Thematische Bibliographien / Neuroectoderme

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Auswahl der wissenschaftlichen Literatur zum Thema „Neuroectoderme“

Autor: Grafiati

Veröffentlicht am 12. April 2025

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Zeitschriftenartikel zum Thema "Neuroectoderme"

Pereira, Mirley Galvão, Luísa Teixeira Fischer Dias, Maria Carolina Rios Fonseca, Ana Carolina da Bouza Ferreira, Larissa Ramos Xavier De Castro, Cinthia Mares Leão, Iúri Leão De Almeida und Renato Resende Mundim. „Meningite recorrente por Sinus Trato Dérmico Lombossacral“. Brazilian Journal of Health Review 6, Nr. 5 (02.10.2023): 23386–96. http://dx.doi.org/10.34119/bjhrv6n5-402.

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Sinus Trato Dérmico (STD) é uma alteração embriológica devido à não disjunção da neuroectoderme e ectoderme nas primeiras semanas de gestação. Mais comum na em região lombossacral, o STD tem como principal complicação as infecções, sendo mandatória correção cirúrgica após o diagnóstico. Pré-escolar masculino de 3 anos e 11 meses, admitido em pronto socorro infantil com quadro de meningite, que recorreu em 4 dias após tratamento antimicrobiano, sendo readmitido para novo tratamento e diagnosticado nesta ocasião o STD. O paciente foi abordado neurocirurgicamente com boa evolução clínica e sem novas infecções após. O diagnóstico e tratamento do STD deve ser idealmente quando assintomático, uma vez que estabelecida complicação como neuroinfecção a morbimortalidade e risco de sequelas neurológicas aumentam substancialmente nas crianças. O caso relatado evoluiu com desfecho favorável e sem sequelas, no entanto, casos de meningite recorrente são potencialmente fatais.

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Berger, Christian, Joachim Urban und Gerhard M. Technau. „Stage-specific inductive signals in the Drosophila neuroectoderm control the temporal sequence of neuroblast specification“. Development 128, Nr. 17 (01.09.2001): 3243–51. http://dx.doi.org/10.1242/dev.128.17.3243.

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One of the initial steps of neurogenesis in the Drosophila embryo is the delamination of a stereotype set of neural progenitor cells (neuroblasts) from the neuroectoderm. The time window of neuroblast segregation has been divided into five successive waves (S1-S5) in which subsets of neuroblasts with specific identities are formed. To test when identity specification of the various neuroblasts takes place and whether extrinsic signals are involved, we have performed heterochronic transplantation experiments. Single neuroectodermal cells from stage 10 donor embryos (after S2) were transplanted into the neuroectoderm of host embryos at stage 7 (before S1) and vice versa. The fate of these cells was uncovered by their lineages at stage 16/17. Transplanted cells adjusted their fate to the new temporal situation. Late neuroectodermal cells were able to take over the fate of early (S1/S2) neuroblasts. The early neuroectodermal cells preferentially generated late (S4/S5) neuroblasts, despite their reduced time of exposure to the neuroectoderm. Furthermore, neuroblast fates are independent from divisions of neuroectodermal progenitor cells. We conclude from these experiments that neuroblast specification occurs sequentially under the control of non-cell-autonomous and stage-specific inductive signals that act in the neuroectoderm.

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Pruitt, S. C. „Expression of Pax-3- and neuroectoderm-inducing activities during differentiation of P19 embryonal carcinoma cells“. Development 116, Nr. 3 (01.11.1992): 573–83. http://dx.doi.org/10.1242/dev.116.3.573.

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A P19 embryonal carcinoma stem cell line carrying an insertion of the E. coli LacZ gene in an endogenous copy of the Pax-3 gene was identified. Expression of the Pax-3/LacZ fusion gene in neuroectodermal and mesodermal lineages following induction of differentiation by chemical treatments (retinoic acid and dimethylsulfoxide) was characterized using this line and is consistent with the previous localization of Pax-3 expression in the embryo to mitotically active cells of the dorsal neuroectoderm and the adjacent segmented dermomyotome. Pax-3/LacZ marked stem cells were also utilized as target cells in mixing experiments with unmarked P19 cells that had been differentiated by pretreatment with chemical inducers. Induction of beta-galactosidase and neuroectodermal markers in the target cells demonstrates that: (1) some differentiated P19 cell derivatives transiently express endogenous Pax-3- and neuroectoderm-inducing activities, (2) undifferentiated target stem cells respond to these activities even in the presence of leukemia inhibitory factor and (3) the endogenous activities can be distinguished from, and are more potent than, retinoic acid treatment in inducing neuroectoderm. These observations demonstrate that P19 embryonal carcinoma cells provide a useful in vitro system for analysis of the cellular interactions responsible for neuroectoderm induction in mammals.

