Дисертації з теми "Glioma Cell Lines"
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Gee, Abigail Louise. "Proton beam irradiation of glioma cell lines in vitro." Thesis, University of Liverpool, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.439489.
Повний текст джерелаFlorian, Catarina Ligia. "Proton nuclear magnetic resonance studies of human glioma cell lines." Thesis, University College London (University of London), 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.309218.
Повний текст джерелаFerreira, Matthew Thomas. "Analysis of how the production and activity of PGD2 affects glioma cell lines." Universidade de São Paulo, 2015. http://www.teses.usp.br/teses/disponiveis/42/42134/tde-10042015-120110/.
Повний текст джерелаA Organização Mundial de Saúde classifica glioblastoma (GBM) como um astrocitoma tipo IV, fazendo uns dos tumores mais fatais que existe. A pesar dos avanços em quimioterapia, cirurgia e radioterapia que melhoram a longevidade de sobrevivência, a trajetória geral da doença permanece imutável. Tem sido demonstrado que células de GBM produzem níveis significativos de prostaglandinas, incluindo prostaglandina D2 (PGD2). PGD2 possui propriedades pro- e anti-tumorigenicos. Então, um entendimento mais completo da atividade de PGD2 em GBM pode gerar tratamentos mais efetivos. Através de técnicas como RT-PCR, imunohistoquimicas e HPLC espectrometria de massa em tandem, conseguimos confirmar a presença da síntese de PGD2 em linhagens de GBM. Tratamos linhagens de GBM com concentrações variáveis de PGD2 exógeno durante 72 horas e observamos seus efeitos na contagem de células, apoptose, mitose e viabilidade. Nossos resultados sugerem que PGD2 possui funções opostas em GBM dependendo em concentração (mM PGD2 vs. nM PGD2) e ativação de receptores.
Giegerich, Anna [Verfasser], Eric Thomas [Gutachter] Hahnen, and Thorsten [Gutachter] Simon. "Identification of CD133-positive cell populations within glioma cell lines / Anna Giegerich ; Gutachter: Eric Thomas Hahnen, Thorsten Simon." Köln : Deutsche Zentralbibliothek für Medizin, 2021. http://d-nb.info/1236928091/34.
Повний текст джерелаMoore, Casey Benjamin. "Cell cycle affects accumulation of β-D-5-o-Carboranyl-2'-Deoxyuridine(D-CDU) in human glioma cell line". Thesis, Georgia Institute of Technology, 2002. http://hdl.handle.net/1853/16348.
Повний текст джерелаCILIBRASI, CHIARA. "CHROMOSOMAL INSTABILITY IN GLIOMA STEM CELL LINES FROM GLIOBLASTOMA MULTIFORME: IMPLICATIONS FOR NEW THERAPEUTIC STRATEGIES." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2017. http://hdl.handle.net/10281/158150.
Повний текст джерелаGlioblastoma is the most common primary malignant brain tumour in the adult population. Despite multimodality treatment with surgery, radiotherapy and chemotherapy, outcomes are very poor, with less than 15% of patients alive after two years. Increasing evidence suggests that Glioma stem cells (GSCs) are likely to play an important role in the biology of this disease and are involved in treatment resistance and tumour recurrence following standard therapy. GSCs are characterized by enhanced self-renewal, highlighted by the expression of stem cell markers, such as CD133 and Nestin, elevated invasive behaviour, chemo and radiotherapy resistance, and the ability to generate multi-lineage progenities. A typical feature of GSCs is also the elevated chromosomal instability (CIN): they are characterized by various numerical and structural aberrations, deletions, amplification and loss of heterozygosity. A variety of alterations have been proposed as being responsible for CIN, including defects in genes involved in the regulation of the mitotic machinery, such as the Aurora Kinases, making them a promising therapeutic target for GSCs depletion. My thesis address two main aspects of this research area, aiming at the identification of new GSCs-targeted therapeutic strategies for GBM complete eradication. In the first part of my project I investigated the effect of Danusertib, a pan-Aurora kinases inhibitor on 5 GSC lines isolated from glioblastoma patients, previously characterized in our laboratory from a cytogenomic and epigenomic point of view. Results showed that response to Danusertib exposure was heterogeneous among GSC lines. Some of them were more sensitive to subtle changes in Aurora kinases activity, which result in huge morphological alterations, a rapid increase in polyploidy and subsequently in senescence, with a consistent reduction in clonogenic survival and proliferation. Interestingly I also observed that the more resistant cell lines showed an increase in ploidy and senescence after repeated rounds of Danusertib exposure, suggesting that there could be the presence of an intolerable ploidy threshold that leads cells to senescence. In the second part of my thesis I presented some preliminary results I achieved in Dr Hochegger’s lab (Genome Damage and Stability Center, University of Sussex, Brighton, UK), where I took part in a project aimed on setting up CrispR/Cas9 mediated GFP or RFP-tagged CD133 (PROM1 gene) and Nestin (NES gene) glioma stem cell lines in order to look, with live cell imaging techniques, for signs for asymmetric cell division, by which a single GSC would be able to both maintain a pool of self-renewing stem cells and produce differential progeny, using live cell imaging. The biological significance of asymmetric or symmetric division modes is not yet fully understood, but improved understanding of this phenomenon may lead to the development of preventative treatments or improved therapeutic options for brain tumour patients through the identification of novel targets that are involved in the control of asymmetric cell division in human brain tissue.
