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1
Panasenkava, Veranika. "Utilisation de cellules souches pluripotentes induites combinée à une approche transcriptomique pour améliorer le diagnostic moléculaire des troubles du neurodéveloppement chez l’homme". Electronic Thesis or Diss., Université de Rennes (2023-....), 2024. http://www.theses.fr/2024URENB060.
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L'holoprosencéphalie (HPE) est une maladie rare qui affecte le développement de la ligne médiane du cerveau antérieur dès les premiers stades embryonnaires, rendant son diagnostic moléculaire complexe. Elle résulte principalement d’altérations génétiques entraînant une réduction de l'activité de la voie de signalisation Sonic Hedgehog (SHH). Cependant, un diagnostic moléculaire précis n’est possible que pour 30% des patients, ce qui souligne l’importance de développer des nouvelles approches diagnostiques. Le principal obstacle réside dans l'impossibilité d'accéder au tissu primaire affectée par la pathologie, soit le neuroectoderme antérieur. Pour surmonter cet obstacle, j’ai mis au point un modèle in vitro du développement du neuroectoderme antérieur en utilisant des cellules souches pluripotentes induites. Ce modèle m’a permis de produire des données transcriptomiques permettant d’évaluer les impacts moléculaires de la déficience en SHH et de définir des signatures transcriptomiques décrivant les variations de l'activité de la voie SHH pouvant être corrélées à la sévérité des phénotypes d’HPE. Ce travail a également révélé de nouveaux gènes co-exprimés et régulés par SHH, qui pourraient constituer de nouveaux marqueurs génétiques de l'HPE. Ces avancées ouvrent la voie à la création d’outils de diagnostic innovants, visant à améliorer la précision du diagnostic pour les patients atteints d'HPEAbstract : Holoprosencephaly (HPE) is a rare disorder that affects the development of the midline of the forebrain during the earliest stages of embryogenesis, making molecular diagnosis challenging. It primarily results from genetic alterations that lead to a reduction in the activity of the Sonic Hedgehog (SHH) signaling pathway. However, a precise molecular diagnosis is only possible for 30% of patients, highlighting the importance of developing new diagnostic approaches. The main challenge is the inaccessibility of the primary tissue, specifically the anterior affected by HPE, namely the anterior neuroectoderm. To overcome this challenge, I established an in vitro model of anterior neuroectoderm using induced pluripotent stem cells. This model allowed me to generate transcriptomic data to assess the molecular impacts of SHH deficiency and define transcriptomic signatures that describe variations in SHH pathway activity, which may correlate with the severity of HPE phenotypes. This work also revealed new co-expressed and SHH-regulated genes, which could serve as new genetic markers for HPE. These advances pave the way for innovative diagnostic tools aimed at improving diagnostic accuracy for patients with HPE
2
Kishi, Masashi. "Requirement of Sox2-mediated Signaling for Differentiation of Early Xenopus Neuroectoderm". Kyoto University, 2000. http://hdl.handle.net/2433/180825.
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Voulgaris, Dimitrios. "Evaluation of Small Molecules for Neuroectoderm differentiation & patterning using Factorial Experimental Design". Thesis, Chalmers Tekniska Högskola, 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-273264.
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Screening for therapeutic compounds and treatments for diseases of the Brain does not only encompass the successful generation of iPS-derived homogenous neural stem cell populations but also the capacity of the differentiation protocol to derive on-demand region-specific cells. Νoggin, a human recombinant protein, has been extensively used in neural induction protocols but its high production costs and batch-to-batch variation have switched the focus to utilizing small molecules that can substitute noggin. Resultantly, the aim of this study was to optimize neuroepithelial stem cell generation in a cost-efficient fashion as well as to evaluate the impact that patterning factors (i.e. small molecules or proteins that enhance the emergence of type-specific neuronal populations) have on the regionality of the neural stem cell population. Findings in this study suggest that DMH1 is indeed a small molecule that can replace noggin in neural induction protocols as previously documented in literature; DMHI appears also to have a ventralizing effect on the generated neural population.QC 20201013
4
Orbegoso-Celis, L., R. Bernuy-Guerrero, F. Imán-Izquierdo, L. Alfaro-Lujan, Espinoza L. Barreto e W. Silva-Caso. "First report of a primitive neuroectodermal tumor of the bladder in a newborn". Elsevier Inc, 2021. http://hdl.handle.net/10757/654519.
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Primitive neuroectodermal tumor (PNET) is part of the Ewing sarcoma family of tumors. The present case reports a primitive neuroectodermal tumor (PNET) of rare location in the bladder in a newborn. It was evaluated with prenatal ultrasound and postnatal tomography that revealed a mass in the posterior wall of the bladder. The patient underwent partial cystectomy with subsequent analysis of the surgical piece removed, the histopathological study indicated a tumor of mesenchymal origin, and immunohistochemical staining confirmed the diagnosis of PNET of the bladder. Satisfactory result and short-term follow-up.Revisión por pares
5
Hayden, James Timothy. "The molecular basis for central nervous system primitive neuroectodermal tumour development". Thesis, University of Newcastle upon Tyne, 2012. http://hdl.handle.net/10443/1598.
