Dissertationen zum Thema „Ependymomas“
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TIXIER, THIERRY. „Les ependymomes sous-cutanes sacrococcygiens“. Clermont-Ferrand 1, 1990. http://www.theses.fr/1990CLF13076.
Der volle Inhalt der QuelleEicker, Monika. „Monosomie 22 in Ependymomen“. [S.l. : s.n.], 2007. http://nbn-resolving.de/urn:nbn:de:bsz:289-vts-58938.
Der volle Inhalt der QuelleKilday, John-Paul. „Genomic and epigenetic characterisation of childhood ependymoma“. Thesis, University of Nottingham, 2011. http://eprints.nottingham.ac.uk/12553/.
Der volle Inhalt der QuelleTourbez, Arthur. „Développement et caractérisation d'organoïdes de tumeurs cérébrales pédiatriques utilisés en recherche fondamentale et translationnelle“. Electronic Thesis or Diss., Lyon 1, 2023. https://n2t.net/ark:/47881/m6416x50.
Der volle Inhalt der QuellePediatric high-grade gliomas (pHGG) and posterior fossa type A ependymomas (EPN-PFA) remain one of the biggest challenges in pediatric oncology. They exhibit vast inter- and intra-tumoral heterogeneity, complicating the development of effective therapeutic strategies. Then to improve their clinical outcome, we absolutely need pre-clinical models that recapitulate key features of their corresponding parental tumors. During my PhD, I developed an optimized protocol for the establishment and biobanking of pHGG organoids (pHGG_O) and EPN-PFA organoids (EPN-PFA_O). These models can be grown long-term and comprehensive histological and molecular analyses showed that they recapitulate inter- and intra-tumoral heterogeneity of their parental tumor even after several passages and cryopreservation as 3D cultures. I further showed that they can be employed to test responses to standard of care therapy as well as new therapeutic options, including drugs from clinical trials as they accurately capture the clinical phenotypes of their respective parental tumors. Moreover, these models led to the identification of the DRD2 inhibitor ONC201 as an unexpected potential therapeutic agent for H3K27M non-altered pediatric brain tumors and helped identify combination strategies to increase the therapeutic response to ONC201. Thus, those models are positioned to support powerful and innovative preclinical studies, particularly those related to personalized assessments of treatment response profiles and identification of novel efficient drug combinations
Sabnis, Durgagauri. „An investigation of druggable prognostic markers in paediatric ependymoma“. Thesis, University of Nottingham, 2016. http://eprints.nottingham.ac.uk/33243/.
Der volle Inhalt der QuelleTALIK, ZYGART NATHALIE. „Les ependymomes intracraniens de l'enfant : a propos de 27 observations“. Lille 2, 1989. http://www.theses.fr/1989LIL2M382.
Der volle Inhalt der QuelleAndreiuolo, Felipe. „Target in context : molecular pathology of pediatric ependymoma and high grade glioma“. Phd thesis, Université Paris Sud - Paris XI, 2012. http://tel.archives-ouvertes.fr/tel-00913042.
Der volle Inhalt der QuelleFeuß, Mareike [Verfasser]. „Die mikrochirurgische Therapie des cerebralen und spinalen Ependymoms / Mareike Feuß. Medizinische Fakultät“. Bonn : Universitäts- und Landesbibliothek Bonn, 2011. http://d-nb.info/1017916136/34.
Der volle Inhalt der QuelleLABORIEUX, ANY. „Ependymomes intracraniens de l'enfant : revue de la litterature a propos de deux cas“. Nice, 1990. http://www.theses.fr/1990NICE6531.
Der volle Inhalt der QuelleGENESTIN, ELISABETH. „Ependymome pan-medullaire : etude clinique du 7eme cas de la litterature, et apports des techniques nouvelles“. Lille 2, 1989. http://www.theses.fr/1989LIL2M241.
Der volle Inhalt der QuelleRitzmann, Timothy. „Recurrent paediatric ependymoma : a multicentre analysis of clinical features and tumour biology in the molecular era“. Thesis, University of Nottingham, 2018. http://eprints.nottingham.ac.uk/51719/.
Der volle Inhalt der QuelleSzathmari, Alexandru. „Étude du transcriptome dans les tumeurs périventriculaires du système nerveux central : recherche des marqueurs diagnostiques et pronostiques“. Thesis, Lyon 1, 2010. http://www.theses.fr/2010LYO10037.
Der volle Inhalt der QuelleNeurosurgery of periventricular tumors, especially of pineal region tumors, is well developed at the Neurosurgical Hospital in Lyon. Taking opportunity of this background, our objective was identification of new diagnostic markers for each of these tumors using microarray transcriptome analysis, characterisation of a pleomorphic pineal parenchyma tumor (PPT) subtype, evaluation of melatonin synthesis in PPTs and the microarray analysis of molecular signature of some of circumventricular organs (CVO) after their laser microdissection in rat. The microarray analysis of periventricular tumors allowed molecular classification of the tumours and revealed different diagnostic markers for each type of tumors. Potentially new prognostic candidate genes (HoxD13, Prame, CD24 and Pou4f2 and Aurora kinase B pathway genes) are proposed for improvement of PPT classification. A PPT multicenter study allowed the characterisation of a pleomorphic subtype frequently managed as a higher grade tumour in the literature. The study of PPT ex vivo and in vivo showed their preserved capacity for melatonin production. However a stable PPT cell line culture could not be obtained. The laser microdissection of OCV in rat, sometimes vestigial in humans and potentially at the origin of the periventricular tumors, associated with a microarray study highlighted some potentially new or already described specific markers of these structures
Bonhns, Michalowski Mariana. „Étude des altérations épigénétiques des tumeurs des enfants : le cas des épendymomes et des neuroblastomes“. Université Joseph Fourier (Grenoble), 2006. http://www.theses.fr/2006GRE10210.