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McDonald, J. A., und C. Q. Doe. „Establishing neuroblast-specific gene expression in the Drosophila CNS: huckebein is activated by Wingless and Hedgehog and repressed by Engrailed and Gooseberry“. Development 124, Nr. 5 (01.03.1997): 1079–87. http://dx.doi.org/10.1242/dev.124.5.1079.

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The Drosophila ventral neuroectoderm produces a stereotyped array of central nervous system precursors, called neuroblasts. Each neuroblast has a unique identity based on its position, pattern of gene expression and cell lineage. To understand how neuronal diversity is generated, we need to learn how neuroblast-specific gene expression is established, and how these genes control cell fate within neuroblast lineages. Here we address the first question: how is neuroblast-specific gene expression established? We focus on the huckebein gene, because it is expressed in a subset of neuroblasts and is required for aspects of neuronal and glial determination. We show that Huckebein is a nuclear protein first detected in small clusters of neuroectodermal cells and then in a subset of neuroblasts. The secreted Wingless and Hedgehog proteins activate huckebein expression in distinct but overlapping clusters of neuroectodermal cells and neuroblasts, whereas the nuclear Engrailed and Gooseberry proteins repress huckebein expression in specific regions of neuroectoderm or neuroblasts. Integration of these activation and repression inputs is required to establish the precise neuroectodermal pattern of huckebein, which is subsequently required for the development of specific neuroblast cell lineages.

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Batsakis, John G., Bruce MacKay und Adel K. El-Naggar. „Ewing's Sarcoma and Peripheral Primitive Neuroectodermal Tumor: An Interim Report“. Annals of Otology, Rhinology & Laryngology 105, Nr. 10 (Oktober 1996): 838–43. http://dx.doi.org/10.1177/000348949610501014.

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The primitive neuroectoderm and its progeny seemingly give rise to an ever-increasing number of clinicopathologic entities. Ewing's sarcoma and peripheral primitive neuroectodermal tumor have recently been united by relatively unique antigens expressed by the MIC-2 gene, commonly coexpressed neural markers, and cytogenetic and molecular genetic abnormalities. Because of these factors, the current thinking is that Ewing's sarcoma and the peripheral primitive neuroectodermal tumor are parts of a phenotypic spectrum. We present an “interim report” on this group of neoplasms, emphasizing their presentation in the head and neck

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José Martin, Toranzo Fernández, Salgado-García Nickte-ha und Santos-Díaz Miguel Ángel. „Primitive neuroectodermal tumor in the jaw: report of a case“. Journal of Clinical Pediatric Dentistry 28, Nr. 2 (01.01.2005): 167–71. http://dx.doi.org/10.17796/jcpd.28.2.d272qrxj804r0403.

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The neuroectodermal tumor is a malignant neoplasm of round cells originated from the neural crest. The occurrence of this tumor in head and neck is rare.A 5 month old Mexican patient with a primitive neuroectodermic tumor stage IV, in the jaw is reported.

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Buc-Caron, MH, JM Launay, PJ Marie und O. Kellermann. „Une stratégie pour immortaliser des lignées orientées vers l'endoderme, le neuroectoderme ou le mésoderme à partir du tératocarcinome de la souris“. Reproduction Nutrition Développement 30, Nr. 3 (1990): 309–16. http://dx.doi.org/10.1051/rnd:19900303.

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Fernández, Mercedes, Micaela Pannella, Vito Antonio Baldassarro, Alessandra Flagelli, Giuseppe Alastra, Luciana Giardino und Laura Calzà. „Thyroid Hormone Signaling in Embryonic Stem Cells: Crosstalk with the Retinoic Acid Pathway“. International Journal of Molecular Sciences 21, Nr. 23 (25.11.2020): 8945. http://dx.doi.org/10.3390/ijms21238945.

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While the role of thyroid hormones (THs) during fetal and postnatal life is well-established, their role at preimplantation and during blastocyst development remains unclear. In this study, we used an embryonic stem cell line isolated from rat (RESC) to study the effects of THs and retinoic acid (RA) on early embryonic development during the pre-implantation stage. The results showed that THs play an important role in the differentiation/maturation processes of cells obtained from embryoid bodies (EB), with thyroid hormone nuclear receptors (TR) (TRα and TRβ), metabolic enzymes (deiodinases 1, 2, 3) and membrane transporters (Monocarboxylate transporters -MCT- 8 and 10) being expressed throughout in vitro differentiation until the Embryoid body (EB) stage. Moreover, thyroid hormone receptor antagonist TR (1-850) impaired RA-induced neuroectodermal lineage specification. This effect was significantly higher when cells were treated with retinoic acid (RA) to induce neuroectodermal lineage, studied through the gene and protein expression of nestin, an undifferentiated progenitor marker from the neuroectoderm lineage, as established by nestin mRNA and protein regulation. These results demonstrate the contribution of the two nuclear receptors, TR and RA, to the process of neuroectoderm maturation of the in vitro model embryonic stem cells obtained from rat.