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Central nervous system primitive neuroectodermal tumours (CNS-PNETs) are highly aggressive tumours with similar histopathological features to other intracranial PNETs (medulloblastomas). These two tumours have accordingly been treated using unified approaches, but CNS-PNETs have a dismal prognosis. Few studies have investigated the genetic features of CNS-PNETs. The molecular basis of CNS-PNET was therefore investigated in a cohort containing CNS-PNETs from children (n=33) and adults (n=5), to aid improvements in disease classification and treatment. The common medulloblastoma molecular defects were investigated in CNS-PNETs, and showed RASSF1A promoter hypermethylation is a frequent event (18/22, 82%), and MYC family gene amplification occurs in a subgroup (MYCN: 3/25 (12%), MYCC: 0/25 (0%)). In contrast and in distinction to medulloblastoma, chromosome 17p loss is not a common feature (2/23, 9%), whilst p53 pathway signalling appears to play a major role (20/22, 91%), and associated with TP53 mutations (4/22, 18%). Aberrant Wnt signalling was identified in 2 cases (2/22, 9%) and coupled with CTNNB1 mutation in a single case. IDH1 mutations (2/25, 8%) however, appear to occur in adult but not childhood CNS-PNETs or medulloblastoma. Subsequent genome-wide investigations of the CNS-PNET DNA methylome aimed at a wider characterisation of the molecular features of CNS-PNETs and its relationships to other childhood tumours identified CNS-PNETs as a heterogenous disease group without defined sub-clusters, which were predominantly distinct from medulloblastomas, but exhibited overlap with high-grade gliomas. A panel of 76 tumour-specific methylation events were identified as disease markers. The combination of either RASSF1A hypermethylation or HLA-DPB1 hypomethylation discerned normal brain from CNS-PNET in 94% of cases (64/68). In addition, hypermethylation of TAL1, MAP3K1 and IGFBP1 is associated with non-infant disease. In conclusion, this study has shown CNS-PNETs are a heterogenous group of tumours that are molecularly distinct from medulloblastomas, and has implicated developmental pathways and genetic events in their tumorigenesis. The associations between molecular events identified and clinical features warrant further investigation to aid classification and treatment advancements.
6
Chng, Z. "The function of Smad-interacting factors in neuroectoderm differentiation of human embryonic stem cells". Thesis, University of Cambridge, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.597623.
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To further understand the molecular mechanisms involving Activin/Nodal signalling in pluripotency, I studied in hESCs the function of two Smad-binding partners, Smad-Interacting Protein 1 (SIP1) and Ectodermin, which are involved in neuroectoderm specification in amphibians and in the mouse. This report demonstrates that Activin/Nodal signalling cooperates with NANOG, OCT4 and SOX2 to tightly control the expression of the SIP1 in hESCs. In turn, SIP1 plays a role in pluripotency by limiting the positive effect of Activin/Nodal signalling on mesendoderm differentiation. Importantly, SIP1 favours neuroectoderm differentiation and protects neuroectodermal cells from the mesoderm-inducing effect of BMP signalling, confirming that SIP1 has a key function in this early cell fate decisions. Similar results were obtained with pluripotent stem cells derived from post-implantation mouse embryos (mEpiSCs) implying that these mechanisms are evolutionarily conserved and suggesting that they could take place in vivo during early development of mammalian embryos. My study on the function of SIP1 explains the mechanisms by which Activin/Nodal signalling and SIP1 regulate the cell fate decision between neuroectoderm and mesendoderm in the progression from pluripotency to primary germ later differentiation. I present my preliminary studies on the function of Ectodermin in hESCs, and I propose that Ectodermin does not play a role in neuroectoderm differentiation, but may be involved in mesendoderm differentiation. Finally, I provide some preliminary results on understanding the function of SMAD4 in hESCs, and propose that the classical effectors of Activin/Nodal signalling, that is, SMAD2, SMAD3 and SMAD4, may have differential roles in propagating Activin/Nodal signalling effects.
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Onai, Takayuki. "Xenopus XsalF : anterior neuroectodermal specification by attenuating cellular responsiveness to Wnt signaling". Kyoto University, 2006. http://hdl.handle.net/2433/143850.
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Kyoto University (京都大学)0048
新制・課程博士
博士(医学)
甲第12217号
医博第2970号
新制||医||921(附属図書館)
24053
UT51-2006-J210
京都大学大学院医学研究科脳統御医科学系専攻
(主査)教授 塩田 浩平, 教授 金子 武嗣, 教授 西川 伸一, 教授 鍋島 陽一
学位規則第4条第1項該当
8
Miller, Suzanne. "Genome-wide molecular characterisation of central nervous system primitive neuroectodermal tumours and pineoblastomas". Thesis, University of Nottingham, 2010. http://eprints.nottingham.ac.uk/11668/.
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CNS PNET and pineoblastomas are highly malignant embryonal brain tumours of poor prognosis. Current treatment strategies are based on the histologically similar medulloblastoma; however, patients with CNS PNET and pineoblastoma have significantly worse outcomes. Specific therapies based on the underlying biology and genetics of CNS PNET and pineoblastoma are needed. To provide evidence of the fundamental genetics driving tumour pathogenesis and to identify novel targets for therapy, 46 CNS PNETs and pineoblastomas were analysed using the Affymetrix 100K/500K mapping sets to identify genome-wide copy number alterations and loss of heterozygosity. Overall, frequent gains of 1q, 2p and 21q and frequent loss of 16q were identified. Unsupervised hierarchical clustering showed marked differences in the frequency of genetic imbalance in the CNS PNETs and pineoblastomas, with pineoblastomas containing fewer genomic changes clustering separately to the CNS PNETs. Novel gene copy number alterations were identified; gain of PCDHGA3 (5q31.3) and FAM129A (1q25) and losses of OR4C12 (11p11.12), CADPS (3p14.2), and SALL1 (16q12.1). Loss of CDKN2A and CDKN2B was also identified, in keeping with previous genetic studies of CNS PNET. Linking gene copy number data with patient clinical information, loss of CADPS was associated with poor prognosis in patients with primary CNS PNETs (p = 0.033 and p = 0.046, by SNP array and real time qPCR analyses, respectively). On comparison of 5 primary and recurrent CNS PNET pairs, gain of 2p21 was the most common alteration maintained in 80% of cases. Immunohistochemistry for p15INK4B (encoded by CDKN2B) was performed which demonstrated the loss in gene copy number had lowered the expression of the encoded protein. Finally an immunohistochemical and mutational screen for INI1 (commonly lost in the malignant embryonal brain tumour, ATRT) was performed in the CNS PNET/pineoblastoma cohort which showed the loss of INI1 protein expression in the tumour cohort was not due to mutations residing in the mutational hotspots of exons 5 and 9 of the INI1 gene. Patients with INI1 immunonegative CNS PNETs had a worse prognosis than those with INI1 immunopositive CNS PNETs (p < 0.0001). This project demonstrated the first application of SNP array technology in the analysis of the largest cohort of CNS PNETs and pineoblastomas to date, identified novel gene copy number alterations, linked genetic alterations with clinical factors and identified 2 potential markers of prognosis.
