CEREBRAIS: IMPORTÂNCIA NA CLASSIFICAÇÃO, SOBREVIDA E TRATAMENTO." In I Congresso Nacional de Pesquisas e Estudos Genéticos On-line. Revista Multidisciplinar em Saúde, 2022. http://dx.doi.org/10.51161/geneticon/9009.
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Introdução: No Brasil os gliomas representam 42% dos tumores cerebrais. Originam-se do parênquima cerebral e tem comportamento variado. Os de alto grau são agressivos e tem sobrevida média global de 15 meses. Os de baixo grau tem sobrevida de 2-5 anos, podem recidivar ou progredir para piores graus. Objetivos: Identificar a genética molecular dos gliomas e sua importância na classificação, sobrevida e tratamento desses tumores. Metodologia: Revisão de literatura através de pesquisa na base de dados MEDLINE, via PubMed, utilizando os termos: “glioma” [and] “molecular genetics” [and] “therapy”. Aplicados os filtros de busca: “textos completos gratuitos”, “dados associados” e “últimos 5 anos”. Foram encontrados 22 resultados e incluídos 6 para esse estudo. Os critérios de elegibilidade foram todos os artigos coincidentes com tema proposto conforme os filtros e termos de busca. Excluiu-se 16 artigos por não contemplarem os critérios elegíveis. Realizada extração de dados, análise dos resultados e redação dessa revisão. Resultados: No contexto do glioma estão os seguintes tumores: astrocitoma, oligodendroglioma, glioblastoma multiforme e ependimoma. Há marcadores genéticos específicos que caracterizam os astrocitomas de acordo com os graus de I até IV. Os glioblastomas secundários apresentam mutações nos genes IDH1 ou IDH2 diferentemente da apresentação primária. Os astrocitomas e os oligodendrogliomas podem expressar mutações dos genes IDH1 ou IDH2. Os oligodendrogliomas frequentemente tem mutação IDH1/2 e codeleção 1p/19q, enquanto que os astrocitomas tem mutação dos genes ATRX, pTP53 e IDH1/2, sem a codeleção 1p/19q. A codeleção 1p/19q é característica dos tumores oligodendrogliais, útil no diagnóstico e também como preditor de melhor sobrevida e melhor resposta à radioterapia e à quimioterapia. A presença da mutação IDH1/2 relaciona o tumor a um melhor prognóstico e melhor resposta à quimioterapia. Existem quatro graus do ependimoma e nove subtipos moleculares distintos, determinado variabilidade genotípica e fenotípica, determinando tratamento e prognóstico diversos. Conclusão: Foi possível identificar que o perfil genético molecular dos gliomas é determinante tanto para subclassificar quanto para predizer sobrevida e tratamento, pois a genética molecular heterogênea dos gliomas mostrou caracterizar doenças com fenótipos distintos. O conhecimento da genética molecular pode abrir novas oportunidades de tratamento indicando estratégias mais específica de tratamento.
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Pereira, Edmundo. "Nanotecnologia em gliomas malignos." In XXXII Congresso Brasileiro de Neurocirurgia. Thieme Revinter Publicações Ltda, 2018. http://dx.doi.org/10.1055/s-0038-1672796.
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Ul Ain, Qurat, Iqra Duaa, Komal Haroon, Faisal Amin, and Muhammad Zia ur Rehman. "MRI Based Glioma Detection and Classification into Low-grade and High-Grade Gliomas." In 2021 15th International Conference on Open Source Systems and Technologies (ICOSST). IEEE, 2021. http://dx.doi.org/10.1109/icosst53930.2021.9683838.
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Muller, Paul J., and Brian C. Wilson. "Photodynamic therapy of supratentorial gliomas." In BiOS '98 International Biomedical Optics Symposium, edited by Thomas J. Dougherty. SPIE, 1998. http://dx.doi.org/10.1117/12.308129.
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Modenese, Alberto, Leena Korpinen, and Fabriziomaria Gobba. "934 Gliomas incidence in italy." In 32nd Triennial Congress of the International Commission on Occupational Health (ICOH), Dublin, Ireland, 29th April to 4th May 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/oemed-2018-icohabstracts.1230.
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Muller, Paul J., and Brian C. Wilson. "Photodynamic therapy of supratentorial gliomas." In BiOS '97, Part of Photonics West, edited by Thomas J. Dougherty. SPIE, 1997. http://dx.doi.org/10.1117/12.273505.
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Pinho, Rafaela Seixas, Afonso Moraes Melo Junior, Rafael Silva Lemos, Amanda da Silva Furtado, and Luís Eduardo Werneck de Carvalho. "Gliomas: tumor markers and prognosis." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.538.