Stutzman, Alan. "The effect of Neuregen nutrient medium on the growth of rat glioma cell lines F98 and 9L /." Available to subscribers only, 2007. http://proquest.umi.com/pqdweb?did=1456287431&sid=9&Fmt=2&clientId=1509&RQT=309&VName=PQD.
Повний текст джерела"Department of Molecular Biology, Microbiology and Biochemistry." Includes bibliographical references (leaves 109-126). Also available online.
Tassone, Evelyne. "Extracellular matrix-degrading enzymes and control of fibroblast growth factor-2 (FGF-2) signaling in pediatric glioma cell lines." Doctoral thesis, Università degli studi di Padova, 2012. http://hdl.handle.net/11577/3422194.
Повний текст джерелаL’obiettivo principale del mio progetto di ricerca è stato analizzare il ruolo di due enzimi che degradano la matrice extracellulare, l’“heparanase” (HPSE) e la “membrane-type 1 matrix metalloproteinase” (MT1-MMP), nei gliomi pediatrici. Ho trascorso i primi due anni di Dottorato nel laboratorio del Dott. Maurizio Onisto (Università di Padova). Ho poi continuato il mio lavoro presso la New York University School of Medicine, sotto la supervisione del Prof. Paolo Mignatti, il cui lavoro sperimentale è focalizzato sull’approfondimento dei meccanismi molecolari alla base dell’attivazione del segnale intracellulare da parte di MT1-MMP e del suo inibitore fisiologico, il “tissue inhibitor of metalloproteinases-2” (TIMP-2). I gliomi, i più comuni tumori cerebrali primari, comprendono un gruppo eterogeneo di neoplasie che originano dalle cellule gliali. Nonostante i recenti progressi raggiunti nel trattamento e nel controllo di tali tumori, la prognosi dei bambini affetti da glioma, ed in particolare dalle sue forme più aggressive, rimane tuttora infausta. Pur essendo confinati nell’organo nel quale originano, i gliomi possono invadere tutte le aree del cervello. Uno degli eventi più importanti che caratterizzano l’invasività dei gliomi è costituito dalla degradazione della matrice extracellulare, un complesso meccanismo che coinvolge enzimi sia glicosidici sia proteolitici. HPSE è una endo-β-D-glucuronidasi secreta nella matrice extracellulare, nella quale taglia le catene di eparan solfato dei proteoglicani solubili e legati alla membrana. MT1-MMP, una proteasi legata alla membrana e composta da un dominio catalitico extracellulare e da una piccola coda citoplasmatica, è coinvolta nella degradazione proteolitica di proteine extracellulari e di membrana. Elevati livelli di HPSE e MT1-MMP sono stati riscontrati in numerosi tipi di tumore e tale evidenza sottolinea il ruolo chiave che essi svolgono nell’invasività tumorale e nella formazione di metastasi. In questo studio sono state caratterizzate cinque linee cellulari di glioma pediatrico derivanti da diversi tipi di glioma: due glioblastomi multiformi, un astrocitoma anaplastico, un astrocitoma diffuso ed un astrocitoma pilocitico. Con lo scopo iniziale di esaminare il ruolo di MT1-MMP nell’attivazione del segnale indotto dall’FGF-2, è stata inoltre utilizzata una linea cellulare di carcinoma mammario, la quale non esprime MT1-MMP e perciò rappresenta un modello ideale per studiare la regolazione della sua espressione. I dati riportati mostrano che, nelle cellule di carcinoma mammario, MT1-MMP regola l’attivazione del segnale intracellulare da parte del “fibroblast growth factor-2” (FGF-2) e controlla il legame di questo fattore di crescita alla superficie delle cellule. Nelle cellule di astrocitoma pediatrico non è stata