9
Burns, Alice Sin Ying Wai. "The role of the p53 tumour suppressor pathway in central primitive neuroectodermal tumours". Thesis, University of Newcastle Upon Tyne, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.300357.
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Wu, Hue-Tsi. "The WNT signalling pathway in Ewing sarcoma/primitive neuroectodermal tumour : an immunohistochemical investigation". Master's thesis, University of Cape Town, 2011. http://hdl.handle.net/11427/11479.
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Includes abstract.Includes bibliographical references.
The WNT pathway is a major developmental pathway that plays an important role in the development of many tumours, including neuroectodermal and bone tumours. Ewing sarcoma (ES) / primitive neuroectodermal tumour (PNET) shows varying degrees of neuroectodermal differentiation and is the second commonest bone malignancy in childhood. A recent study on ES cell lines using RT-PCR analysis and biological response assays suggests that an intact WNT pathway exists in ES and that addition of exogenous WNT ligands enhances cell motility. Based on this we hypothesize that the WNT pathway may play a role in the biology of ES/PNET and we aim to investigate this by immunohistochemical stains on archival tissue.
11
Thompson, Samantha Lee. "A genetic basis for the development of prognostic indication in childhood primitive neuroectodermal tumours". Thesis, University of Nottingham, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.324697.
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Aramaki, Toshihiro. "Jiraiya Attenuates BMP Signaling by Interfering with Type-II BMP Receptors in Neuroectodermal Patterning". Kyoto University, 2011. http://hdl.handle.net/2433/142060.
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Opel, Daniela. "Role of phosphoinositide-3-kinase (PI3K)/Akt signaling in apoptosis regulation of neuroectodermal tumors". [S.l. : s.n.], 2008. http://nbn-resolving.de/urn:nbn:de:bsz:289-vts-63916.
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Roche-Durst, Evodie. "Le progonome melanique ou melanotique : (mnti : melanotic neuroectodermal tumor of infancy) : a propos d'une observation". Université Louis Pasteur (Strasbourg) (1971-2008), 1985. http://www.theses.fr/1985STR1M024.
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McBride, Sean Matthew. "Radiation is an important component of multimodality therapy for pediatric supratentorial non-pineal neuroectodermal tumors". [New Haven, Conn. : s.n.], 2008. http://ymtdl.med.yale.edu/theses/available/etd-12092008-141837/.
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Mittal, Bina. "In vitro characterization of a cell surface molecule expressed by certain cells of neuroectodermal and mesenchymal origin". Thesis, McGill University, 1994. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=41718.
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Adhesive interactions between neurons and astroglia are likely to play an important role during central nervous system development. Using a monoclonal antibody (designated MAb 1A1) raised against purified neonatal rat astrocytes, I have characterized some of the in vitro functional and biochemical properties of a potentially novel cell surface molecule. By indirect immunofluorescence, the antibody labels subpopulations of astrocytes (flat type-1 astrocytes and Bergmann glia) and cells derived from the mesenchyme (leptomeninges and fibroblasts). The latter showed 1A1$ sp{+}$ immunoreactivity only when grown to confluency. Cell-cell contact and extracellular matrix molecules were found to play a role in the regulation of 1A1 antigen expression on leptomeninges. 1A1 Fab fragments inhibited the binding of neuron to astrocyte and astrocyte to astrocyte, but not of neuron to neuron in an in vitro adhesion assay, thus indicating that this surface antigen may function as a cell adhesion molecule on astrocytes. Addition of Fab fragments of MAb 1A1 also reduced leptomeningeal cell adhesion. Further functional antibody perturbation experiments indicated that this surface molecule mediates neurite outgrowth on astrocytes and neuronal migration on Bergmann glia via a heterophilic-binding mechanism. Both immunoprecipitation and immunocytochemical analysis showed the timing of 1A1 antigen expression in postnatal rat cerebellum to coincide with the developmental period of granule cell migration along Bergmann glia. On SDS-PAGE, the immunopurified 1A1 surface molecule migrated as a single molecular weight band of $ approx$135 kd and appeared to be poorly glycosylated. Based on its unique cell-type distribution, functional properties and biochemical analysis, this 135 kd glycoprotein is likely to be distinct from other known cell adhesion molecules expressed on astrocytes.
17
Edwards, Amanda Lee. "Dissecting and Targeting the PUMA and OLIG2 Control Points of Tumors of Neuroectodermal Origin with Stapled Peptides". Thesis, Harvard University, 2013. http://dissertations.umi.com/gsas.harvard:10886.
