Relevant bibliographies by topics / Glioma tumors

Academic literature on the topic 'Glioma tumors'

Author: Grafiati
Published: 10 December 2022
Last updated: 29 January 2023

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Journal articles on the topic "Glioma tumors"

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Rao, Rohit, Feng Zhang, Ravinder Verma, Jincheng Wang, Dazhuan Xin, and Richard Lu. "TMIC-55. CHARACTERIZATION OF TUMOR-MICROENVIRONMENT INTERACTIONS IN GLIOBLASTOMAS AT THE SINGLE-CELL LEVEL." Neuro-Oncology 21, Supplement_6 (November 2019): vi259—vi260. http://dx.doi.org/10.1093/neuonc/noz175.1089.

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Abstract Glioblastomas are malignant brain tumors that carry a poor prognosis. The tumor microenvironment has been identified as an important regulator of tumor growth and may represent a novel target for therapy. Transcriptional subtypes of glioma are a major source of heterogeneity of expression in gliomas. Gliomas are highly heterogeneous diseases and can be classified into different subtypes including proneural, classical and mesenchymal tumors. We hypothesized that different subtypes of glioma will have different microenvironmental composition and exhibit distinct responses to therapies. To understand whether gliomas induced by different oncogenic drivers affect microenvironment composition, we induced mouse gliomas using a PDGFB and dnp53 driver to model proneural glioma and HRasV12 and dnp53 to model mesenchymal glioma, respectively. We performed single cell transcriptomic profiling to characterize the tumor microenvironment in these glioma models. We found that in the PDGFB/dnp53 glioma model had a large microglia contribution with about 30% tumor-associated microglia. In contrast, the HRasV12/dnp53 glioma model had only sparse microenvironmental cells. In addition, microglia in each model displayed subtype-specific gene expression programs, with microglia in the HRasV12/dnp53 tumor model expressing increased antigen presenting genes while increased levels of osteopontin in the PDGFB/dnp53 tumor model. To determine the tumor-microenvironment interactions, we performed receptor-ligand analysis using CellPhoneDb to identify secretory ligands that support tumor cell growth in microenvironmental cells. We found that tumor-associated pericytes are an important source of growth factor ligands in both PDGFB/dnp53 and HRasV12/dnp53 glioma models. We are investigating the contribution of microglia and pericytes to tumor growth and survival through cell depletion and pharmacological inhibition and determining whether the differences in tumor microglia between the models affects sensitivity to therapies including immunotherapy. Understanding how tumor-intrinsic signaling modulates microenvironment niches and tumor-microenvironment communications aids rational design of combinations targeting the malignant brain tumors.
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Morrone, Fernanda Bueno, Pedro Vargas, Liliana Rockenbach, and Thamiris Becker Scheffel. "P2Y12 Purinergic Receptor and Brain Tumors: Implications on Glioma Microenvironment." Molecules 26, no. 20 (October 12, 2021): 6146. http://dx.doi.org/10.3390/molecules26206146.

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Gliomas are the most common malignant brain tumors in adults, characterized by a high proliferation and invasion. The tumor microenvironment is rich in growth-promoting signals and immunomodulatory pathways, which increase the tumor’s aggressiveness. In response to hypoxia and glioma therapy, the amounts of adenosine triphosphate (ATP) and adenosine diphosphate (ADP) strongly increase in the extracellular space, and the purinergic signaling is triggered by nucleotides’ interaction in P2 receptors. Several cell types are present in the tumor microenvironment and can facilitate tumor growth. In fact, tumor cells can activate platelets by the ADP-P2Y12 engagement, which plays an essential role in the cancer context, protecting tumors from the immune attack and providing molecules that contribute to the growth and maintenance of a rich environment to sustain the protumor cycle. Besides platelets, the P2Y12 receptor is expressed by some tumors, such as renal carcinoma, colon carcinoma, and gliomas, being related to tumor progression. In this context, this review aims to depict the glioma microenvironment, focusing on the relationship between platelets and tumor malignancy.
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Amin, Samirkumar, Kevin Anderson, Beth Bourdreau, Emmanuel Martínez, Emre Kocakavuk, Kevin C. Johnson, Floris Barthel, et al. "GENE-57. COMPARATIVE MOLECULAR LIFE HISTORY OF SPONTANEOUS CANINE AND HUMAN GLIOMA." Neuro-Oncology 21, Supplement_6 (November 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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Irvin, David, Hannah Roberts, Vladislav Sharin, Ahsan Farooqi, Sharvari Dharmaiah, Christian Alvarez, and Jason Huse. "CSIG-09. ATRX DEFICIENCY IN GLIOMA IMPACTS TRANSCRIPTIONAL PROFILES AND THE IMMUNE MICROENVIRONMENT IN VIVO." Neuro-Oncology 22, Supplement_2 (November 2020): ii29. http://dx.doi.org/10.1093/neuonc/noaa215.121.

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Abstract Current treatment for diffuse astrocytoma fails to address its underlying molecular mechanisms leading to inevitable disease progression and eventual patient death. Genomic studies have implicated ATRX alterations as critical to low grade glioma biology. Our lab has previously shown in vitro that ATRX influences glioma motility, cellular differentiation state, and epigenetic programming, however, the influence of ATRX alterations in vivo remains unclear. Here, we leveraged an RCAS/tva mouse tumor model to probe the role of ATRX deficiency in glioma. Atrx deficient murine tumors exhibited lower histopathological grade and were associated with longer survival than Atrx-intact counterparts, and syngeneic allografts of cell lines derived from primary tumors mirrored the differential degrees of aggressiveness seen in primary tumors. Tumor-derived Atrx-deficient cell lines showed increased susceptibility to G-quadruplex stabilizing compounds, pointing to increased replication stress and recapitulating a key phenotype of ATRX-mutant gliomas in humans. Transcriptional profiling revealed enrichments in MYC target genes, E2F targets as well as G2/M checkpoint pathways in Atrx-intact tumors and cells, and enrichment in RAS signaling in Atrx-deficient tumors and cells. Finally, Atrx deficient murine gliomas displayed increased levels of NK cells, a phenotype recapitulated in ATRX-mutant human gliomas, and primary Atrx-deficient glioma lines exhibited increased levels of NK cell-attracting cytokines. These latter findings suggest that ATRX deficiency could influence interactions between glioma cells and their immune microenvironment by way of phenotypically relevant molecular mechanisms.
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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.
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Nguyen, Hoang Dong, Phedias Diamandis, Michelle S. Scott, and Maxime Richer. "Deciphering of Adult Glioma Vulnerabilities through Expression Pattern Analysis of GABA, Glutamate and Calcium Neurotransmitter Genes." Journal of Personalized Medicine 12, no. 4 (April 14, 2022): 633. http://dx.doi.org/10.3390/jpm12040633.