identificata alcuna chiara correlazione tra espressione di HPSE, MT1-MMP o FGF-2 ed aggressività tumorale. I risultati inoltre dimostrano che il silenziamento genico di HPSE in una linea cellulare di glioblastoma pediatrico non influenza l’espressione del “vascular endothelial growth factor” (VEGF) o la proliferazione cellulare, ma determina la sovraespressione della “matrix metalloproteinase-2” (MMP-2) e di MT1-MMP. Inoltre, nelle cellule di glioma, l’attivazione di ERK1/2 da parte di FGF-2 non correla con l’espressione di MT1-MMP e risulta modificata dal trattamento con un inibitore di MMP. Infine, in tutte le cellule di glioma, anche TIMP-2 regola l’attivazione del segnale intracellulare. In conclusione, i risultati ottenuti mostrano che MT1-MMP non ha gli effetti nelle cellule di carcinoma mammario e di glioma pediatrico, indicando l’esistenza di un differente e più complesso meccanismo di controllo del segnale intracellulare. La caratterizzazione delle linee cellulari di astrocitoma pediatrico presentata in questa tesi offre una più completa conoscenza di questo gruppo di tumori ancora poco studiati.
BARONCHELLI, SIMONA. "Cytogenetic, genimic, epigenomic and drug sensitivity landscapes to unravel the complexity of glioma stem cell lines: a multi-level approach." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2011. http://hdl.handle.net/10281/27138.
Повний текст джерелаHammerbacher, Katharina [Verfasser], and Ralf [Akademischer Betreuer] Kinscherf. "Effects of novelly synthesized nucleolipides on different tumor cell lines (HT29, HepG2, Panc-1, RenCa) with special respect to glioma cell lines (BT4Ca, GOS3, G28, G112, U251, U87) of human or other species / Katharina Hammerbacher ; Betreuer: Ralf Kinscherf." Marburg : Philipps-Universität Marburg, 2020. http://d-nb.info/120746967X/34.
Повний текст джерелаNoë, Adrian J. (Adrian James). "Characterization of the transport of sarcosinamide chloroethylnitrosourea by the catecholamine extraneuronal uptake2 carrier in human glioma cell lines and its relation to its selective cytotoxicity." Thesis, McGill University, 1996. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=40413.
Повний текст джерелаLundblad, Dan. "Studies on the antiproliferative action of interferon : effects on proteins synthesized in the G1 and S phase of the cell cycle in 2 anchorage-dependent cell lines." Doctoral thesis, Umeå universitet, Molekylärbiologi (Teknat- och Medfak), 1991. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-100575.
Повний текст джерелаDiss. (sammanfattning) Umeå : Umeå universitet, 1991, härtill 6 uppsatser
digitalisering@umu
Keßler, Jaqueline Verfasser], Ralph [Akademischer Betreuer] Golbik, Dirk [Akademischer Betreuer] Vordermark та Daniel [Akademischer Betreuer] [Zips. "Effect of molecular markers HIF-1α and IDH1 on the radiobiological behavior of human malignant glioma cell lines in normoxia and hypoxia / Jaqueline Keßler ; Ralph Golbik, Dirk Vordermark, Daniel Zips". Halle, 2016. http://d-nb.info/1118500555/34.
Повний текст джерелаKenney-Herbert, Emma Mary. "Molecular and cellular characterisation of human glioblastoma tumour-initiating cell lines." Thesis, University of Cambridge, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.608958.
Повний текст джерелаSilva, Roseli da. "Expressão gênica da família das lisil oxidases e papel funcional de LOX em astrocitomas." Universidade de São Paulo, 2014. http://www.teses.usp.br/teses/disponiveis/5/5138/tde-12012015-091413/.