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Tumors of neuroectodermal origin are among the most aggressive and treatment-refractory forms of human cancer. While such tumors arise from a variety of defects, two key targets are the transcription factors p53 and OLIG2. We have developed stabilized peptides to study and target deregulated p53 and OLIG2 pathways in neuroectodermal cancers. PUMA (p53-upregulated modulator of apoptosis) is a BH3-only member of the BCL-2 protein family that regulates apoptosis in response to p53-dependent and p53-independent stress signals. The specific interactions that mediate the pro-apoptotic activity of PUMA remain controversial. We generated stabilized alpha-helices of BCL-2 domains (SAHB) peptides modeled after the BH3 effector domain of PUMA. Structural analyses determined that PUMA SAHB contacts BAX at both the N-terminal \(\alpha1/\alpha6\) trigger site and the canonical BH3 binding pocket, binding events that functionally activate BAX. Notably, both PUMA SAHB and PUMA protein pull-downs identified anti- and pro-apoptotic binding partners in a cellular context. As PUMA has been implicated in driving apoptosis in multiple neural cell types, we further demonstrated that treatment of neuroblastoma cell lines with a cell-permeable PUMA SAHB analog triggered dose-dependent apoptosis. Together, we find that the PUMA BH3 domain activates apoptosis through multimodal interactions with BCL-2 family proteins, and its mimetics may serve as prototype therapeutics in tumors of neural origin. Whereas suppression of p53 signaling and apoptosis are features of diverse tumor types, the basic helix-loop-helix (bHLH) transcription factor OLIG2 is selectively overexpressed in gliomas. Early in development, OLIG2 is responsible for maintaining progenitor cells in a replication-competent state. Tumor stem cells are believed to co-opt this OLIG2 functionality to continually repopulate glial tumors. To achieve its transcriptional function, OLIG2 must dimerize via its bHLH domain. Stabilized alpha-helices of OLIG2 (SAH-OLIG2) peptides of the OLIG2 bHLH domain were generated in an effort to disrupt this pathologic dimerization. While helical stabilization of several SAH-OLIG2 peptides was achieved, specific engagement and disruption of the native bHLH dimer did not occur, informing alternative design strategies for future targeting efforts. These studies underscored the importance of interrogating the OLIG2 dimeric structure and catalyzed the discovery of candidate OLIG2 interaction partners for therapeutic targeting.
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CESARINI, VALERIANA. "Regulation of neuroectodermal cancers invasive behavior: role of PDE5 in Glioblastoma Multiforme and of Sox2 in Melanoma". Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2014. http://hdl.handle.net/2108/203040.
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Neuroectoderm is one of the earliest cell lineages that establish at gastrulation. Neuroectodermal tumors arise from cells originating from the primitive neuroectoderm, which include glial cells, neurons, neural crest cells, parenchymal cells of the pineal gland and primitive embryonic cells of brain and retina. Both melanocytes and glial cells are derived embryologically from the neuroectoderm. Their malignant transformed counterparts, melanoma and glioma cells, respectively, may share common antigens. Numerous tumor-associated antigens have been identified in melanomas but only a few in gliomas. We undertook a study of how invasiveness of tumor cells can be regulated in gliomas as well as in melanomas, focusing our attention on two genes, Sox2 and PDE5, which have been hypothesized to play a role in melanoma invasiveness. In particular, we modulated PDE5 expression in glioblastoma cell lines and Sox2 in a melanoma animal model to evaluate the invasiveness potential of this tumor cell types in vitro and in vivo.
19
Wang, Min. "Importance of insulin-like growth factor-1 receptor and EWS/FLI-1 fusion protein in growth and survival of two different types of neuroectodermal tumor cells /". Stockholm, 1998. http://diss.kib.ki.se/1998/91-628-3293-X/.
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Machado, Lucas Faria Abrahão. "Pesquisa de biomarcadores como fator prognóstico nos tumores da família do sarcoma de Ewing". Universidade de São Paulo, 2017. http://www.teses.usp.br/teses/disponiveis/5/5140/tde-10112017-115117/.
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INTRODUÇÃO: Os tumores da família do sarcoma de Ewing (TFSE) compreendem um espectro de neoplasias de células neuroectodérmicas dos ossos e partes moles de comportamento biológico agressivo e prognóstico reservado, caracterizadas por translocações envolvendo um dos genes da família TET/FET e um dos genes da família ETS, mais comumente EWSR1 e FLI1. Com o avanço da medicina personalizada, cresce a demanda por biomarcadores em TFSE que tenham valor como fatores prognósticos e potencial para futuras terapias-alvo específicas. Este estudo propôs biomarcadores, incluindo proteínas relacionadas à supressão tumoral, proliferação celular, metabolismo energético, atividade imune, vias de reparo do DNA e células tronco. MÉTODOS: A expressão imuno-histoquímica dos biomarcadores MTAP, p16, STAG2, p53, USP22, PTEN, RKIP, Ciclina D1, MCTs (1, 2 e 4), CD147, CA IX, GLUT1, BRACHYURY, PD-L1, OCT4 e SALL4 foi analisada em uma série bem caracterizada de 113 TFSE através de amostras em tissue microarrays (TMA). Os perfis de expressão foram então associados aos parâmetros clínico-patológicos dos pacientes e à sobrevida global para uma análise do impacto no prognóstico. RESULTADOS: A hiperexpressão de p53 mostrou associação estatisticamente significativa com menor sobrevida global (p < 0,001), doença metastática no diagnóstico (p = 0,017) e idade acima de 20 anos (p = 0,04). A perda de expressão de MTAP (p = 0,039) e de Brachyury (p = 0,008) também se associaram significativamente com menor sobrevida global. Em relação às características clínicas dos pacientes, doença metastática no diagnóstico e etnia não-branca foram associados a um pior prognóstico. CONCLUSÕES: Os biomarcadores p53, MTAP e Brachyury foram identificados como fatores independentes relacionados ao prognóstico. A utilização destes biomarcadores como fator prognóstico nos TFSE pode auxiliar na estratificação de risco dos pacientes e até mesmo estimular o desenvolvimento de drogas-alvo específicasINTRODUCTION: The Ewing sarcoma family of tumors (ESFT) comprises a spectrum of neoplasms of neuroectodermal cells of the bones and soft tissues with an aggressive biological behavior and poor outcome, characterized by translocations involving one of the genes of the TET/FET family and one of the genes of the ETS family, most commonly EWSR1 and FLI1. With the progress of personalized medicine, there is a great demand for biomarkers in ESFT that could have prognostic values and the potential for future targeted therapies. This study proposed the evaluation of protein expression of different classes of biomarkers, including proteins related to tumor suppression, cell proliferation, energy metabolism, immune activity, DNA repair pathways and stem cells. METHODS: Immunohistochemical expression of the biomarkers MTAP, p16, STAG2, p53, USP22, PTEN, RKIP, Cyclin D1, MCTs (1, 2 and 4), CD147, CA IX, GLUT1, BRACHYURY, PD-L1, OCT4 and SALL4 was analyzed in a well-characterized series of 113 ESFT in a tissue microarray (TMA) platform. Expression profiles were then associated with patients\' clinical-pathological parameters and overall survival for analysis of the prognostic impact. RESULTS: p53 hyperexpression showed a statistically significant association with lower overall survival (p <0.001), metastatic disease at diagnosis (p = 0.017) and age over 20 years (p = 0.04). Loss of MTAP (p = 0.039) and Brachyury (p = 0.008) were also significantly associated with lower overall survival. Regarding the clinical characteristics of the patients, metastatic disease at diagnosis and non-white ethnicity were associated with a worse prognosis. CONCLUSIONS: The biomarkers p53, MTAP and Brachyury were identified as independent factors related to the prognosis. The use of these biomarkers as a prognostic factor in ESFT may aid in the risk stratification of patients and even stimulate the development of specific targeted drugs
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Aragón, Manresa Ferran. "The role of vHnf1 and Fgf Signaling in the caudal Hindbrain Patterning". Doctoral thesis, Universitat Pompeu Fabra, 2008. http://hdl.handle.net/10803/7147.