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Kramatschek, B., und J. A. Campos-Ortega. „Neuroectodermal transcription of the Drosophila neurogenic genes E(spl) and HLH-m5 is regulated by proneural genes“. Development 120, Nr. 4 (01.04.1994): 815–26. http://dx.doi.org/10.1242/dev.120.4.815.

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The Enhancer of split gene complex (E(SPL)-C) of Drosophila comprises seven genes encoding bHLH proteins, which are required by neuroectodermal cells for epidermal development. Using promoter and gene fusions with the lacZ gene, we determined the location of cis-acting sequences necessary for normal expression of two of the genes of the E(SPL)-C, E(spl) and HLH-m5. About 0.46 kb of E(spl) and 1.9 kb of HLH-m5 upstream sequences are necessary to reproduce the normal transcription pattern of these genes. The gene products of achaete, scute and lethal of scute, together with that of ventral nervous system condensation defective, act synergistically to specify the neuroectodermal E(spl) and HLH-m5 expression domains. Negative cross- and autoregulatory interactions of the E(SPL)-C on E(spl) contribute, directly or indirectly, to this regulation. Interactions involve DNA binding, since mutagenesis of binding sites for bHLH proteins in the E(spl) promoter abolishes neuroectodermal expression and activates ectopic expression in neuroblasts. A model for activation and repression of E(spl) in the neuroectoderm and neuroblasts, respectively, is proposed.

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Stüttem, Isabella, und José A. Campos-Ortega. „Cell commitment and cell interactions in the ectoderm of Drosophila melanogaster“. Development 113, Supplement_2 (01.04.1991): 39–46. http://dx.doi.org/10.1242/dev.113.supplement_2.39.

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The separation of neural from epidermal progenitor cells in the ventral neuroectoderm of Drosophila is thought to be mediated by cellular interactions. In order to verify the occurrence of regulatory signals and to test the neurogenic capabilities of cells from various regions of the ectoderm, we have carried out homotopic and heterotopic transplantations of single ectodermal cells. We found that cells from any of the tested regions, with the exception of the proctodeal anlage, are capable of developing as neuroblasts following their transplantation into the ventral neuroectoderm. These neurogenic capabilities are gradually distributed. Cells from the procephalic and ventral neurogenic regions exhibit maximal capabilities, as shown by their behavior in heterotopic transplantations. However, the two neurogenic regions differ from each other in that no epidermalising signals can be demonstrated to occur within the procephalic neuroectoderm, whereas such signals are strong within the ventral neuroectoderm; in addition, neuralising signals from neighbouring cells seem to be necessary for neuroectodermal cells to develop as neuroblasts. Other ectodermal regions whose cells exhibit weaker neurogenic capabilities are, in decreasing order of capability, the dorsal epidermal anlage, the anterolateral region of the procephalic lobe, comprising the anlage of the pharynx, and the anterior pole of the embryo, corresponding to the anlagen of the stomodeum and ectodermal anterior midgut. We assume that, during development in situ, the neurogenic capabilities of all these cells are suppressed by inhibitory signals, which are released upon heterotopic transplantation into the neuroectoderm. A community effect which prevents groups of dorsal epidermal cells from taking on a neural fate upon their transplantation into the ventral neuroectoderm, is shown. Finally, we hypothesize that the lack of neurogenic capability in the cells from the proctodeal anlage is due to the absence of products of the proneural genes.

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Dissertationen zum Thema "Neuroectoderme"

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'HPE
Abstract : 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

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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

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Orbegoso-Celis, L., R. Bernuy-Guerrero, F. Imán-Izquierdo, L. Alfaro-Lujan, Espinoza L. Barreto und 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

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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.

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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

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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.

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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.

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Bücher zum Thema "Neuroectoderme"

J, Staal Gerard E., und Veelen, Cees W. M. van., Hrsg. Markers of human neuroectodermal tumors. Boca Raton, Fla: CRC Press, 1986.

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Huang, Yuan-Ping. Transcriptional Regulation of Neuroectodermal Lineage Commitment in Embryonic Stem Cells. [New York, N.Y.?]: [publisher not identified], 2014.

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Taylor, Roger E. Principles of paediatric radiation oncology. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199696567.003.0020.