Повний текст джерелаThe development and invasion of primary brain tumors are directly influenced by the extracellular matrix. Considering that lysyl oxidase (LOX) and other lysyl oxidase family members (LOXL1, LOXL2, LOXL3 e LOXL4) have both structural and functional complexity and that they are involved in vital biological processes such as cell motility, cell signaling and gene regulation, a deregulation of these proteins can lead to the genesis and tumor progression. This study aimed to evaluate the expression levels of genes that code for the lysyl oxidase family members in astrocytomas of different malignant grades and to correlate to the expression of BMP1 and HIF1A, IDH1 mutation and overall patients\' survival. Moreover, protein expression coded by these genes was also analyzed, besides an in vitro functional study of LOX role in astrocytomas. Gene expression analysis was performed by quantitative real-time PCR in a series of 153 astrocytomas and 22 samples of non-neoplastic brain. Protein expression was analyzed by immunohistochemistry in astrocytoma samples. LOX knockdown was performed in cells of human glioblastoma U87MG and A172 transfected with siRNA. Expression levels of all genes (LOX, LOXL1, LOXL2, LOXL3, LOXL4, BMP1 e HIF1A) increased with the malignant grade of astrocytomas, glioblastomas presenting the higher levels. Positive correlations of gene expression values were observed specially in glioblastomas. Only LOXL3 expression impacted in the overall survival of glioblastoma cases. Patients with higher expression presented longer survival time than those with lower LOXL3 expression. Astrocytoma grade II cases with IDH1 mutation presented lower LOXL1 and LOXL4 expression when compared to those cases with wild type IDH1. On the other hand, GBM cases with IDH1-mutated presented lower LOX and LOXL1 expression than GBM cases without IDH1 mutation. Protein expression levels of lysyl oxidase family members were also higher in glioblastoma samples, with both nuclear and cytoplasmic localization, and also endothelium staining. Interestingly, a glioblastoma case with IDH1-mutated had lower LOX expression, including endothelial cells. For functional analysis, LOX knockdown by siRNA and treatment with inhibitor BAPN of U87MG and A172 cell lines affected migration behavior. Furthermore, lower LOX expression affected invasion capacity and anchorage independent growth. Altogether, these results corroborate LOX role in important processes of astrocytoma tumorigenesis. Additionally, LOX expression is influenced by IDH1 mutational status in glioblastomas. Therefore, our work provides new insights for possible therapeutic interventions for patients with astrocytomas
Rabah, Yasmine. "Satellite glial cell-proprioceptor interactions in dorsal root ganglia Characterization of transgenic mouse lines for selectively targeting glial cells in dorsal root ganglia Satellite glial cells modulate proprioceptive neuron function." Thesis, Sorbonne Paris Cité, 2018. http://www.theses.fr/2018USPCB208.
Повний текст джерелаProprioceptive neurons (one’s own neurons) are necessary for controlling motor control and locomotion. They arise from muscle spindles and tendons and synapse onto ventral horn motoneurons to deliver information about the length and contraction of muscles. Proprioceptor somata reside within the dorsal root ganglia (DRG) and are tightly enwrapped in a thin sheath of GFAP-expressing glial cells, called satellite glial cells (SGCs). Interestingly, SGCs express a number of Gq protein- coupled receptors (Gq GPCRs), which can be activated by neurotransmitters released by sensory neuron somata. Sensory neuron somata also express a number of receptors and transmitters. Both the expression of receptors and the close contact between SGCs and sensory neurons led to the hypothesis that these two cell types communicate. There is emerging evidence that SGCs and nociceptive sensory neuron (pain-sensing neurons) somata can communicate. Furthermore, to date, there is no study conducted on SGC-proprioceptor interaction. We hypothesized that SGC Gq GPCR signaling induces the release of neuroactive molecules from SGCs, leading to the modulation of proprioceptor activity. The main goal of this project has been to test this hypothesis using complementary technical approaches (2-photon Ca2+ imaging, immunohistochemistry, biochemistry and behavior) combined with a powerful chemogenetic DREADD-based tool to activate SGC Gq GPCR activity. We have demonstrated ex vivo that SGCs modulate proprioceptive neuron activity through a purinergic pathway. In order to test the physiological relevance of this discovery in vivo, we performed sensorimotor behavioral experiments and have shown that activating GFAP-expressing glial cells induces sensorimotor deficits. Determining whether SGC-induced proprioceptor activity has profound implications in the understanding of sensorimotor functions in health and diseases
Pernod, Gilles. "Propriétés pro-fibrinolytiques des cellules de la lignée gliomateuse C6 : implication dans la survenue d'hémorragie intra-tumorale." Université Joseph Fourier (Grenoble ; 1971-2015), 1998. http://www.theses.fr/1998GRE10230.