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Durant els primers estadis del desenvolupament embrionari dels metazous els teixits embrionaris son progressivament regionalitzats fins que adquireixen destins específics. En els vertebrats, el tub neural, que és el primordi del sistema nerviós central, es tempranament regionalitzat en el seu eix antero-posterior i queda dividit en les tres vesícules cerebrals i la medul·la espinal. La vesícula cerebral més posterior rep el nom de rombencèfal. En el rombencèfal un següent estadi de regionalització condueix cap a una organització en una serie de segments anomenats rombomers. Aquesta organització primària serveix de patró per les estructures que es van generant en el rombencèfal. A part d'unitats morfològiques els rombomers també son compartiments que observen restricció del llinatge cel·lular i expressen combinacions específiques de gens que els hi confereixen una identitat posicional. L'assoliment d'una identitat posicional per part de cadascun dels rombomers implica un procés jeràrquic i gradual en el qual intervenen tota una serie de factors de transcripció de tipus Hox i no Hox així com diferents molècules de senyalitzacióvHnf1 es un dels primers factors de transcripció expressats en el rombencèfal. En aquest projecte s'ha estudiat el paper de vHnf1 així com la implicació de la senyalització FGF en la regionalització del rombencèfal caudal del embrió de pollet. Els resultats mostren que vHnf1 s'expressa tempranament en el rombencèfal amb un límit rostral d'expressió coincident amb la frontera prospectiva entre els rombomers 4 i 5. Experiments de sobrexpressió mostren que vHnf1 es capaç de conferir caràcter caudal a rombomers rostrals tot induint Krox20 in MafB i reprimint Hoxb1 a r4. Les induccions de Krox20 i MafB resultaren ésser dependents de la senyalització per FGFs. Sorprenentment, els nostres resultats també mostren que vHnf1 indueix fortament la expressió de Fgf3. És més, anàlisis per RT-PCRs semiquantitatives demostraren que aquesta inducció es molt ràpida suggerint que Fgf3 és directament regulat per vHnf1. En aquest projecte també es presenta l'anàlisi dels perfils d'expressió d'alguns gens del grup de "sinexpressió" dels FGFs en el rombencéfal caudal. Finalment es determina que la senyalització FGF funciona a través de la via intracel·lular Ras-MAPK en el procés de regionalització del rombencéfal caudal sense implicació de la via PI3K-Akt.
Aquests resultats ofereixen nova informació sobre els mecanismes moleculars implicats en la regionalització del rombencèfal caudal en vertebrats. De manera interessant aquests resultats posen de manifest certes diferencies en els mecanismes de regulació que operen en la regionalització del rombencéfal de diferents especies.
During early embryonic development of chordates, the hindbrain, which is the caudalmost brain vesicle, is transiently organized along the AP axis in a series of segments called rhombomeres (r). This segmental organization serves as scaffold for several structures that develop within the hindbrain in repeated patterns. Each rhombomere has a molecular identity given by a specific combination of gene expression. Rhombomeric identity is the result of a progressively refined patterning that involves the interplay of different cell signaling pathways and rhombomere-specific transcription factors.
In the present project the role of vHnf1, one of the earliest transcription factors expressed in the hindbrain, and its interplay with FGF signaling has been analyzed during the chick embryo development. The results show that vHnf1 is very early expressed in the chick neuroepithelium with a sharp boundary of expression coinciding with the presumptive r4/r5 interrhombomeric boundary. Gain-of-function experiments demonstrated that vHnf1 is able to confer partial caudal character to rostral rhombomeres through the mediation of FGF signaling. We also analyzed the expression of genes of the FGF synexpression group in the caudal hindbrain. Finally, we determined that the role of FGF signaling in regulating the caudal rhombomeric markers Krox20 and MafB is mediated through the Ras-ERK1/2 intracellular pathway.
The results of this project provide new information about the molecular mechanisms involved in patterning the vertebrate caudal hindbrain. Interestingly, while requirement of vHnf1 and FGF signaling for caudal hindbrain patterning is an evolutionary conserved feature, the ways by which FGF signals are regulated during this process differ across species.
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Huang, Yuan-Ping. "Transcriptional Regulation of Neuroectodermal Lineage Commitment in Embryonic Stem Cells". Thesis, 2014. https://doi.org/10.7916/D8RB72XW.