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Adult infiltrating gliomas are highly aggressive tumors of the central nervous system with a dismal prognosis despite intensive multimodal therapy (chemotherapy and/or radiotherapy). In this study, we studied the expression, methylation and interacting miRNA profiles of GABA-, glutamate- and calcium-related genes in 661 adult infiltrating gliomas available through the TCGA database. Neurotransmitter-based unsupervised clustering identified three established glioma molecular subgroups that parallel major World Health Organization glioma subclasses (IDH-wildtype astrocytomas, IDH-mutant astrocytomas, IDH-mutant oligodendroglioma). In addition, this analysis also defined a novel, neurotransmitter-related glioma subgroup (NT-1), mostly comprised of IDH-mutated gliomas and characterized by the overexpression of neurotransmitter-related genes. Lower expression of neurotransmission-related genes was correlated with increased aggressivity in hypomethylated IDH-wildtype tumors. There were also significant differences in the composition of the tumor inflammatory microenvironment between neurotransmission-based tumor categories, with lower estimated pools of M2-phenotype macrophages in NT-1 gliomas. This multi-omics analysis of the neurotransmission expression landscape of TCGA gliomas—which highlights the existence of neurotransmission-based glioma categories with different expression, epigenetic and inflammatory profiles—supports the existence of operational neurotransmitter signaling pathways in adult gliomas. These findings could shed new light on potential vulnerabilities to exploit in future glioma-targeting drug therapies.
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Berg, Tracy, Carolina Marques, Vasiliki Pantazopoulou, Elinn Johansson, Kristoffer von Stedingk, David Lindgren, Elin Pietras, et al. "TAMI-05. THE IRRADIATED BRAIN MICROENVIRONMENT SUPPORTS GLIOMA STEMNESS AND SURVIVAL VIA ASTROCYTE-DERIVED TRANSGLUTAMINASE 2." Neuro-Oncology 22, Supplement_2 (November 2020): ii213—ii214. http://dx.doi.org/10.1093/neuonc/noaa215.894.

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Abstract The highest-grade gliomas invariably recur as incurable tumors following standard of care comprising surgery, radiotherapy, and chemotherapy. The majority of the recurrent tumors form within the area of the brain receiving high-dose irradiation during treatment of the primary tumor, indicating that the recurrent tumor forms in an irradiated microenvironment. The tumor microenvironment has been demonstrated to influence the therapeutic response and stemness characteristics of tumor cells, but the influence of radiation on the microenvironment and its subsequent consequences for tumor cells are incompletely understood. Here, we used genetically engineered glioma mouse models and human glioma samples to characterize the impact of standard of care radiotherapy on the brain tumor microenvironment. We found that tumor-associated astrocytes subjected to radiation in vitro could enhance tumor cell stemness and survival of co-cultured glioma cells. More aggressive gliomas formed in vivo when mouse brains were irradiated prior to tumor cell implantation, suggesting that the irradiated brain microenvironment supports tumor growth. We isolated the effect of irradiated astrocytes to extracellular matrix secreted by these cells, and specifically found that astrocyte-derived transglutaminase 2 (TGM2) is a stromal promoter of glioma stemness and radioresistance. TGM2 levels were increased after radiation in glioma mouse models. Recombinant TGM2 enhanced, and TGM2 inhibitors blocked, glioma cell stemness. In human GBM tissue, TGM2 levels were increased in recurrent vs. primary tumors. In summary, in addition to supporting TGM2 as a potential therapeutic target in glioma, our data indicate that radiotherapy results in a tumor-supportive microenvironment, the targeting of which may be necessary to overcome tumor cell therapeutic resistance and recurrence.
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Mellinghoff, Ingo K., Benjamin M. Ellingson, Mehdi Touat, Elizabeth Maher, Macarena I. De La Fuente, Matthias Holdhoff, Gregory M. Cote, et al. "Ivosidenib in Isocitrate Dehydrogenase 1–Mutated Advanced Glioma." Journal of Clinical Oncology 38, no. 29 (October 10, 2020): 3398–406. http://dx.doi.org/10.1200/jco.19.03327.

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PURPOSE Diffuse gliomas are malignant brain tumors that include lower-grade gliomas (LGGs) and glioblastomas. Transformation of low-grade glioma into a higher tumor grade is typically associated with contrast enhancement on magnetic resonance imaging. Mutations in the isocitrate dehydrogenase 1 ( IDH1) gene occur in most LGGs (> 70%). Ivosidenib is an inhibitor of mutant IDH1 (mIDH1) under evaluation in patients with solid tumors. METHODS We conducted a multicenter, open-label, phase I, dose escalation and expansion study of ivosidenib in patients with m IDH1 solid tumors. Ivosidenib was administered orally daily in 28-day cycles. RESULTS In 66 patients with advanced gliomas, ivosidenib was well tolerated, with no dose-limiting toxicities reported. The maximum tolerated dose was not reached; 500 mg once per day was selected for the expansion cohort. The grade ≥ 3 adverse event rate was 19.7%; 3% (n = 2) were considered treatment related. In patients with nonenhancing glioma (n = 35), the objective response rate was 2.9%, with 1 partial response. Thirty of 35 patients (85.7%) with nonenhancing glioma achieved stable disease compared with 14 of 31 (45.2%) with enhancing glioma. Median progression-free survival was 13.6 months (95% CI, 9.2 to 33.2 months) and 1.4 months (95% CI, 1.0 to 1.9 months) for the nonenhancing and enhancing glioma cohorts, respectively. In an exploratory analysis, ivosidenib reduced the volume and growth rates of nonenhancing tumors. CONCLUSION In patients with m IDH1 advanced glioma, ivosidenib 500 mg once per day was associated with a favorable safety profile, prolonged disease control, and reduced growth of nonenhancing tumors.
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Wroblewski, Tadeusz, Philip Tatman, Anthony Fringuello, Sam Scherer, William Foreman, Denise Damek, Samy Youssef, Kevin Lillehei, David Ormond, and Michael Graner. "DDRE-20. HIGH-THROUGHPUT SCREENING OF FDA-APPROVED COMPOUNDS IN GLIOMA AND GLIOBLASTOMA IDENTIFIES NOVEL THERAPEUTICS." Neuro-Oncology 23, Supplement_6 (November 2, 2021): vi78. http://dx.doi.org/10.1093/neuonc/noab196.304.