Повний текст джерелаCraperi, Delphine. "Thérapie génique des gliomes : caractérisation des voies cytotoxiques déclenchées par le système thymidine kinase herpétique/ganciclovir." Université Joseph Fourier (Grenoble ; 1971-2015), 1998. http://www.theses.fr/1998GRE10073.
Повний текст джерелаHuang, Yan. "Comparative cellular uptake studies of a carborane cholesteryl ester by human glioma cell lines." 2003. http://purl.galileo.usg.edu/uga%5Fetd/huang%5Fyan%5F200312%5Fms.
Повний текст джерелаBhargava, Shruti. "Panoramic View of RNA Binding Proteins (RBPs) in Glioblastoma : IMP3, an RBP, is Essential for Glioma Stem-like Cell Maintenance." Thesis, 2016. https://etd.iisc.ac.in/handle/2005/4377.
Повний текст джерела李漢傑. "Mitogenic response of malignant glioma cell lines of Chinese brain to three growth factors in the serum-free medium and chromosome karyotypic analysis." Thesis, 1991. http://ndltd.ncl.edu.tw/handle/81136925488536161919.
Повний текст джерелаCurtis, VF, H. Wang, P. Yang, RE McLendon, X. Li, QY Zhou, and XF Wang. "A PK2/Bv8/PROK2 antagonist suppresses tumorigenic processes by inhibiting angiogenesis in glioma and blocking myeloid cell infiltration in pancreatic cancer." Thesis, 2013. http://hdl.handle.net/10161/4982.
Повний текст джерелаDissertation
Deng, Lingxiao. "Regeneration and plasticity of descending propriospinal neurons after transplantation of Schwann cells overexpressing glial cell line-derived neurotrophic factor following thoracic spinal cord injury in adult rats." 2015. http://hdl.handle.net/1805/7347.
Повний текст джерелаAfter spinal cord injury (SCI), poor axonal regeneration of the central nervous system, which mainly attributed to glial scar and low intrinsic regenerating capacity of severely injured neurons, causes limited functional recovery. Combinatory strategy has been applied to target multiple mechanisms. Schwann cells (SCs) have been explored as promising donors for transplantation to promote axonal regeneration. Among the central neurons, descending propriospinal neurons (DPSN) displayed the impressive regeneration response to SCs graft. Glial cell line-derived neurotrophic factor (GDNF), which receptor is widely expressed in nervous system, possesses the ability to promote neuronal survival, axonal regeneration/sprouting, remyelination, synaptic formation and modulate the glial response. We constructed a novel axonal permissive pathway in rat model of thoracic complete transection injury by grafting SCs over-expressing GDNF (SCs-GDNF) both inside and caudal to the lesion gap. Behavior evaluation and histological analyses have been applied to this study. Our results indicated that tremendous DPSN axons as well as brain stem axons regenerated across the lesion gap back to the caudal spinal cord. In addition to direct promotion on axonal regeneration, GDNF also significantly improved the astroglial environment around the lesion. These regenerations caused motor functional recovery. The dendritic plasticity of axotomized DPSN also contributed to the functional recovery. We applied a G-mutated rabies virus (G-Rabies) co-expressing green fluorescence protein (GFP) to reveal Golgi-like dendritic morphology of DPSNs and its response to axotomy injury and GDNF treatment. We also investigated the neurotransmitters phenotype of FluoroGold (FG) labeled DPSNs. Our results indicated that over 90 percent of FG-labeled DPSNs were glutamatergic neurons. DPSNs in sham animals had a predominantly dorsal-ventral distribution of dendrites. Transection injury resulted in alterations in the dendritic distribution, with dorsal-ventral retraction and lateral-medial extension of dendrites. Treatment with GDNF significantly increased the terminal dendritic length of DPSNs. The density of spine-like structures was increased after injury and treatment with GDNF enhanced this effect.