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Lineage commitment of pluripotent cells is a critical step in the development of multicellular organisms and a prerequisite for efficient differentiation of stem cells into terminal cell types. During successful neuroectodermal lineage commitment, extracellular signals terminate the pluripotency program, activate neural transcriptional program, and suppress alternative mesendodermal fate. Retinoic acid (RA) has been identified as a potent inducer of neural differentiation in embryonic stem cells (ESCs), yet the transcriptional program initiated by RA is poorly understood. Expression profiling of differentiating ESCs revealed delayed response of the pluripotency marker Oct4 and neural marker Sox1 following RA treatment, suggesting that RA regulates the pluripotency program and neural transcriptional program indirectly through induction of additional transcription factors.
In this study, I identified a zinc finger factor Zfp703 as a downstream effector of RA-mediated neuroectodermal lineage commitment. Zfp703 expression in ESCs resulted in Oct4 repression, Sox1 induction, and neural differentiation. Moreover, Zfp703 strongly suppresses mesendodermal fate by repressing genes such as Brachyury, Eomes, and Mixl1 even under conditions favoring mesendoderm specification. Zfp703 binds to and represses Lef1 promoter, raising the possibility that it might modulate Wnt signaling via regulating Lef1. Finally, Zfp703 is not required for RA-mediated Oct4 repression and Sox1 induction. However, it is necessary for efficient Brachyury repression by RA. Based on these data, I propose that Zfp703 is involved in the transcription regulation during neural progenitor specification. Through downregulating of both mesendodernal fate and pluripotency, Zfp703 de-represses neural transcriptional program and indirectly promotes the default neuroectodermal lineage commitment.
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Tsai, Hung-Li, e 蔡弘曆. "Extracellular Matrix-Cytokine Guides Transdifferentiation from Mesoderm Stem Cells to Neuroectoderm Stem Cells". Thesis, 2014. http://ndltd.ncl.edu.tw/handle/s3rpj5.
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博士臺北醫學大學
醫學科學研究所
102
Mesenchymal stem cells (MSCs) can differentiate into neural stem cells (NSCs) under specific conditions. Wnt was reported to be crucial during embryonic development and adult tissue homeostasis. Wnts regulate neurogenesis, such as neurite and synapse formation, of the neural stem or progenitor cells. In addition to Wnts, tenascin (Tn) family members, TnC and TnR, have been demonstrated to regulate differentiation and migration, as well as neurite outgrowth and survival in numerous types of neurons and progenitor cells. Thus, we hypothesize that Wnt signaling and different forms of Tn regulate the terminal neuronal differentiation in neurotrophin-induced hMSCs. Wnt was also reported, to stimulate hMSC with neurotrophins containing medium (retinoic acid, nerve growth factor, and brain-derived neurotrophic factor; NBR) resulting in the expression of Wnt7a, which enhanced the hMSCs to express neuronal markers in our subsequent analysis, Synapsin-1 (SYN) was induced by Wnt7a and lithium, a glycogen synthase kinase (GSK)-3βinhibitor, in the NBR-induced hMSCs, but was further inhibited by the Wnt inhibitors. Furthermore, hrWnt7a triggered the formation of cholinergic, dopaminergic, GABAergic, and serotonergic neurons. hMSCs were then further cultured in media incorporated with soluble Tn, or on pre-coated Tn. In a qualitative PCR analysis, adding a soluble TnC and TnR mixture to the medium significantly enhanced the expression of neuronal and glial markers, whereas no synaptic markers were expressed. Conversely, in the groups of cells treated with coated TnC, hMSCs showed neurite outgrowth and synaptic marker expression. A combination of TnC and TnR significantly promoted hMSC differentiation in neurons or oligodendrocytes, induced neurite and synapse formation, and inhibited differentiation into astrocytes. In a functional blocking study, integrin α7 and α9β1 blocking antibodies inhibited, respectively, 80% and 20% of the mRNA expression by the hMSCs in the coated Tn mixture. In summary, our results demonstrated novel mechanisms and functions of Wnt7a and Tn for regulating neural differentiation. Data can be broadly employed in the use of MSC to treat neurodegenerative disease.
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Poirier, Steve. "Implication de la convertase NARC-1 / PCSK9 au cours de la différenciation neuroectodermale". Thèse, 2006. http://hdl.handle.net/1866/15585.
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"Molecular analysis of candidate tumor suppressor genes in medulloblastoma and supratentorial primitive neuroectodermal tumor". Thesis, 2005. http://library.cuhk.edu.hk/record=b6073992.
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Medulloblastoma (MB) and supratentorial primitive neuroectodermal tumor (stPNET) are pediatric embryonic brain tumors, which arise in a brain that is in the process of growth and development. They differ significantly from adult lesions and may involve unique genetic and epigenetic factors. However, the pathogenesis of these tumors is still elusive. My project consisted of four parts, investigating major genetic and epigenetic alterations of these tumors.Multiple genetic studies have shown high frequency of loss (30--60%) on chromosome 8p in MBs. Microcell-mediated transfer of chromosome 8 suppressed tumorigenesis or the proliferation of colon and breast cancer cell, indicating that chromosome 8p is likely to include several TSGs in human cancers. In previous studies from our laboratory, results showed the frequency of loss on chromosome 8p is also rather high (66.7%). An overlapping HD region was identified in a 1.8cM interval on 8p22-23.1, between markers D8S520 and D8S1130, in two MBs (Yin et al., 2002), indicating that several candidate TSGs are located within or near this region. PinX1 on 8p23.1, a potential inhibitor of telomerase, is most likely the candidate TSG in MBs due to its location and function. To evaluate the genetic alterations of PinX1 and to investigate its role in MBs, the first part of my study is to perform mutation analysis in a series of 52 primary MBs, 3 MB cell lines and 4 primary stPNETs. Transcript expression of PinX1 was evaluated by reverse transcription-polymerase chain reaction (RT-PCR) in microdissected tumors and normal cerebellum. Using the telomeric repeat amplification protocol (TRAP) assay, 19 MBs, 2 stPNETs and all 3 MB cell lines were analyzed for telomerase activity. No somatic point mutations and loss of expression of PinX1 were detected in our series, suggesting that PinX1 is not the target gene on 8p23.1 in MBs. Although we did not find a significant association between PinX1 expression and telomerase activity, the presence of telomerase activity in 16 of 22 MBs and 1 of 2 stPNETs indicate that telomerase activation is associated with the development of this malignant disease. Our study represents the largest series of MB examined by telomerase repeat amplification protocol (TRAP) assay. (Abstract shortened by UMI.)