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Abstract BACKGROUND Glioma and glioblastoma comprise 28% of all primary central nervous system tumors and cause the majority of primary brain tumor deaths. Despite substantial research into the molecular pathogenesis and genetic landscape of glioma, no currently approved therapies are curative for any glioma or glioblastoma. Patients with glioblastoma have an average survival time of 12-15 months, while patients with grade III gliomas have an average survival time of 3-5 years, and patients with grade II gliomas have an average survival time of 8-15 years. The lack of a curative treatment for these tumors necessitates additional research into novel therapies. METHODS In this study, we developed a high-throughput drug screen and culture system to identify existing FDA-approved therapies with the potential to inhibit glioma viability. RESULTS In total, we screened 39 tumors: 21 glioblastoma, 10 oligodendroglioma, and 8 astrocytoma. Carfilzomib was the most effective compound across the cohort, decreasing the average tumor viability to 39.0% +/- 16.5%SD. Regardless of tumor grade, MGMT methylation, EGFR amplification, tumor recurrence and etiology, tumor histology, prior treatment, and patient gender, carfilzomib significantly reduced cell viability in every tumor; though was not necessarily the most effective compound in each of these groups. We found HDAC inhibition to be the most effective treatment in grade 1 astrocytomas. However, HDAC inhibition was surpassed by carfilzomib and RNA transcription inhibitors in all higher grades. Interestingly, EGFR inhibition, while significantly effective in 36 tumors, was consistently less effective than carfilzomib across the cohort, though did surpass the effectiveness of HDAC inhibition in grade III gliomas. CONCLUSIONS FDA approved compounds can effectively inhibit glioma tumor viability. Specifically, carfilizomib holds great promise. Further in vivo studies are needed to confirm these findings.
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Pedersen, L. K. "P05.02.A 18F-FACBC PET/MRI in diagnostic assessment of gliomas." Neuro-Oncology 24, Supplement_2 (September 1, 2022): ii36. http://dx.doi.org/10.1093/neuonc/noac174.121.

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Abstract Background and Theory MRI and histopathological tissue sampling are routinely done as part of the diagnostic work-up of patients with glioma. MRI provides anatomical images with high resolution and excellent soft-tissue contrast. But this modality has limitations in identifying tumor grade, true tumor extension and differentiate viable tumor tissue from treatment induced changes. PET can provide quantitative information of cellular activity and metabolism, and may therefore have additional value compared to MRI alone. Objective The aim of this study was to find the sensitivity of [18F]FACBC PET in gliomas, and evaluate if PET imaging with this tracer can improve differentiation between low-and high-grade gliomas. Methods Patients with suspicion of primary (n=19) or recurrent gliomas (n=8) were recruited to this study from St. Olavs hospital, Trondheim University Hospital, Trondheim, and from the University Hospital of North Norway, Tromsø. PET acquisitions (30-45 min post injection) using the amino acid radiotracer [18F]FACBC (3 MBq/kg) were performed simultaneously to MRI acquisitions (T1 with and without contrast, FLAIR, and UTE for attenuation correction. The sensitivity of [18F]FACBC PET in glioma detection was assessed using histopathology as reference. Tumor-to-background ratios (TBRs) were compared to tumor subtype and grade to assess the diagnostic value of this tracer for glioma diagnostics. Results Histopathology revealed 2 WHO grade 1 gliomas (pilocytic astrocytoma n=1, pilocytic astrocytoma/ganglioglioma n=1), 7 WHO grade 2 gliomas(astrocytoma n=4, oligodendroglioma n=3), 7 WHO grade 3 gliomas(astrocytoma n=5, oligodendroglioma n=2) and 12 WHO grade 4 tumors(astrocytoma n=1, glioblastoma n=11). [18F]FACBC PET provided a sensitivity of 74.1% in the detection of gliomas. PET uptake was observed in all grade 4 tumors, 5/7 grade 3 tumors, 2/7 grade 2 tumors, and all grade 1 tumors. TBRpeak was high with a median value of 9.4 (range: 2.1-34.9) in PET positive tumors. Only tumors with a TBRpeak > 2.0 were detected with [18F]FACBC PET. TBRpeak was highest for grade 1 gliomas with a median value of 20.6, and increased significantly from grade 2 to grade 4 tumors with median values of 1.7 (grade 2), 6.2 (grade 3) and 12.4 (grade 4) (Kruskal-Wallis, p=0.001). Conclusion [18F]FACBC PET demonstrated high uptake in the majority of gliomas, and there was a clear tendency to higher uptake in the higher grade tumors. [18F]FACBC PET may be useful in the differentiation between glioms grades and subtypes. A future study using the same patient data will be performed to evaluate the assessment of [18F]FACBC PET in neurosurgical treatment planning. Image-localized biopsies from different regions of each tumor will be correlated to fused PET/MRI images to evaluate if [18F]FACBC PET can be used to guide surgical resection and to improve accuracy in histopathological tissue sampling.
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Dissertations / Theses on the topic "Glioma tumors"

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Konnully, Augustus Meera Bessy. "Characterization of cellular heterogeneity in Diffuse Low Grade Glioma." Thesis, Montpellier, 2020. http://www.theses.fr/2020MONTT038.