Der volle Inhalt der QuelleDuring the last 10 years, a new mechanism of tumor development has been described: the hypermethylation of tumor suppressor genes. These epigenetic modifications were rarely studied in childhood cancer and large series of patients didn't exist before 2003. We studied two groups of childhood tumors; ependymoma and neuroblastome. Ependymomas (EP) represent the third most frequent type of central nervous system (CNS) tumor of childhood. No prognostic biological markers are available, and differentiation from choroid plexus papilloma (CPP) is difficult. On the other hand, neuroblastoma, the most common extracranial solid cancer diagnosed in infancy and childhood, has some genetic abnormalities that are clearly related to prognosis as NMYC amplification. Our objectives were to describe a methylation profile in these two childhood cancers and try to find a relationship between genes methylation and clinical evolution. In the first study, for a sample of 27 children with intracranial EP and 7 with CPP, we described and compared the methylation status of 19 genes. On the second study, 62 neuroblastomas were studied in terms of the methylation status of the same genes. Although we did not observe a statistical relationship between methylation and clinical outcome, the methylation pattern does not appear to be randomly distributed in ependymoma and in neuroblastoma and may represent a mechanism of tumor development and evolution. Hypermethylation was related to clinical stage in neuroblastoma: stages 1, 2 and 4s were less frequently methylated than those at stages 3 and 4 (p = 0. 002). In conclusion, the results from our series indicate that hypermethylation of tumor suppressor genes may be important in the development and evolution of childhood cancers. Thus, these epigenetic alterations could be used as a marker of the disease and genes regulating methylation should be considered as possible novel therapeutic targets
Sander, Milena Lucia [Verfasser], und Matthias [Akademischer Betreuer] Reinhard. „Zerebrale Hämodynamik nach Schädelbestrahlung im Kindesalter bei Patienten mit Medulloblastom oder anaplastischem Ependymom“. Freiburg : Universität, 2020. http://d-nb.info/1205256598/34.
Der volle Inhalt der QuelleDiop, Seynabou. „Étude de la contribution maternelle d'EZHIP à la distribution de H3K27me3 au cours du développement précoce de la souris“. Electronic Thesis or Diss., Sorbonne université, 2022. https://accesdistant.sorbonne-universite.fr/login?url=https://theses-intra.sorbonne-universite.fr/2022SORUS544diff.pdf.
Der volle Inhalt der QuelleThe Polycomb machinery, through its chromatin regulating activities, maintains gene silencing of many developmental genes. Alteration of its function impairs embryonic development and is frequently reported in pathologies including cancer. We previously showed that EZHIP is a direct interactor of the Polycomb Repressive Complexe 2 (PRC2) and inhibits its enzymatic activity, thereby limiting H3K27me3 deposition. Importantly, EZHIP is primarily expressed in gametes and its knockout in mice result in reduced female fertility (Ragazzini et al 2019). Further investigating the role of EZHIP in gametes, we observed that the maternal pool of EZHIP is important to regulate a set of transiently imprinted genes in preimplantation embryos. In the absence of EZHIP, both parental alleles are expressed, in correlation with important changes with global H3K27me3 deposition. Importantly, absence of EZHIP has also important consequences on X linked gene expression. We will present our extensive characterization of transcriptome changes and H3K27me3 alterations which reveal the crucial role of EZHIP as a new maternal component of the Polycomb machinery in early mouse development
Santos, Marcos Juliano dos 1980. „A avaliação da evolução pós-operatória dos ependimomas intramedulares“. [s.n.], 2013. http://repositorio.unicamp.br/jspui/handle/REPOSIP/309592.
Der volle Inhalt der QuelleDissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas
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Resumo: Os ependimomas intramedulares são tumores de crescimento lento que acarretam déficits neurológicos progressivos e pode levar os pacientes a dependência funcional. Embora a remoção microcirúrgica seja o tratamento de escolha para a lesão, questionamento existe sobre se pacientes com apenas sinais clínicos leves devem ser submetidos a ressecções cirúrgicas radicais. Este estudo avaliou, segundo a escala funcional de McCormick, a evolução pós-operatória de uma série de vinte pacientes submetidos à ressecção microcirúrgica total para ependimomas intramedulares. A ressecção completa foi atingida em 19 dos 20 pacientes (95%), somente 1 paciente apresentou piora clínica (5%). Nos pacientes com independência funcional pré-operatória, com McCormick grau I e II, não houve piora clínica e todos os tumores foram ressecados completamente. No subgrupo de pacientes grau II, a média do status funcional pós-operatória apresentou melhora estatisticamente significativa. Nenhum paciente com grau IV melhorou após o tratamento cirúrgico. O tratamento cirúrgico foi eficaz para ressecar completamente os tumores sem agregar déficits neurológicos na maioria dos pacientes. Nos pacientes com McCormick graus I e II pré-operatório a cirurgia deve ser indicada no momento do diagnóstico
Abstract: Intramedullary ependymomas are slow-growing lesions that progressively lead to neurological compromise and functional dependence. Although surgical excision is the treatment of choice for such lesions, there is questioning as to whether patients with only subtle clinical findings should be subjected to radical surgical resections. This study has evaluated according to the McCormick functional scale the surgical outcome of a series of twenty patients with intramedullary ependymomas submitted to microsurgical resection. Total surgical resection was achieved in 19 of the 20 patients (95%). Only one patient experienced clinical worsening (5%). Patients classified as McCormick grade I and II who were independent pre-operatively remained so in the post-operative period and had their tumors completely removed. In grade II patients there was a significant improvement in their post-operative status. None of the grade IV patients improved after surgical treatment. Surgical treatment has proven to be efficient in completely removing tumors without adding neurological deficits in most patients. In patients McCormick grades I and II pre-operatively surgery should be indicated early in the diagnosis
Mestrado
Neurologia
Mestre em Ciências Médicas
Pein, Anna von [Verfasser], und Christian [Akademischer Betreuer] Hagel. „Untersuchungen zur Expression von Nestin und Glykoprotein nmb in kindlichen Ependymomen / Anna von Pein ; Betreuer: Christian Hagel“. Hamburg : Staats- und Universitätsbibliothek Hamburg, 2019. http://d-nb.info/1194547915/34.