Chang Qing.
"April 2005."
Adviser: Ho-Keung Ng.
Source: Dissertation Abstracts International, Volume: 67-01, Section: B, page: 0191.
Thesis (Ph.D.)--Chinese University of Hong Kong, 2005.
Includes bibliographical references (p. 201-228).
Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web.
Electronic reproduction. [Ann Arbor, MI] : ProQuest Information and Learning, [200-] System requirements: Adobe Acrobat Reader. Available via World Wide Web.
Abstracts in English and Chinese.
School code: 1307.
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Tobin, Desmond J. "Ex vivo organ culture of human hair follicles: a model epithelial-neuroectodermal-mesenchymal interaction system". 2010. http://hdl.handle.net/10454/7452.
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noThe development of hair follicle organ culture techniques is a significant milestone in cutaneous biology research. The hair follicle, or more accurately the "pilo-sebaceous unit", encapsulates all the important physiologic processes found in the human body; controlled cell growth/death, interactions between cells of different histologic type, cell differentiation and migration, and hormone responsitivity to name a few. Thus, the value of the hair follicle as a model for biological scientific research goes way beyond its scope for cutaneous biology or dermatology alone. Indeed, the recent and dramatic upturn in interest in hair follicle biology has focused principally on the pursuit of two of biology's holy grails; post-embryonic morphogenesis and control of cyclical tissue activity. The hair follicle organ culture model, pioneered by Philpott and colleagues, ushered in an exceptionally accessible way to assess how cells of epithelial (e.g., keratinocytes), mesenchymal (e.g., fibroblasts), and neuroectodermal (e.g., melanocytes) origin interact in a three-dimensional manner. Moreover, this assay system allows us to assess how various natural and pharmacologic agents affect complex tissues for growth modulation. In this article, I focus on the culture of the human hair follicle mini-organ, discussing both the practical issues involved and some possible research applications of this assay.
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Opel, Daniela [Verfasser]. "Role of phosphoinositide-3-kinase (PI3K), Akt signaling in apoptosis regulation of neuroectodermal tumors / Daniela Opel". 2008. http://d-nb.info/997788496/34.
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Tao, Wei-Yu, e 陶威宇. "Expression of PCSK and Proteolytic Processing of BMP Propeptide on Dorso-Ventral Patterning of Helobdella Neuroectoderm: a Preliminary Study". Thesis, 2015. http://ndltd.ncl.edu.tw/handle/47271389432792250729.
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碩士國立臺灣大學
生命科學系
103
Bone morphogenetic protein (BMP) morphogen is known to play a vital role in body axis patterning during embryogenesis. Unlike BMP4/Dpp functions as a morphogen patterning embryo dorsoventral (DV) axis in vertebrate and fly, BMP5-8 in leech, the key BMP signaling ligand specifies DV patterning, acts in a “cell-cell contact” fashion. Evidences indicate that the ligand BMP proprotein’s differential proteolytic processing by proprotein convertases (PCs or PCSKs) influences its signaling range. Further, different signaling ranges were found between teloblast lineages (N/Q and O/P), above which make the proteolytic processing of BMP5-8 in leech embryo DV patterning an unsolved question. To characterize the role of PCSK-mediated cleavage in leech DV patterning, I carried out the following experiments. First, by reverse transcription-PCR and whole mount in situ hybridization, expressions of all 12 PCSK-related genes in leech have been confirmed and localized at embryogenesis stage 8. Second, a cell surface-linked indicator of proteolysis assay (CLIP) is prepared to test PC activity in vivo. Third, ectopic expression of cleavage site-mutated BMP5-8 in leech has been used. The above results indicate that the proteolytic processing of BMP5-8 is not required for development of normal neuroectodermal, which is also a key event of body axis formation.
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Harris, Kathryn P. "Cdc42 and Par Proteins Regulate the Trafficking of Apical Membrane Proteins to Stabilize Dynamic Adherens Junctions in the Drosophila Neuroectoderm". Thesis, 2010. http://hdl.handle.net/1807/32028.
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Epithelial sheets line the surfaces of the body, forming a barrier between the external environment and internal tissues. During development, regulation of epithelial architechture can drive morphogenesis and build the three-dimensional structures of the body. Epithelial form and function derive from the polarized morphology of epithelial cells, which have apical surfaces that face the external environment, lateral surfaces containing cell-cell junctions and basal surfaces that connect to the underlying tissue. A network of polarity proteins establishes the apico-basolateral axis, while a system of polarized membrane traffic ensures delivery of specialized cargo to distinct membrane surfaces. How these systems of polarity and trafficking are integrated is still poorly understood.
The focus of my study was to investigate how the apical polarity proteins Cdc42, Par6, Bazooka and aPKC (the “Par complex”) regulate polarity and adherens junction (AJ) integrity during Drosophila development. Upon perturbation of Cdc42/Par activity during embryogenesis, apical membrane proteins accumulate in sorting endosomes. This trafficking defect occurs throughout the ectoderm, but in the ventral neuroectoderm (VNE) is accompanied by a concomitant depletion of the apical proteins from the plasma membrane (PM) and a loss of AJ integrity. I have demonstrated that the VNE phenotype is a consequence of the relatively high morphogenetic activity of this tissue. Furthermore, I have shown that the AJ defects are likely a downstream consequence of the depletion of important apical polarity factors, such as Crumbs, from the PM. To further characterize the mechanism of apical trafficking, I searched for interactors of Cdc42/Par in the membrane trafficking machinery. I describe interactions between several trafficking genes and Cdc42/Par and provide evidence that Vps26, a component of the retromer complex that retrieves proteins from endosomal membrane and delivers them to the Golgi for re-secretion, is phosphorylated by aPKC and acts as an aPKC effector in the recycling of apical membrane proteins. I propose that Cdc42/Par regulate the retromer to promote the PM localization of apical proteins, which is important to maintain AJ integrity in morphogenetically active tissues.