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Les gliomes diffus de bas grade (DLGG) sont des tumeurs gliales de grade II qui affectent principalement les jeunes adultes. Elles sont caractérisées par une croissance lente et une activité mitotique réduite. Cependant, ces tumeurs diffusent et envahissent le cerveau sain via les vaisseaux sanguins et les fibres nerveuses. Après plusieurs années de croissance lente, ces tumeurs peuvent évoluer vers des glioblastomes, des tumeurs cérébrales très agressives dont la survie médiane moyenne est alors de 12 à 15 mois après le diagnostic. La caractérisation cellulaire des DLGG est encore limitée ce qui nuit à la recherche d’un traitement à un stade précoce. Dans ma thèse de doctorat, je me suis focalisée sur la caractérisation de 'hétérogénéité cellulaire des DLGG mutés pour IDH1. En effectuant une analyse d'immunofluorescence sur des astrocytomes et oligodendrogliomes de grade II, j'ai identifié deux sous-populations cellulaires largement non chevauchantes et exprimant respectivement les facteurs de transcription SOX9 et OLIG1. Ces cellules s’apparentent à des cellules de type astrocytaire et oligodendrocytaire et expriment des marqueurs moléculaires distincts. Les cellules SOX9 expriment APOE, KCNN3, CRYAB et ID4, tandis que les cellules OLIG1 expriment préfentiellement PDGFRA, SOX8, MASH1 et SOX4. Par ailleurs, j’ai montré que les cellules SOX9 présentent une activation particulière des voies de signalisation, notamment Notch, BMP et leurs cibles en aval. Pour étudier le rôle de la voie de signalisation Notch dans la formation de ces 2 sous-populations tumorales, j'ai purifié par tri magnétique les cellules tumorales à partir d'échantillons de gliomes fraîchement réséqués et j'ai surexprimé le domaine intracellulaire Notch (NICD), une forme active de Notch. J’ai ainsi montré que cette activation augmentait l’expression des marqueurs cellulaires associés aux cellules SOX9+ et une baisse de ceux associés aux cellules OLIG1+. J'ai ensuite étendu ces analyses à une lignée cellulaire anaplasique dérivée d'un patient et mutée pour IDH1. Ces résultats indiquent un rôle clé de la signalisation Notch dans la régulation de la plasticité des cellules tumorales. Des expériences similaires pour étudier l'activation de la signalisation BMP (bone morphogenetic protein) n'ont pas montré d'effet notable sur la plasticité. Néanmoins, le traitement des cellules par des membres de la famille BMP a fortement augmenté l’expression de CRYAB, un marqueur associé à SOX9, et a diminué l’expression de OLIG1 et OLIG2. En conclusion, j'ai identifié deux sous-populations tumorales non chevauchantes dans des gliomes diffus de bas grade et j'ai démontré le rôle déterminant de la voie de signalisation Notch dans leur formation. Ces résultats permettront de mieux comprendre l'hétérogénéité tumorale dans les DLGG et de concevoir de nouvelles stratégies thérapeutiques contre ces tumeurs
Diffuse Low-Grade Gliomas (DLGG) are WHO grade II glial tumors affecting younger adults. They are characterized as silent, slow growing tumors with fewer mitotic activities. However, they diffuse and invade the healthy brain via blood vessels and nerve fibers. These, over a period of years develop to malignant Glioblastoma, aggressive brain tumors where patients have an average medial survival of 12-15 months after diagnosis. Ill-defined phenotypic and cellular diversity of DLGG poses serious limitation to treatment and prevention at the early stage.In my PhD thesis, I aimed to address this limitation by characterizing the cellular heterogeneity in IDH1-mutated DLGG. By performing immunofluorescence analysis on grade II astrocytoma and oligodendroglioma, I have identified two largely non-overlapping cellular subpopulations expressing SOX9 and OLIG1 transcription factors, which represent astrocyte-like and oligodendrocyte-like cells, respectively. Upon further investigation, I have shown that these subpopulations express distinct molecular markers. Sox9 cells are associated with APOE, KCNN3, CRYAB and ID4, while Olig1 cells showed strong correlation with the expression of PDGFRA, SOX8, MASH1, and SOX4. In addition, the sox9 cells show a particular activation of signaling pathways including Notch, BMP and their downstream targets.To ascertain the role of Notch signaling in regulating the formation of these tumoral subpopulations, I used magnetic sorting of tumor cells from freshly resected glioma samples and overexpressed Notch Intracellular Domain (NICD), an active form of Notch. Increased Notch activation resulted in an upregulation of Sox9- and downregulation of Olig1-associated cell markers. I have then extended these analyses on one anaplastic IDH1 mutated patient derived cell line which reproduced similar gene expression profile confirming the robustness of the role of Notch signaling in regulating the plasticity of the cells. Parallel experiments performed by activation of Bone Morphogenetic Protein (BMP) signaling on IDH1 mutated cell line did not show a prominent effect on the plasticity. Nevertheless, BMP signal activation highly upregulated CRYAB, a SOX9 related marker and downregulated OLIG1 and OLIG2.In conclusion, I have identified two non-overlapping tumor subpopulations in diffuse low-grade gliomas and demonstrated the deterministic role of Notch signaling pathway in their formation. I believe that these findings would aid in better understanding tumoral heterogeneity in DLGG and be extended in designing new therapeutic strategies against these tumors
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Safdar, Shahana. "Peptide-targeted nitric oxide delivery for the treatment of glioblatoma multiforme." Diss., Georgia Institute of Technology, 2012. http://hdl.handle.net/1853/45797.

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Glioblastoma multiforme (GBM) is the most common malignant central nervous system tumor. The ability of glioma cells to rapidly disperse and invade healthy brain tissue, coupled with their high resistance to chemotherapy and radiation have resulted in extremely poor prognoses among patients. In recent years, nitric oxide (NO) has been discovered to play a ubiquitous of role in human physiology and studies have shown that, at sufficient concentrations, NO is able to induce apoptosis as well as chemosensitization in tumor cells. This thesis discusses the synthesis and characterization of targeted NO donors for the treatment of GBM. Two glioma targeting biomolecules, Chlorotoxin (CTX) and VTWTPQAWFQWVGGGSKKKKK (VTW) were reacted with NO gas to synthesize NO donors. These NO donors, CTX-NO and VTW-NO, released NO for over 3 days and were able to induce cytotoxicity in a dose dependent manner in glioma cells. The biggest advantage, a result of the targeted delivery of NO, was that the NO donors did not have toxic effects on astrocytes and endothelial cells. To characterize the chemosensitizing effects of CTX-NO, cells were incubated with CTX-NO prior to exposure to temozolomide (TMZ) or carmustine (BCNU). These drugs are the most popular chemotherapeutics used in the treatment of GBM, but have only shown modest improvements in patient survival. Viability studies showed that CTX-NO selectively elicited chemosensitivity in glioma cells, whereas the chemosensitivty of astrocytes and endothelial cells remained unaffected. Further investigation showed that CTX-NO pretreatment decreased O6-methylguanine DNA methyltransferase (MGMT) and p53 levels, suggesting that a decrease in DNA repair ability may be the mechanism by which chemosensitivity is induced. Lastly, the effects of CTX-NO on glioma cell invasion and migration were studied using Boyden chamber and modified scratch assays. Non-toxic doses of CTX-NO decreased glioma cell invasion in a dose dependent manner. Studies quantifying matrix metalloproteinase-2 (MMP-2) and matrix metalloproteinase-9 (MMP-9) surface expression demonstrated that while MMP-2 expression was decreased by both CTX and CTX-NO, MMP-9 expression was decreased only by CTX-NO. Furthermore quantifying MMP-2 and MMP-9 activity levels showed that NO and CTX work synergistically to decrease the activity of the enzymes. These studies demonstrate that the decrease in glioma invasion resulting from CTX-NO treatment was partially a consequence of decreased levels of surface and activated MMP-2 and MMP-9. The work presented in this thesis describes a novel approach to treating GBM that can be modified to develop treatments for various other tumors. Furthermore this is the first study to develop glioma-targeting NO donors.
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Munson, Jennifer Megan. "Novel nanocarriers for invasive glioma." Diss., Georgia Institute of Technology, 2011. http://hdl.handle.net/1853/41226.