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Background: Gliomas are classified based from the molecular parameters involved in their pathogenesis, which influence their prognosis. The parameters are based on the mutation of the genes encoding the enzyme isocitrate dehydrogenase 1 and 2 (IDH1 and IDH2), on the codelection of the arms of chromosome 1p/19q and the promoting hypermethylation of the MGMT gene. Objectives: identify tumor markers related to gliomas and their prognostic values. Methods: integrative review of the literature based on pubmed, lilacs and scielo platforms. Articles published in English, Portuguese and Spanish between 2016 and 2021 were included. Articles that were not related to the theme were excluded from the analysis. Results: The IDH1 and 2 genes are traditional markers and mutations in these genes are associated with a better prognosis. The codeletion 1p/19q, on the other hand, is indicative of a more favorable prognosis when related to tumors without codeletion. MGMT gene hypermethylation has strong prognostic value in patients treated with radiotherapy and chemotherapy with alkyl agentes, because the low expression of the MGMT gene allows better efficacy of the therapy, which would be prevented by the MGMT enzyme. The circulating marker microRNA – 221 (miRNA), obtained by less invasive techniques, is an indicator of poor prognosis, however, it has not yet obtained clinical validation for use. Conclusion: It is concluded that the tumor markers that indicate a better prognosis are the genes IDH-I and II, the codelection 1p / 19q and the hypermethylation of the MGMT gene. While miRNA showed a worse prognosis.
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Stupak, E. V., V. V. Stupak, V. M. Glotov, et al. "METHOD OF RAMAN SPECTROSCOPY IN MINIMALLY INVASIVE DIAGNOSTICS OF GLIOMAS OF VARIOUS GRADES OF MALIGNANCY USING MACHINE LEARNING TECHNOLOGIES." In X Международная конференция молодых ученых: биоинформатиков, биотехнологов, биофизиков, вирусологов и молекулярных биологов — 2023. Novosibirsk State University, 2023. http://dx.doi.org/10.25205/978-5-4437-1526-1-376.
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Gliomas are one of the most frequently reported malignant tumors of the CNS. Currently, there are no methods for diagnosing brain tumors, such as determining blood plasma markers. In our study, Raman spectroscopy of blood plasma in combination with machine learning technologies makes it possible to differentiate patients with brain gliomas from patients without oncological pathology, this method can be used for minimally invasive diagnosis and determination of the degree of malignancy of brain gliomas.
Reports on the topic "Gliomas"
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Keating, Amy. Targeting Pediatric Glioma with Apoptosis and Autophagy Manipulation. Defense Technical Information Center, 2012. http://dx.doi.org/10.21236/ada567861.
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Keating, Amy. Targeting Pediatric Glioma with Apoptosis and Autophagy Manipulation. Defense Technical Information Center, 2014. http://dx.doi.org/10.21236/ada614915.
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Zhang, Hui-Mei, Xiao-Bing Huo, Hua-Long Wang, and Chen Wang. Recurrent glioma and radiation necrosis: a meta-analysis of MRI diagnosis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, 2021. http://dx.doi.org/10.37766/inplasy2021.12.0028.
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Becher, Oren, and Alex Chung. Genetically Engineered Mouse Model of Diffuse Intrinsic Pontine Glioma as a Preclinical Tool. Defense Technical Information Center, 2012. http://dx.doi.org/10.21236/ada569511.
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Chen, Qian, Yuhua Hu, Haihua Zhan, and Yawei He. The diagnostic value of miR-221/222 in glioma : a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, 2021. http://dx.doi.org/10.37766/inplasy2021.3.0064.
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Jin, Yin, and Xingchen Ye. Prognostic and clinicopathological role of C-reactive protein in glioma: a meta-analysis of 2,064 patients. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, 2023. http://dx.doi.org/10.37766/inplasy2023.10.0010.
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Yang, Chao, Tao-junjin Lu, Jie Wang, Qing Zhang, Ze-Fen Wang, and Zhi-Qiang Li. Association of systemic immune-inflammation index with grade and prognosis in glioma patients: a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, 2022. http://dx.doi.org/10.37766/inplasy2022.4.0072.
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Gu, Xindong, Xining He, Hualong Wang, et al. Dynamic susceptibility contrast-enhanced perfusion-weighted imaging in differentiation between recurrence and pseudoprogression in high-grade glioma: a meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, 2023. http://dx.doi.org/10.37766/inplasy2023.2.0056.
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Mahmoudi, Farhad, Mahtab Mokarram, Sadegh Sabouhi, Sara Hashemi, Parastoo Saberi, and Hadi Zamanian. Application of digital health for improving medication adherence in MS patients. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, 2021. http://dx.doi.org/10.37766/inplasy2021.10.0058.
Full textAbstract:
Review question / Objective: The aim of this study is to evaluate the efficacy of digital health interventions in monitoring and improving medication adherence in Multiple Sclerosis patients. Condition being studied: Multiple sclerosis (MS) is the most prevalent chronic inflammatory disease of the central nervous system (CNS), which leads to focal lesions in the white matter, characterized by selective primary demyelination with partial preservation of axons and reactive astrocytic gliosis. The disease is thought to be due to a complex interaction between different genetic and environmental factors. The prevalence of MS is rising all over the world, due on one hand to earlier diagnosis and prolonged survival, and on the other to a true increase in incidence of the disease. The diagnosis of MS remains clinical despite recent advances in diagnostics and relies on demonstrating dissemination in space and time while excluding alternative diagnoses.