Der volle Inhalt der QuellePein, Anna von Verfasser], und Christian [Akademischer Betreuer] [Hagel. „Untersuchungen zur Expression von Nestin und Glykoprotein nmb in kindlichen Ependymomen / Anna von Pein ; Betreuer: Christian Hagel“. Hamburg : Staats- und Universitätsbibliothek Hamburg, 2019. http://nbn-resolving.de/urn:nbn:de:gbv:18-99531.
Der volle Inhalt der QuelleStein, Roland Gregor [Verfasser], und Wolfgang [Akademischer Betreuer] Roggendorf. „Immunhistochemische Marker für die Prognose und Proliferation in Ependymomen bei Kindern und Erwachsenen / Roland Gregor Stein. Betreuer: Wolfgang Roggendorf“. Würzburg : Universität Würzburg, 2012. http://d-nb.info/1102819956/34.
Der volle Inhalt der QuelleKamaly-Asl, Ian. „Molecular, genetic, patient and surgical factors involved in the development and outcome of central nervous system tumours“. Thesis, University of Manchester, 2011. https://www.research.manchester.ac.uk/portal/en/theses/molecular-genetic-patient-and-surgical-factors-involved-in-the-development-and-outcome-of-central-nervous-system-tumours(3e42d00e-b543-452e-bd71-ff53e194d944).html.
Der volle Inhalt der QuelleDünschede, Jutta [Verfasser]. „Retrospektive Analyse des postoperativen Outcome zur Diskussion des therapeutischen Vorgehens unter Beleuchtung diverser neurologischer Variablen bei Patienten mit intramedullären Ependymomen / Jutta Dünschede“. Tübingen : Universitätsbibliothek Tübingen, 2020. http://d-nb.info/1214640028/34.
Der volle Inhalt der QuelleKolevatova, Larissa [Verfasser], und Markus [Akademischer Betreuer] Glatzel. „Untersuchungen zum Epidermal-growth-factor-receptor-Status in Ependymomen : Vergleich von immunhistochemischen Färbungen und Floureszenz-in-situ-Hybridisierung / Larissa Kolevatova. Betreuer: Markus Glatzel“. Hamburg : Staats- und Universitätsbibliothek Hamburg, 2011. http://d-nb.info/1020427930/34.
Der volle Inhalt der QuelleWening, Janna [Verfasser], und Stefan [Akademischer Betreuer] Rutkowski. „Auswertung des Studienzweigs E-HIT2000 – Therapie von Kindern mit Ependymom in der prospektiven multizentrischen HIT2000 Studie / Janna Wening ; Betreuer: Stefan Rutkowski“. Hamburg : Staats- und Universitätsbibliothek Hamburg, 2019. http://d-nb.info/1175092010/34.
Der volle Inhalt der QuelleWening, Janna Verfasser], und Stefan [Akademischer Betreuer] [Rutkowski. „Auswertung des Studienzweigs E-HIT2000 – Therapie von Kindern mit Ependymom in der prospektiven multizentrischen HIT2000 Studie / Janna Wening ; Betreuer: Stefan Rutkowski“. Hamburg : Staats- und Universitätsbibliothek Hamburg, 2019. http://nbn-resolving.de/urn:nbn:de:gbv:18-94816.
Der volle Inhalt der QuelleLuzuric, Dominique. „Tumeurs intra-médullaires de l'enfant : aspect particulier de l'épendymome géant de la queue de cheval“. Montpellier 1, 1990. http://www.theses.fr/1990MON11137.
Der volle Inhalt der QuelleDe, Bustos Cecilia. „Genetic and Epigenetic Variation in the Human Genome : Analysis of Phenotypically Normal Individuals and Patients Affected with Brain Tumors“. Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-6629.
Der volle Inhalt der QuelleWild, Florian [Verfasser], und Makoto [Akademischer Betreuer] Nakamura. „Die Behandlung intraspinaler Ependymome in den letzten 20 Jahren in der Klinik für Neurochirurgie der Medizinischen Hochschule Hannover : Ergebnisse von 49 Patienten / Florian Wild. Klinik für Neurochirurgie des Zentrums Neurologische Medizin Medizinische Hochschule Hannover. Betreuer: Makoto Nakamura“. Hannover : Bibliothek der Medizinischen Hochschule Hannover, 2014. http://d-nb.info/1066605165/34.