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The invasive nature of glioblastoma (GBM) represents a significant challenge to the standard of care and contributes to poor clinical outcomes. Invasion of tumors into healthy brain restricts chemotherapeutic access and complicates surgical resection. The central hypothesis of the thesis is that an effective anti-invasive agent can enhance the standard chemotherapeutic response in invasive brain tumors. Through a screen of novel compounds, a new anti-invasive small molecule, Imipramine Blue (IB), was identified. This triphenylmethane compound inhibits invasion of highly invasive glioma in vitro and in vivo. To elicit a response in vivo, Imipramine Blue was liposomally encapsulated to yield better delivery to tumor. Using this formulation, it is shown that IB attenuates invasion of glioma in vivo leading to a more compact tumor in an aggressively invasive rodent glioma model. Further, it is shown that this novel compound binds NADPH oxidases and alters expression of actin regulatory elements to elicit this anti-invasive activity. To test our hypothesis that anti-invasive therapy coupled with chemotherapy will enhance efficacy, nano-IB therapy was followed by liposomally encapsulated doxorubicin (DXR) chemotherapy. Additionally, a co-encapsulated formulation of IB and DXR was developed and tested in vivo. This combination therapy significantly enhanced survival compared to IB or DXR alone, resulting in long-term survival in the syngeneic invasive rat astrocytoma model RT2. It was seen that sequential treatment was more effective than the co-encapsulated treatment indicating a benefit of pre-treating the tumor with the anti-invasive. This thesis demonstrates that novel anti-invasive IB mediated 'containment' of diffuse glioma significantly enhances the efficacy of DXR chemotherapy compared to chemotherapy or anti-invasive therapy alone.
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Dan, Michael. "Human anti-glioma monoclonal antibodies from patients with neurological tumors." Thesis, McGill University, 1989. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=74367.

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The current management of malignant gliomas is unsatisfactory compared to other solid tumors. Expected median survival is less than one year with even the best of care. At some point in their illness, most patients with neurological tumors are capable of mounting an immune response to their disease. This study focused on the humoral immune response of brain tumor patients by preparing human-human B cell hybridomas from autologous peripheral blood lymphocytes and a human myeloma-like cell line, designated as TM-H2-SP2. Eighteen fusions were successfully performed, and 15.8% of all microwells screened contained human immunoglobulin with anti-tumor activity. Five hybridomas, designated as BT27/1A2, BT27/2A3, BT32/A6, BT34/A5, and BT54/B8 were selected for detailed study. All five produced monoclonal IgM in a range of 2.4-44 $ mu$g/ml, had a similar (but not identical) pattern of reactivity against a panel of human tumor cell lines, and did not react with normal human astrocytes. All five human monoclonal antibodies (HmAbs) recognized a subpopulation of tumor cells based on multiparameter flow cytometric studies. Cell sorting experiments suggested that the identified subpopulation may share certain properties with hypothetical tumor stem cells. Preliminary antigen characterization indicated that the HmAbs are directed to cell surface glycolipids. These HmAbs possess certain properties of reactivity that suggest potential roles for them in the future diagnosis and clinical management of human malignant gliomas.
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Murren, Robert John. "Intracytoplasmic lipid droplets in high grade glioma : metabolism and target for therapy." Thesis, University of Birmingham, 2018. http://etheses.bham.ac.uk//id/eprint/8134/.

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Glioblastoma is a highly malignant and aggressive high grade glioma with a poor prognosis. The low survival rates stem from tumour progression, late intervention, ineffective therapies and drug resistance, requiring new therapeutic and diagnostic approaches. Lipid droplets are dynamic organelles suggested to be influential facets of cancer metabolism and biology in many tumours. In glioblastoma lipid droplets have been associated with hypoxia higher clinical grades and poor survival however the cellular pathways underlying lipid droplet metabolism remain unclear. Using a publically available database of grade 2 ta 4 glioma gene expression, we observed that genes associated with lipid droplet metabolism were important prognostic survival and tumour progression indicators. Moreover, through confocal microscopy, flow cytometry and NMR-based methods, we observed that uptake of exogenous lipids and adipose triglyceride lipase-mediated lipid shuttling produced lipid droplets whilst autophagy was vital to lipid droplet breakdown. ATGL-mediated lipid shuttling was further observed to prevent unsaturated fatty acid oxidative damage. Finally, we investigated the effect of pharmacological lipid droplet manipulation and observed that autophagy inhibition can improve temozolomide and irradiation cytotoxicity. Taken together our data suggests that understanding lipid droplet metabolic pathways may generate prognostic bio-markers of survival and progression and improve current therapies.
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Mörén, Lina. "Metabolomics and proteomics studies of brain tumors : a chemometric bioinformatics approach." Doctoral thesis, Umeå universitet, Kemiska institutionen, 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-111309.