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Lee, Kyle Francis. "High resolution DNA copy number analysis of supratentorial primitive neuroectodermal tumours indicates frequent alterations in the cadherin-catenin adhesion pathway". 2009. http://link.library.utoronto.ca/eir/EIRdetail.cfm?Resources__ID=968294&T=F.
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Yang, Shang-Chih, e 楊上知. "Establish an RNA interference based high-throughput screening in human embryonic stem cell and reveal a novel function of ATF1 in early neuroectoderm differentiation". Thesis, 2019. http://ndltd.ncl.edu.tw/handle/9j499p.
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博士國立陽明大學
生化暨分子生物研究所
107
By a shRNA high-throughput screen, I reveal that Activating Transcription Factor 1 (ATF1) is a novel pluripotent regulator in human embryonic stem cells (hESCs). The knockdown of ATF1 expression significantly upregulated neuroectoderm genes but not mesoderm, endoderm, and trophectoderm genes. Of note, downregulation or knockout of ATF1 with shRNA, siRNA, or CRISPR/Cas9 was sufficient to upregulate SOX2 and PAX6 expression under the undifferentiated or differentiated conditions, while overexpression of ATF1 suppressed neuroectoderm differentiation. Endogenous ATF1 was spontaneously downregulated after day(s) 1-3 of neural induction. By double knockdown experiments, upregulation of SOX2 was critical for the increase of PAX6 and SOX1 expression in shATF1 hESCs. Using the luciferase reporter assay, ATF1 acted as a negative transcriptional regulator of SOX2 gene expression. In summary, the novel function of ATF1 was discovered and these findings contribute to a broader understanding of the very first steps of regulating neuroectoderm differentiation in hESCs.
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Hrindová, Božidara. "Dôkaz somatických mutácií významných pre neuroektodermálne nádory (CTNNB1, BRAF, ALK)". Master's thesis, 2015. http://www.nusl.cz/ntk/nusl-343751.
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The diploma thesis was focused on evidence of selected somatic mutations in genes ALK (Anaplastic lymphoma receptor tyrosine kinase), BRAF (v-Raf murine sarcoma viral oncogene homolog B1) and β-catenin (CTNNB1) through molecular - genetic methods in the target group of neuroectodermal tumors (neuroblastoma, medulloblastoma, brain tumors, paraganglioma and pheochromocytoma). Some of them are already considered as prognostic indicators which help to identify the subtype of various tumors and on the basis of this molecular - biological classification choosing the appropriate treatment. The genetic material of 133 patients was used for the analysis divided by the type of cancer. The presence of the mutation was detected in seven cases, of which two of them beloged to the gene BRAF, one to the gene ALK and four to the gene β-catenin. The subject of research in the cases of this genes were hotspot mutation sites. The purpose was to confirm the presence of the mutation in the hotspots and contribute to the studies which are aimed at the introduction of more suitable treatment through the inhibitors of mutated genes. Keywords: ALK, BRAF, β-catenin (CTNNB1), neuroectodermal tumors, sequencing, MLPA
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Žídek, Radim. "Wnt/β-kateninová signalizace ve vývoji mořského kroužkovce Platynereis dumerilii". Doctoral thesis, 2019. http://www.nusl.cz/ntk/nusl-397475.
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Radim Žídek "Wnt/β-catenin signalling in the development of the marine annelid Platynereis dumerilii" (dissertation) Abstract: Wnt/β-catenin signalling is absolutely crucial for the early embryonic development of metazoan animals from the establishment of body axes, through the specification of germ layers and tissues to the development of organ systems. I used pharmacological manipulations of the Wnt/β-catenin pathway activity in the planktonic larvae of the marine polychaete annelid Platynereis dumerilii, the representative of the clade Spiralia, to investigate the role of Wnt/β- catenin signalling in the development and evolution of three hallmarks of Bilateria: the central nervous system, the body segmentation and the digestive tube. Wnt proteins are produced in all three aforementioned systems in Platynereis where they trigger the Wnt/β-catenin pathway in neighbouring cells. I describe here, for the first time in Platynereis, a homologue of the endpoint transcription factor of the entire pathway, Pdu-Tcf, which is subjected to an alternative splicing and along with a Wnt target gene Pdu-Axin is expressed in tissues with the active Wnt signalling - in the brain ganglia, in the neuroectoderm along the ventral midline, in segments, in the posterior growth zone and in the gut. Pharmacological manipulations...
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Vosecká, Tatiana. "Genetické změny u neuroektodermálních nádorů detekované pomocí molekulárně biologických metod". Master's thesis, 2012. http://www.nusl.cz/ntk/nusl-312525.
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9 ABSTRACT Tatiana Labudová: Genetic changes in neuroectodermal tumours detected by molecular biological methods. Charles University in Prague, Faculty of Science, Department of Anthropology and Human Genetics Thesis, 75 pages,8 supplements, 2012 This thesis is concerned to neuroectodermal tumours that make a major group of infant tumour diseases. Genetic material gained from patients with neuroectodermal tumours was examined using comparative genomic hybridization (CGH) and interphasic fluorescence in situ hybridization (I-FISH). The aim of this Thesis is to prove chromosomal changes and to create the whole genetic profile. According to these profiles can be determined tumourgenetic cascade or specific genetic changes that lead to malignant tumours. In some cases (f.e. neuroblastoms) the genetic profile helps us to determine a subtype of disease and it's biological behaviour. Keywords: tumour diseases, neuroblastoma, CNS tumours, pheochromocytoma, Ewing's sarcoma, neuroectodermal tumour, comparative genomic hybridization, interphase fluorescence in situ hybridization