Der volle Inhalt der QuelleAndrade, Fernanda Gonçalves de. „Estudo das alterações na expressão gênica dos ependimomas“. Universidade de São Paulo, 2014. http://www.teses.usp.br/teses/disponiveis/5/5138/tde-01092014-154140/.
Der volle Inhalt der QuelleEpendymomas are rare glial cell-derived tumors. They can be found in any central nervous system localization and despite the histological similarity, they seem to display distinct genomic abnormalities. Clinical variables are intercorrelated and they are usually unable to predict the disease course. We aimed to analyze increased gene and protein expression in ependymomas and to correlate with patients\' clinical data. We studied patients with ependymoma submitted to surgical resections at Hospital das Clinicas, University of São Paulo, from 1996 to 2011 (33 fresh-frozen samples for gene expression analysis by quantitative real-time PCR and 149 formalin-fixed, paraffin-embedded samples, relative to 121 patients due to relapses, for protein analysis by tissue microarray immunohistochemistry). Immunohistochemical reactions were analyzed semi-quantitatively and scored with a labeling index (LI) calculated as the product of the percentage of the positively stained nuclei by the intensity of staining. Eighty-one cases were adults (mean 27.2 years). There were 60 intracranial and 61 spinal cases, of which 10 tumors were myxopapillary, 92 were grade II and 19 were grade III. Gross total resection was achieved in 62% of cases and relapse was confirmed in 41.4% of cases. We observed a shorther time to relapse in children and supratentorial intracranial tumor localization (p<0.001 for both), anaplastic histology and incomplete resections (p<0.05 for both). The following genes were selected based on public SAGE database and literature: ARMC3, CCND1, CHST5, DNALI1, FGFRL1, GNA13, IGF2, MSX1, NOTCH1 and RSPH3. ARMC3, RSHL3, CHST5 and DNALI1 presented higher expression levels in intramedullary ependymomas (p < 0.05) and FGFRL1, NOTCH1 and CCND1 in supratentorial cases (p < 0.01). IGF2 presented higher expression levels in pediatric cases and CHST5 in adults cases (p < 0.05 in both). Higher expression levels of FGFRLI1 (p < 0.05), CCND1 and IGF2 (p < 0.01 for both) were observed in anaplastic histology cases. None of the genes impacted in progression free survival or overall survival of patients. The expression of protein codified by CCND1, cyclin D1, was also evaluated by immunohistochemistry, because its overexpression has been related with several types of neoplasias and its prognostic value has not yet been fully established in ependymomas. There was a correlation of cyclin D1 expression at mRNA and protein levels (p < 0.0001). Correlations between cyclin D1 and anaplastic histology and supratentorial localization were confirmed by protein analyses (p < 0.0001 for both parameters). Additionally, high expression of cyclin D1 was observed in younger patients (p < 0.01). The higher cyclin D1 expression in supratentorial tumor localization was independent of histological grade and age of patient. Relapse was more frequent in cases with higher cyclin D1 expression levels (p < 0.05) although correlation with progression free survival was just observed in gross total resection cases (p < 0.001). Ependymomas presented differential gene expression according to age, tumor localization and histological grade in our study. Determination of cyclin D1 expression levels may be useful to guide follow-up and treatment in supratentorial cases with gross total resection
Liang, Muh-Lii, und 梁慕理. „The Mechanism of MicroRNAs/mRNAs Interactomes in Pediatric High-grade Gliomas and Radio-resistance in Pediatric Ependymomas“. Thesis, 2018. http://ndltd.ncl.edu.tw/handle/5vpjng.
Der volle Inhalt der Quelle國立陽明大學
臨床醫學研究所
106
High-grade gliomas and ependymomas are two main challenging malignancies in children, and which composed of a majority of central nervous system (CNS) tumors of young patients. In addition to maximal safe surgical resection and limited efficacy of chemotherapy, the applications of adjuvant irradiation play an important role for the tumor treatment. However, in the young ages, the resistance of residual and recurrent tumor, and long-term intellectual sequelae remain the major obstacles of radiotherapy. The advancement of high-throughput next-generation sequencing and molecular clustering technologies largely promoted the study of neuro-oncology from diagnosis based molecular to therapeutic targets in the last decade. In order to identify potential targets for the development of new therapeutic strategies, we compared the miRNome and transcriptome of pediatric low- (pLGGs) and high-grade gliomas (pHGGs) using small RNA sequencing (smRNA-Seq) and gene expression microarray, respectively in the first study. Through integrated bioinformatics analyses and experimental validation, we identified miR-137 and miR-6500-3p are significantly downregulated in pHGGs. Overexpression of miR-137 or miR-6500-3p reduced cell proliferation in two pHGG cell lines, SF188 and UW479. We also identified mRNA/miRNA interactions and confirmed that CENPE, KIF14 and NCAPG levels were direct targets of miR-137 or miR-6500-3p and were significantly higher in pHGGs than pLGGs. Furthermore, knockdown of CENPE, KIF14 or NCAPG combined with temozolomide treatment resulted in a combined suppressive effect on pHGG cell proliferation. These targets combined with chemotherapy are also potential therapeutic strategy. In the secondary study, we focused on the mechanism of therapeutic failure caused by radio-resistance and identified the significance of cyclin D1 overexpression in progression and radio-resistance of pediatric ependymomas. Here we analyze clinic-pathological factors in 82 cases of ependymoma less than 20 years old and 31 out of 82 (37.8%) patients are under 3-year-old. The 10 years PFS and OS are 38% and 60%. Gross-total resection is the single significant prognostic factor for longer 10 years progression free survival (PFS) and overall survival (OS) in the multi-variant analysis (p<0.05). We demonstrated that 24 primary (92%) and 16 recurrent (95%) ependymomas were up-regulated, and 5 out of 7 paired samples exhibited higher CCND1 expression in recurrent tumors. Knocking down CCND1 reduced cell proliferation and repressed genes associated with S-phase and DNA repair. Homologous recombination activities of DNA repair were significantly decreased in CCND1-deficient cells while the level of H2AX was increased after irradiation. We treated ependymoma cells with palbociclib plus irradiation significantly suppressed expression of CDC6, MCM2, MAD2L1, CDK2, BRCA2 and RAD51 genes, and induced higher H2AX level after 24 hours and also reduced cell proliferation. In summary, our findings identify novel mRNA/miRNA interactions in pediatric high-grade gliomas and also suggest a robust role of CCND1 in regulating cell proliferation and radio-resistance in ependymomas, which providing insight of mechanism related to the radio-resistance and the potential therapeutic targets for both pediatric high-grade gliomas and ependymomas.