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The WHO classification of brain tumors is based on histological features and the aggressiveness of the tumor is classified from grade I to IV, where grade IV is the most aggressive. Today, the correlation between prognosis and tumor grade is the most important component in tumor classification. High grade gliomas, glioblastomas, are associated with poor prognosis and a median survival of 14 months including all available treatments. Low grade meningiomas, usually benign grade I tumors, are in most cases cured by surgical resection. However despite their benign appearance grade I meningiomas can, without any histopathological signs, in some cases develop bone invasive growth and become lethal. Thus, it is necessary to improve conventional treatment modalities, develop new treatment strategies and improve the knowledge regarding the basic pathophysiology in the classification and treatment of brain tumors. In this thesis, both proteomics and metabolomics have been applied in the search for biomarkers or biomarker patterns in two different types of brain tumors, gliomas and meningiomas. Proteomic studies were carried out mainly by surface enhanced laser desorption ionization time of flight mass spectrometry (SELDI-TOF-MS). In one of the studies, isobaric tags for relative and absolute quantitation (iTRAQ) labeling in combination with high-performance liquid chromatography (HPLC) was used for protein detection and identification. For metabolomics, gas-chromatography time-of-flight mass spectrometry (GC-TOF-MS) has been the main platform used throughout this work for generation of robust global metabolite profiles in tissue, blood and cell cultures. To deal with the complexity of the generated data, and to be able to extract relevant biomarker patters or latent biomarkers, for interpretation, prediction and prognosis, bioinformatic strategies based on chemometrics were applied throughout the studies of the thesis. In summary, we detected differentiating protein profiles between invasive and non-invasive meningiomas, in both fibrous and meningothelial tumors. Furthermore, in a different study we discovered treatment induce protein pattern changes in a rat glioma model treated with an angiogenesis inhibitor. We identified a cluster of proteins linked to angiogenesis. One of those proteins, HSP90, was found elevated in relation to treatment in tumors, following ELISA validation. An interesting observation in a separate study was that it was possible to detect metabolite pattern changes in the serum metabolome, as an effect of treatment with radiotherapy, and that these pattern changes differed between different patients, highlighting a possibility for monitoring individual treatment response.  In the fourth study of this work, we investigated tissue and serum from glioma patients that revealed differences in the metabolome between glioblastoma and oligodendroglioma, as well as between oligodendroglioma grade II and grade III. In addition, we discovered metabolite patterns associated to survival in both glioblastoma and oligodendroglioma. In our final work, we identified metabolite pattern differences between cell lines from a subgroup of glioblastomas lacking argininosuccinate synthetase (ASS1) expression, (ASS1 negative glioblastomas), making them auxotrophic for arginine, a metabolite required for tumor growth and proliferation, as compared to glioblastomas with normal ASS1 expression (ASS1 positive). From the identified metabolite pattern differences we could verify the hypothesized alterations in the arginine biosynthetic pathway. We also identified additional interesting metabolites that may provide clues for future diagnostics and treatments. Finally, we were able to verify the specific treatment effect of ASS1 negative cells by means of arginine deprivation on a metabolic level.
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McNeeley, Kathleen Margaret. "Modulating liposomal stealth properties to evade RES and target tumors." Diss., Atlanta, Ga. : Georgia Institute of Technology, 2008. http://hdl.handle.net/1853/26650.

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Thesis (Ph.D)--Biomedical Engineering, Georgia Institute of Technology, 2009.
Committee Chair: Ravi V. Bellamkonda; Committee Member: Ananth V. Annapragada; Committee Member: Andrew Lyon; Committee Member: Gang Bao; Committee Member: Niren Murthy. Part of the SMARTech Electronic Thesis and Dissertation Collection.
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Ghasimi, Soma. "Genotype-phenotype studies in brain tumors." Doctoral thesis, Umeå universitet, Onkologi, 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-83185.

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Meningioma and glioma are the most common primary brain tumors, but their etiologies are largely unknown. Although meningioma is usually benign, their intracranial location can lead to lethal consequences, and despite progress in surgery, radiotherapy, and chemotherapy the prognosis for patients with glioma remains poor. The only well-established environmental risk factor for meningioma and glioma is ionizing radiation. Evidence for inherited predisposition to meningioma and glioma is provided by a number of rare inherited syndromes where collectively these diseases account for only a small proportion of the twofold increased risk of brain tumors seen in first-degree relatives for meningioma and glioma patients. It is very possible that much of the excess familial risk is a consequence of co-inheritance of multiple low-risk genetic variations. With this in mind, the aims of the studies in this thesis were to discover genetic risk variants influencing the probability of acquiring the disease and to identify the association between risk variants on the tumor phenotype. To identify genetic variants influencing meningioma risk, a comprehensive tagging of the selected genes in a case-control study was performed. We identified nine risk variants in EGF, ERBB2, and LRIG2 genes. However, these findings could not be confirmed in another larger independent dataset. In addition, the study identified a correlation between LRIG2 protein expression and ER status when analyzed with different parameters. In a separate study with a larger sample of meningioma patients, the same correlation between LRIG2 and ER status was observed. To explore the potential association between reported germline risk variants and somatic genetic events, matched tumor and blood samples from glioma patients were analyzed by SNP array. The results identified correlations between EGFR gene variants and somatic aberrations within the EGFR locus and CDKN2A/B locus. To further study the relationship between germline risk variants and tumor phenotype, the same patient material was used and analyzed by three different techniques: SNP array, IHC, and FISH. The results revealed EGFR risk variants effecting copy number variation of the EGFR gene and the expression of the IDH1 and p53. Further comparison between different techniques such as SNP array and FISH analysis revealed the difficulty in achieving consistent results with different techniques. To summarize, the glioma studies show a link between genotype and phenotype where genetic risk variants in the EGFR gene were found to be associated with specific somatic aberrations. These associations are biologically interesting because EGFR is involved in multiple cellular processes. Additional studies of the direct functional role of these observations need to be conducted to elucidate the molecular mechanisms underlying the identified association between germline gene variants and somatic aberrations. For the meningioma studies, no significant risk variants influencing the disease were found but a correlation between LRIG2 and ER status was observed. This result suggests a potential role for the LRIG protein in the pathogenesis of meningioma, but more studies are needed to confirm this hypothesizes.

Cancer research foundation in northern Sweden and Lions cancer research foundation at Umeå university

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Uyar, Ramazan [Verfasser], and Rainer [Akademischer Betreuer] Glaß. "Glioma-associated mesenchymal stem cells have profound effects on brain tumors / Ramazan Uyar ; Betreuer: Rainer Glaß." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2019. http://d-nb.info/1202011683/34.

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Kao, Chen-Yu. "Developing a Minimally Invasive Sustained Release System for Glioma Therapy." Thesis, Georgia Institute of Technology, 2007. http://hdl.handle.net/1853/19757.

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Malignant brain tumor is one of the most lethal forms of cancers. In the United States alone, approximately 20,500 new cases of primary malignant brain and central nervous system tumors are expected to be diagnosed in 2007 with 12,740 deaths estimated. Treatment of malignant brain tumor remains a major challenge despite recent advance in surgery and other adjuvant therapies, such as chemotherapy. The failure of potential effective chemotherapeutics for brain tumor treatment is usually not due to the lack of potency of the drug, but rather can be attributed to lack of therapeutic strategies capable of overcoming blood brain barrier for effective delivery of drug to the brain tumor. In this thesis, we developed a minimally invasive sustained release system for glioma therapy. The present study was initiated in an effort to incorporated Doxorubicin (DOX) loaded PLGA particle into an agarose gel, which can provide a continuous release of DOX locally to the tumor site. DOX, a toposiomearase II inhibitor, is not currently used clinically for brain tumor treatment because when delivered systemically it does not cross BBB. Our hydrogel particle system can overcome this shortcoming of DOX. The results from this study demonstrate that the DOX/PLGA particle gel system can maintain the bioactivity of DOX and sustained release DOX for at least 15 day in vitro. The result of in vivo study showed the DOX/PLGA particle gel treated group had significantly extend the medium survival of 9L glioma bearing rat from 21 days to 29 days. Therefore, the success experience of this local and sustained delivery device might benefit the development of future glioma therapy strategy.
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Books on the topic "Glioma tumors"

1

Gliomas. Berlin: Springer, 2009.

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Yamanaka, Ryuya. Glioma: Immunotherapeutic approaches. New York, N.Y: Springer Science+Business Media, 2012.

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G, Broggi, and Gerosa M. A, eds. Cerebral gliomas: Proceedings of the International Workshop on Brain Tumors, held in Santa Margherita Ligure, Italy, 20-22 June 1988. Amsterdam: Excerpta Medica, 1989.

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P, Rock Jack, ed. The practical management of low-grade primary brain tumors. Philadelphia: Lippincott Williams & Wilkins, 1999.

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1940-, Tabuchi K., ed. Biological aspects of brain tumors: Proceedings of the 8th Nikko Brain Tumor Conference, Karatsu (Saga) 1990. Tokyo: Springer-Verlag, 1991.

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Primary central nervous system tumors: Pathogenesis and therapy. New York: Humana Press, 2011.

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Hayat, M. A. Tumors of the Central Nervous System, Volume 2: Gliomas: Glioblastoma (Part 2). Dordrecht: Springer Science+Business Media B.V., 2011.

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Hayat, M. A. Tumors of the Central Nervous System, Volume 1: Gliomas: Glioblastoma (Part 1). Dordrecht: Springer Science+Business Media B.V., 2011.

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Binding distribution and cellular uptake of Na2B12H11SH (BSH) in tumor tissue of glioma patients: Investigations for boron neutron capture therapy. Aachen: Shaker, 1997.

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Omlor, Georg H. Isolated hyperthermic limb perfusion. New York: Springer-Verlag, 1995.

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Book chapters on the topic "Glioma tumors"

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Liu, Dongyou. "Chordoid Glioma, Angiocentric Glioma, and Diffuse Midline Glioma." In Tumors and Cancers, 31–36. Boca Raton : Taylor & Francis, 2018. | Series: Pocket guides to biomedical sciences | “A CRC title, part of the Taylor & Francis imprint, a member of the Taylor & Francis Group, the academic division of T&F Informa plc.”: CRC Press, 2017. http://dx.doi.org/10.1201/9781315120522-6.

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Noureldine, Mohammad Hassan A., Nir Shimony, and George I. Jallo. "Diffuse Midline Glioma – Diffuse Intrinsic Pontine Glioma." In Brainstem Tumors, 159–93. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-38774-7_8.

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Tabatabai, Ghazaleh. "Infiltrative Glioma." In Malignant Brain Tumors, 243–49. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-49864-5_16.

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Hatanaka, H. "Boron-Neutron Capture Therapy for Tumors." In Glioma, 233–49. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-84127-9_18.

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Virgin, Frank W., and Reza Rahbar. "Nasal Glioma." In Pediatric Head and Neck Tumors, 171–74. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-8755-5_22.

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Karajannis, Matthias A., Matija Snuderl, Brian K. Yeh, Michael F. Walsh, Rajan Jain, Nikhil A. Sahasrabudhe, and Jeffrey H. Wisoff. "High-Grade Glioma, Including Diffuse Intrinsic Pontine Glioma." In Brain Tumors in Children, 193–221. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-43205-2_9.

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Kobets, Andrew J., and James T. Goodrich. "History of Brainstem Glioma Surgery." In Brainstem Tumors, 1–40. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-38774-7_1.

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Deutsch, Melvin. "Cerebral Hemisphere Glioma." In Management of Childhood Brain Tumors, 325–42. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4613-1501-8_12.

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Kortmann, Rolf-Dieter, and Arnold C. Paulino. "Low-Grade Glioma." In Radiation Oncology for Pediatric CNS Tumors, 189–211. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-55430-3_10.

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Bradley, Julie A., Ronny L. Rotondo, and Daniel J. Indelicato. "Optic Pathway Glioma." In Radiation Oncology for Pediatric CNS Tumors, 213–28. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-55430-3_11.

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Conference papers on the topic "Glioma tumors"

1

Day, Emily S., Linna Zhang, Nastassja A. Lewinski, Patrick A. Thompson, Rebekah A. Drezek, Susan M. Blaney, and Jennifer L. West. "Photothermal Therapy of Glioma in a Mouse Model With Near-Infrared Excited Nanoshells." In ASME 2010 First Global Congress on NanoEngineering for Medicine and Biology. ASMEDC, 2010. http://dx.doi.org/10.1115/nemb2010-13179.

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Glioblastoma multiforme is the most common and aggressive primary brain tumor, with median survival of approximately 10 months and only 5% of patients surviving greater than 5 years after treatment (1). Surgery and radiotherapy are the main treatment modalities for primary brain tumors, but the associated risks are high when infiltrative tumors are positioned near sensitive regions in the brain. Nanoshells, nanoparticles characterized by a spherical silica core and a gold shell, may provide the opportunity to treat brain tumors in a minimally invasive manner, reducing the risk associated with treatment. Upon exposure to a near-infrared laser, nanoshells convert light energy into heat that can thermally ablate cancerous cells (2). Targeted photothermal ablation of human glioma and medulloblastoma cells has already been demonstrated with this technique in vitro (3).
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Torquette, Sarah Louredo, Bruno Henrique Gonçalves Almada, Juliana Vieira Queiroz Almeida, and Sérgio Augusto Vieira Cançado. "Case Report: High-grade glioma resection in the Broca area without functional loss." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.305.