Gentner, Doreen. „Chromosom 9 in Ependymomen - Eine Mikrosatellitenanalyse“. Doctoral thesis, 2010. https://nbn-resolving.org/urn:nbn:de:bvb:20-opus-55975.
Der volle Inhalt der QuelleBased on a former study of the departmentof neuropathology of the pathologic instisute of the university of Wuerzburg, in which aberrations on chromosome 9 in ependymomas had been described, the whole chromosome should be screened and a finer analysis of previously aberrated regions should be carried out. The aim of the thesis was defining possible tumor suppressor genes or oncogenes being involved in the development and progression of ependymomas. Moreover there should be a correlation to the clinical data. Adults with ependymomas harboring aberrations on chromosome 9 showed significantly longer overall survival than patients of the same group without this aberration, irrespective of the extent of resection in multivariate analysis. Aberrations of chromosome 9, and particularly of DCR1 (DBCCR1), may play a role in the prognostic evaluation for ependymomas in adults in the future. In pediatric patients, genetic aberrations were found significantly more often in supratentorial tumors than in tumors with infratentorial location. Two common regions of deletions were identified (9p21.1 approximately p22.3 and 9q31.3 approximately q33.2). Localization and extend of resection could be confirmed as prognostic factors
„Combining CGH and high-resolution allelotyping study for ependymoma“. 2001. http://library.cuhk.edu.hk/record=b5890889.
Der volle Inhalt der QuelleThesis submitted in: December 2001.
Thesis (M.Phil.)--Chinese University of Hong Kong, 2001.
Includes bibliographical references (leaves 118-159).
Abstracts in English and Chinese.
ACKNOWLEDGEMENTS --- p.i
ABSTRACT(ENGLISH/CHINESE) --- p.iii
CONTENTS --- p.viii
LIST OF TABLES --- p.xi
LIST OF FIGURES --- p.xii
PUBLICATION --- p.xiii
Chapter CHAPTER I --- INTRODUCTION
Chapter I.1. --- Preface --- p.1
Chapter I.2. --- Overview of Carcinogenesis --- p.2
Chapter I.3. --- Oncogene --- p.5
Chapter I.4. --- Tumor Suppressor Genes (TSGs) --- p.6
Chapter I.5 --- Detection of Oncogene and Tumor Suppressor Genes --- p.9
Chapter I.5.1 --- Detaction of Oncogene --- p.9
Chapter I.5.2. --- Detection of Tumor Suppressor Genes --- p.11
Chapter I.6. --- Profiles of Oncogenes/TSGs and Molecular Subtype about Astrocytic Tumors --- p.17
Chapter I.7. --- Intratumoral Heterogeneity and Microsatellite Instability --- p.20
Chapter I.8. --- Outline of Ependymoma --- p.20
Chapter I.9. --- Clinicopathological Factors and Prognosis --- p.22
Chapter I.9.1. --- Histology and Grading (2000) --- p.22
Chapter I.9.2. --- Prognosis Factors --- p.23
Chapter I.9.2.1. --- Age/Sex/Location --- p.23
Chapter I.9.2.2. --- Extent of Resection --- p.25
Chapter I.9.2.3. --- Radiotherapy and Chemotherapy --- p.25
Chapter I.9.2.4. --- Histology --- p.26
Chapter I.10. --- "Cytogenetic, Molecular Genetic and Molecular Studies" --- p.27
Chapter I.11. --- Advantages and Disadvantages of The Research Methods --- p.34
Chapter CHAPTER II --- AIM OF STUDY --- p.36
Chapter CHAPTER III --- MATERIALS AND METHODS --- p.37
Chapter III.1. --- Tumor Samples and DNA Preparations --- p.37
Chapter III.1.1. --- Tumor Samples --- p.38
Chapter III.1.2. --- DNA Preparation --- p.38