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Context: The Broca’s (BA) and Wernicke’s Area (WA) are fundamental for the language function. Surgical interventions in proximal areas can cause functional deficits. The left brain (LB) contains BA and WA in 92.5-97% of the right-handed individuals and 2/3 of the left-handed. The mapping of these functional areas is done with functional magnetic resonance (fMRI), which identifies which cerebral hemisphere is responsible for to the language function. In slow-growing tumor lesions, there might be plasticity in these areas, which allows tumor resection with functional recovery. In high-grade tumors, growth is fast and there is usually no significant plasticity. This article aims to demonstrate that even in high-grade tumors, brain plasticity in language areas can occur. Case report: T.R.P., male, 20 years old, right-handed, with type-2 neurofibromatosis. Evaluated due to the epileptic seizure with a lesion suggestive of high-grade glioma (IV-WHO) affecting the lower frontal gyrus in magnetic resonance imaging. Results: Undergoing surgical resection with awake craniotomy for functional language mapping. Functional studies have shown that the anatomical area corresponding to BA had no function and was surgically removed. T.R.P. evolved without functional deficits and fMRI showed complete resection of the Broca’s area and the anatomo-pathological exam confirmed that the tumor was a high-grade Glioma (IV-WHO). Conclusions: Even in the presence of a fast-growing lesion, the possibility of brain plasticity in the language areas should be considered. When plasticity is found, complete resection of the tumor is possible using invasive brain mapping, which has a direct impact on prognosis and survival.
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Dutra, Milla Giancristofaro, Bernardo Valle Zanetti, Ana Luiza Badini Tubenchlak, Bárbara Gomes Muffato, Leonardo Moreira Dutra, Maria Clara Lopes Resende, Mariana Vanon Moreira, and Yves Henrique Faria Dias. "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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Silva, Pedro Felipe Camelo Correa Alves Ferreira e., Gustavo Ferreira Martins, Eduardo Augusto Guedes de Souza, Renato Miguel Rezende, Karine Cin Assenço, Yuri José Almeida da Silva, João Cícero Lima Vale, et al. "Dejérine-Roussy syndrome associated with unilateral thalamic glioma." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.594.

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Context: Déjérine-Roussy Syndrome is a rare entity that occurs after an ischemia located in the ventral posterolateral nucleus, and it is characterized by hemiplegia, superficial hemianesthesia, mild hemiataxia and astereognosis, pain on the paretic side and choreoathetosis movements. This unusual condition can be caused by haemorrhage or neoplasm. Thalamic tumors make up less than 5% of all intracranial tumors. The rare clinical presentation of a thalamic tumor is a diagnostic and therapeutic challenge for neurology and neurosurgery practice and generally requires treatment without biopsy. Case report: A 54-years-old man presented complaining of burning and tingling paraesthesias, decreased sensitivity in left dimidium, associated with decreased visual acuity in the left eye. Physical examination showed complete left hemiparesis provided grade 4-, normoreflexia with athetoid movements of the left arm and hand, painful, thermal hemihipoesthesia and epicritic touch, allodyne in the left hemibody, pressure sensitivity present globally, visual campimetry by confrontation with heteronymous hemianopia without changes in the cranial nerves. Magnetic Resonance Imaging of the Skull Base showed an oval mass, with hyposignal in T1 and hypersignal in T2 and FLAIR, with peripheral contrast uptake in the thalamus and nuclei from the right base. The patient showed good clinical-surgical evolution after surgery with Glasgow Outcome Scale 4 and modified Rankin scale 2. Anatomical Pathology confirmed low-grade glioma. Conclusions: Early diagnosis and immediate therapy can delay a fatal outcome or decrease treatment-related morbidity.
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Pishko, Gregory L., Morad Nasseri, Seymur Gahramanov, Leslie L. Muldoon, and Edward A. Neuwelt. "Blood-Tumor Barrier Normalization Effects on Cytotoxic Drug Delivery to Brain Tumors." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14648.

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The blood-brain barrier (BBB) restricts delivery of anti-cancer drugs to brain tumors, but the leaky neovasculature of the blood-tumor barrier (BTB) permits systemically delivered cytotoxic agents to reach the tumor. Anti-angiogenic therapies such as bevacizumab (BEV) have been shown to “normalize” brain tumor vasculature,1 but the impact on chemotherapy delivery remains unclear.2 The goal of this study was to use magnetic resonance imaging (MRI) to investigate the consequences of BTB normalization, via BEV, on temozolomide (TMZ) chemotherapy. Non-invasive MRI techniques were used to track the transport of a chemotherapy surrogate, a low molecular contrast agent (Gd-DTPA), in an intracerebrally implanted human glioma. MRI-derived Gd-DTPA concentration curves were fit to a transvascular exchange model to measure vascular permeability changes and were used to quantify initial area under the gadolinium curve (IAUGC) over the course of treatment.
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RM, Vinaya, and Geeta C. Mara. "Transfer Learning Approach to Detect and Classify Glioma Tumors." In 2022 8th International Conference on Advanced Computing and Communication Systems (ICACCS). IEEE, 2022. http://dx.doi.org/10.1109/icaccs54159.2022.9785206.

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Papaioannou, Thanassis, Reid C. Thompson, Babak Kateb, Oleg Sorokoumov, Warren S. Grundfest, and Keith L. Black. "Thermal imaging of brain tumors in a rat glioma model." In International Symposium on Biomedical Optics, edited by Tuan Vo-Dinh, David A. Benaron, and Warren S. Grundfest. SPIE, 2002. http://dx.doi.org/10.1117/12.466653.

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Sijilmassi, Ouafa. "MRI histogram analysis to differentiate three brain tumor types: meningioma, glioma, and pituitary tumors." In Frontiers in Optics. Washington, D.C.: Optica Publishing Group, 2022. http://dx.doi.org/10.1364/fio.2022.jtu4b.62.

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The objective of this study was to examine histogram analysis parameters derived from MRI to distinguish between different types of brain tumors according to the type of tissue in which they arise and where they are located.
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Ziegler, Jadith, Nataliya Smith, Debra Saunders, Blake Evans, James D. Battiste, Michael Sughrue, Paul Tompkins, et al. "Abstract 3267: Eltd1 as an anti-angiogenic therapy against glioma tumors." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-3267.

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Wu, Binlin, Yan Zhou, Liang Zhang, Shengjia Zhang, Xinguang Yu, Eric Wang, Ke Zhu, Cheng-hui Liu, and Robert R. Alfano. "Glioma Tumors Classified using Visible Resonance Raman Spectroscopy and Machine Learning." In Frontiers in Optics. Washington, D.C.: OSA, 2020. http://dx.doi.org/10.1364/fio.2020.jw6a.17.

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