Chapter III.2. --- Comparative Genomic Hybridization --- p.42
Chapter III.2.1. --- Metaphase Preparation --- p.42
Chapter III.2.2. --- "DNA Labeling, Hybridization, and Detection" --- p.43
Chapter III.2.3. --- Digital Image Analysis --- p.45
Chapter III.3 --- High-Resolution Allelotying (Microsatellite Analysis) --- p.46
Chapter III.3.1 --- General Outline --- p.46
Chapter III.3.2 --- Multiplex PCR --- p.47
Chapter III.3.3 --- Pooling of PCR Products --- p.49
Chapter III.3.4 --- Electrophoresis --- p.50
Chapter III.3.5. --- Assessment of Allelic Imbalance by Calculating Allelic Ratio --- p.52
Chapter III.3.6 --- Standards of Evalution --- p.53
Chapter III.3.7 --- Separating Allelic Loss from Allelic Duplication --- p.54
Chapter III.3.8 --- Statistical Analyses --- p.54
Chapter CHAPTER IV --- RESULTS --- p.54
Chapter IV.1. --- CGH Study --- p.54
Chapter IV.1.1 --- Overview --- p.54
Chapter IV.1.2 --- Common Deletion Regions --- p.58
Chapter IV.1.3 --- Common duplication Regions --- p.60
Chapter IV.2. --- High-Resolution Allelotyping (Microsatellite Analysis) --- p.60
Chapter IV.2.1. --- Overview of Results --- p.60
Chapter IV.2.2. --- LOH profile of Individual Chromosome --- p.93
Chapter IV.2.3. --- Overlapping Small Deletion Regions --- p.95
Chapter CHAPTER V --- DISCUSSION --- p.97
Chapter V.1. --- . General Outline --- p.98
Chapter V.2. --- Chromosome 22 --- p.99
Chapter V.3. --- Chromosome 17 --- p.102
Chapter V.4. --- Chromosome 6 --- p.104
Chapter V.5. --- Chromosome 16 --- p.105
Chapter V.6. --- Chromosome 19 --- p.107
Chapter V.7. --- Chromosome 20 --- p.108
Chapter V.8. --- Chromosome 7 --- p.109
Chapter V.9. --- Chromosome 12 --- p.110
Chapter V.10. --- Chromosome 9 --- p.111
Chapter V.11. --- Chromosome 5 --- p.112
Chapter V.12. --- Chromosome 4 --- p.112
Chapter V.13. --- Correlation of CGH with Allelotyping in the Study --- p.112
Chapter V.14. --- Conclusion --- p.114
Chapter CHAPTER VI --- LIMITATIONS OF THE STUDY --- p.115
Chapter CHAPTER VII --- FUTURE STUDY --- p.116
REFERENCES --- p.118
Eicker, Monika [Verfasser]. „Monosomie 22 in Ependymomen / vorgelegt von Monika Eicker“. 2006. http://d-nb.info/995894825/34.
Der volle Inhalt der QuelleBarszczyk, Mark. „Telomerase as a Prognostic Marker and Therapeutic Target in Paediatric Ependymoma“. Thesis, 2013. http://hdl.handle.net/1807/42680.
Der volle Inhalt der QuelleGentner, Doreen [Verfasser]. „Chromosom 9 in Ependymomen : eine Mikrosatellitenanalyse / vorgelegt von Doreen Gentner“. 2010. http://d-nb.info/1011275961/34.
Der volle Inhalt der QuelleHeinemann, Uta [Verfasser]. „Molekulargenetische Veränderungen auf Chromosom 22 in Ependymomen / vorgelegt von Uta Heinemann“. 2008. http://d-nb.info/987363387/34.
Der volle Inhalt der QuelleStein, Roland Gregor. „Immunhistochemische Marker für die Prognose und Proliferation in Ependymomen bei Kindern und Erwachsenen“. Doctoral thesis, 2012. https://nbn-resolving.org/urn:nbn:de:bvb:20-opus-71082.
Der volle Inhalt der QuelleImmunohistochemical markers for prognosis and proliferation in ependymomas of children and adults
Stettner, Georg Martin. „Immunhistologische und morphometrische Untersuchung der Ependymome im Kindesalter in Korrelation zu den klinischen Befunden“. Doctoral thesis, 2003. https://nbn-resolving.org/urn:nbn:de:bvb:20-opus-6932.
Der volle Inhalt der QuelleIn this dissertation the tumor’s clinical course of 40 children, who developed an ependymoma, was observed and 58 tumor samples were investigated by immunohistochemical methods. p53-accumulation, proliferation (detected by the antibody MIB-1) as well as the expression of HLA-DR by tumor cells and the prognostic value of these factors had been the focus of interest. Furthermore the EMA-expression and the distribution and proliferative activity of cells belonging to the microglia(MG)/macrophage-system in childhood ependymomas was investigated. The mean age at the time of diagnosis was 61 months (8 months to 15 4/12 years, median 41 months), the male/female ratio was balanced. 22,5% of primary tumors were located supratentorial, 60% infratentorial and 17,5% spinal. 52,5% of primary tumors were anaplastic ependymomas (WHO grade III), 40% ependymomas (WHO grade II) and 7,5% myxopapillary ependymomas (WHO grade I). A total resection was achieved in 30,8% of the primary tumors and in 27,3% of recurrent tumors. The mean follow-up was 52 months (6-163 months), the median progression free survival (PFS) and the overall survival (OS) 28 and 64 months respectively. All recurrences developed within 36 months after surgery with one exception, where a recurrence occurred after 84 months. Out of the clinical parameters a prognostic value was only seen in the extent of resection (total vs. subtotal resection: p=0.035 related to the median PFS and p=0.12 related to the median OS respectively). None of the other clinical parameters including tumor grade was correlated to the course of the disease. p53-accumulation was shown in 56,9% and there were correlations with WHO-tumor grade, MIB-1 labeling index (LI) and tumor localization. There was a wide range in MIB-1 LI (1,4% - 63,3%) with a higher mean and median (21,8% and 19,8% respectively) as reported in investigations in ependymomas of adults. There were significant correlations of MIB-1 LI with WHO-tumor grade, tumor localization and p53-accumulation as above mentioned. Out of the immunohistochemical investigated factors in this study only the MIB-1 LI was of prognostic relevance, but without statistical significance (MIB-1 LI <10% vs. MIB-1 LI >10%: p=0.17 related to the median PFS). None of the other immunohistochemical investigated factors mentioned below was related to the outcome in this study. For the first time proliferation of cells belonging to the MG/macrophage-system was documented in 80,4% of ependymal neoplasm. But there was no difference between different tumor grades in relative or absolute counts of proliferating microglial cells as previously shown in astrocytic tumors. The distribution of cells belonging to the MG/macrophage-system show a very heterogeneous pattern with a likely septal arrangement of ameboid microglia and macrophages in particular. Different distribution pattern of subgroups of the microglial cells and macrophages exist, but there is no relation to other variables except the density of microglial cells and macrophages in primary tumors. Although the HLA-DR expression in CNS neoplasms is a well known phenomenon, this is the first report of HLA-DR expression in ependymomas in 52,6% of all tumor samples. As a characteristic of ependymal neoplasms an EMA-expression was detected in 84,5%. EMA-expression can therefore be used as a criteria in differential diagnosis. The results of this study confirm the prognostic importance of a total resection of childhood ependymomas. Furthermore the relevance of proliferative activity related to the clinical course was emphasized. Further studies are needed to explain the reason and meaning of p53-accumulation and to define the role of the MG/microphage-system in the immunological tumor defense
„Molecular genetic studies of oligodendroglial and ependymal tumors“. 1998. http://library.cuhk.edu.hk/record=b5889797.
Der volle Inhalt der QuelleThesis (M.Phil.)--Chinese University of Hong Kong, 1998.
Includes bibliographical references (leaves 124-141).
Abstract also in Chinese.
acknowledgements --- p.i
Abstract (English/Chinese) --- p.ii
contents --- p.vi
list of tables --- p.viii
ost of figures --- p.x
Chapter I. --- introduction --- p.1
Chapter I.1. --- Tumors of the Central Nervous System --- p.1
Chapter I.2. --- Histopathological Classification of Human Glial Tumors --- p.3
Chapter I.2.1. --- Histopathology of Astrocytic Gliomas --- p.3
Chapter I.2.1.1. --- Diffuse Astrocytomas --- p.3
Chapter I.2.1.2. --- Others --- p.6
Chapter I.2.2. --- Histopathology of Non-Astrocytic Gliomas --- p.6
Chapter I.2.2.1. --- Oligodendroglial Tumors --- p.6
Chapter I.2.2.2. --- Ependymal Tumors --- p.9
Chapter I.3. --- Tumor Suppressor Genes --- p.14
Chapter I.3.1. --- p53 --- p.14
Chapter I.3.1.1. --- Historical Perspectives --- p.14
Chapter I.3.1.2. --- Structure of p53 Gene and Protein --- p.15
Chapter I.3.1.3. --- Functions of Wild-Type p53 Protein --- p.18
Chapter I.3.1.4. --- Regulation and Modulation of the Functions of p53 --- p.21
Chapter I.3.1.5. --- Mechnism of p53 Inactivation --- p.23
Chapter I.3.1.6. --- p53 Mutation Profiles in Human Tumors --- p.25
Chapter I.3.2. --- Novel Genes --- p.28
Chapter I.3.2.1. --- PTEN/MMAC1 --- p.28
Chapter I.3.2.2. --- DMBT1 --- p.31
Chapter I.4. --- Cytogenetic and Molecular Genetic Studies in Gliomas --- p.34
Chapter I.4.1. --- Astrocytic Gliomas --- p.34
Chapter I.4.2. --- Non-Astrocytic Gliomas --- p.39
Chapter I.4.2.1. --- Oligodendroglial Tumors --- p.39
Chapter I.4.2.2. --- Ependymal Tumors --- p.46
Chapter II. --- objectives of study --- p.49
Chapter III. --- materials and methods --- p.52
Chapter III.l. --- Patients and Materials --- p.52
Chapter III.2. --- Collection of Samples --- p.57
Chapter III.3. --- DNA Extraction --- p.58
Chapter III.3.1. --- Extraction of Genomic DNA from Formalin-Fixed Paraffin Embedded Tissues --- p.58
Chapter III.3.2. --- Extraction of Genomic DNA from Blood --- p.60
Chapter III.4. --- Loss of Heterozygosity (LOH) Analysis on Chromosome 10q --- p.61
Chapter III.4.1. --- Microsatellite Markers --- p.62
Chapter III.4.2. --- Amplification of Target Sequences by PCR --- p.63
Chapter III.4.3. --- Denaturing Polyaerylamide Gel Electrophoresis --- p.64
Chapter III.4.4. --- Detection of Loss of Heterozygosity (LOH) --- p.64
Chapter III.5. --- Mutational Analysis of p53 and PTEN/MMAC1 --- p.66
Chapter III.5.1. --- Polymerase Chain Reaction-Single Strand Conformation Polymorphism (PCR-SSCP) Analysis --- p.66
Chapter III.5.1.1. --- PCR Primers --- p.66
Chapter III.5.1.2. --- PCR Amplification of Target Sequences --- p.68
Chapter III.5.1.3. --- Non-denaturing Polyacrylamide Gel Electrophoresis --- p.71
Chapter III.5.2. --- Direct DNA Sequencing Analysis --- p.72
Chapter III.5.2.1. --- Cycle Sequencing --- p.72
Chapter III.5.2.2. --- Denaturing Gel Electrophoresis --- p.73
Chapter III.6. --- Differential PCR for Detection of MDM2 Amplification --- p.74
Chapter III.6.1. --- DNA Amplification by PCR --- p.74
Chapter III.6.2. --- Polyacrylamide Gel Electrophoresis --- p.75
Chapter III.6.3. --- Detection of Gene Amplification --- p.75
Chapter IV. --- Results --- p.77
Chapter IV.1. --- LOH Analysis of Chromosome l0q --- p.77
Chapter IV.2. --- Mutational Analysis ofp53 and PTEN/MMAC1 --- p.92
Chapter IV.3. --- Differential PCR Analysis of MDM2 Amplification --- p.103
Chapter V. --- discussion --- p.109
Chapter V.l. --- p53 Gene Inactivation Studies --- p.110
Chapter V.2. --- Molecular Genetic Studies on Chromosome l0q --- p.113
Chapter V.3. --- Microsatellite Instability in Non-Astrocytic Gliomas --- p.117
Chapter V.4. --- Significance of This Study --- p.118
Chapter V.5. --- Limitations of This Study --- p.119
Chapter V.6. --- Future Studies --- p.122
Chapter VI. --- REFERENCES --- p.124
Michalowski, Mariana. „ETUDE DES ALTÉRATIONS EPIGENETIQUES DES TUMEURS DESENFANTS : LE CAS DES ÉPENDYMOMES ET DES NEUROBLASTOMES“. Phd thesis, 2006. http://tel.archives-ouvertes.fr/tel-00115184.
Der volle Inhalt der Quellel'hyperméthylation des gènes suppresseurs de tumeur (GST). Les modifications « épigénétiques » ont été peu étudiées dans les cancers de l'enfant et aucune grande série de tumeurs pédiatriques existait avant 2002. Nous avons recherché ce type altérations dans deux groupes de tumeurs de l'enfant: les ependymomes et les neuroblastomes. Les ependymomes (EP) représentent la troisième tumeur la plus fréquente du système nerveux central (SNC) de l'enfant et n'a pas de marqueurs biologiques pronostiques identifiés. Le neuroblastome, quant à lui, est la tumeur solide extra crânienne la plus fréquente chez l'enfant et présente des anomalies génétiques et moléculaires qui ont été clairement liées au pronostic. Nos objectifs étaient de décrire un profil de méthylation de ces deux cancers de l'enfant et chercher des relations possibles avec l'évolution clinique. Dans la première étude, une série de 27 enfants avec un EP intracrânien et 7 avec papillome du plexus choroïde a été étudiée. Nous avons décrit et comparé le statut de méthylation de 19 gènes. Dans la deuxième étude, 62 neuroblastomes (NB) ont été évalués pour le statut de la méthylation de ces gènes. Nous n'avons pas trouvé de relation statistiquement significative entre la méthylation et l'évolution clinique, mais les méthylations ne semblent pas être distribuées sous une forme aléatoire dans les EP et les NB et peut représenter un mécanisme de développement et d'évolution tumorale. L'hyperméthylation a été corrélée au stade clinique des NB: stades 1, 2 et 4s étaient moins fréquemment méthylés que les stades 3 et 4 (p = 0.002). En conclusion, les résultats de nos séries indiquent que la méthylation des gènes suppresseurs peut avoir un rôle dans l'évolution et le développement des cancers de l'enfant.
L'étude des altérations épigénétiques est nécessaire pour améliorer la comprehension des mécanismes de la carcinogenèse dans les tumeurs pédiatriques. Ces altérations pourraient, donc, être utilisées comme des marqueurs de maladies ou d'évolutivité et les gènes méthylés pourraient être considérés comme des nouvelles cibles thérapeutiques.
Stein, Anne-Katrin [Verfasser]. „Evaluation von Antikörpern gegen ependymale Proteine auf ihre Eignung als diagnostische Marker für Ependymome / vorgelegt von Anne-Katrin Stein“. 2009. http://d-nb.info/993332218/34.
Der volle Inhalt der QuelleStettner, Georg Martin [Verfasser]. „Immunhistologische und morphometrische Untersuchung der Ependymome im Kindesalter in Korrelation zu den klinischen Befunden / vorgelegt von Georg Martin Stettner“. 2003. http://d-nb.info/96919823X/34.
Der volle Inhalt der QuellePal, Jagriti. „Elucidating Deregulated Novel Pathways in Glioma through Genetic and Epigenetic Approaches“. Thesis, 2016. http://etd.iisc.ac.in/handle/2005/4284.
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