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Chapter 15 discusses the principles of paediatric radiation oncology, and addresses quality assurance, chemotherapy/radiotherapy interactions, Leukaemia, Hodgkin lymphoma, Non-Hodgkin lymphoma, Neuroblastoma, Rhabdomyosarcoma, Ewing’s sarcoma/peripheral primitive neuroectodermal tumour, Osteosarcoma, central nervous system tumours, Intensity-modulated radiotherapy, and proton therapy for paediatric tumours.

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Acton, Ronald T., G. Bennett Humphrey, Louis P. Dehner und Gerald B. Grindey. Pediatric Oncology 1: With a Special Section on Rare Primitive Neuroectodermal Tumors. Springer Netherlands, 2011.

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Acton, Ronald T., G. Bennett Humphrey, Louis P. Dehner und Gerald B. Grindey. Pediatric Oncology 1: With a Special Section on Rare Primitive Neuroectodermal Tumors. Springer, 2012.

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Biochemistry of Neuroectodermal Tumours: A special issue of the journal Clinical Chemistry and Enzymology Communications. Routledge, 1990.

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Publications, ICON Health. The Official Parent's Sourcebook On Childhood Supratentorial Primitive Neuroectodermal And Pineal Tumors: Directory For The Internet Age. Icon Health Publications, 2005.

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Mason, Peggy. Cells of the Nervous System. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190237493.003.0002.

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The nervous system is made up of neurons and glia that derive from neuroectoderm. Since neurons are terminally differentiated and do not divide, primary intracranial tumors do not arise from mature neurons. Tumors outside the nervous system may metastasize inside the brain or may release a substance that negatively affects brain function, termed paraneoplastic disease. Neurons receive information through synaptic inputs onto dendrites and soma and send information to other cells via a synaptic terminal. Most neurons send information to faraway locations and for this, an axon that connects the soma to synaptic terminals is required. Glial cells wrap axons in myelin, which speeds up information transfer. Axonal transport is necessary to maintain neuronal function and health across the long distances separating synaptic terminals and somata. A common mechanism of neurodegeneration arises from impairments in axonal transport that lead to protein aggregation and neuronal death.

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Melino, Gerry. Biochemistry of Neuroectodermal Tumours: A special issue of the journal Clinical Chemistry and Enzymology Communications (Clinical Chemistry and Enzymology Communications,). Routledge, 1994.

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Lundh, Barbro. Neurovirulence of enveloped RNA viruses: Studies of neuroectodermal cell infection and neuroinvasion of vesicular stomatitis and sendai viruses in the mouse. 1988.

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Buchteile zum Thema "Neuroectoderme"

Michaels, Leslie, und Henrik B. Hellquist. „Neuroectodermal Tumours“. In Ear, Nose and Throat Histopathology, 203–17. London: Springer London, 2001. http://dx.doi.org/10.1007/978-1-4471-0235-9_18.

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Michaels, L. „Neuroectodermal Tumours“. In Ear, Nose and Throat Histopathology, 189–201. London: Springer London, 1987. http://dx.doi.org/10.1007/978-1-4471-3332-2_18.

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Abada, Evi. „Neuroectodermal Tumors“. In Encyclopedia of Pathology, 1–3. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-319-28845-1_5589-1.

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Goldstein, Bram. „Primitive Neuroectodermal Tumor“. In Encyclopedia of Clinical Neuropsychology, 2025–26. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-0-387-79948-3_150.

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Goldstein, Bram. „Primitive Neuroectodermal Tumor“. In Encyclopedia of Clinical Neuropsychology, 1–2. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-56782-2_150-2.

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Goldstein, Bram. „Primitive Neuroectodermal Tumor“. In Encyclopedia of Clinical Neuropsychology, 2817. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-57111-9_150.

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Peraud, Aurelia, Jörg-Christian Tonn und James T. Rutka. „Dysembryoplastic Neuroectodermal Tumors“. In Oncology of CNS Tumors, 555–60. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-04152-6_29.

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Peraud, Aurelia, Jörg-Christian Tonn und James T. Rutka. „Dysembryoplastic Neuroectodermal Tumors“. In Oncology of CNS Tumors, 533–37. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-02874-8_38.

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Fisher, Cyril. „Neuroectodermal and Neural Tumors“. In Atlas of Soft Tissue Tumor Pathology, 99–106. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-7025-0_10.

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Singh, Mohit, und Juliette Hukin. „Supratentorial Primitive Neuroectodermal Tumors“. In Tumors of the Central Nervous System, Volume 4, 15–24. Dordrecht: Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-94-007-1706-0_2.

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Konferenzberichte zum Thema "Neuroectoderme"

Seixas, João Alfredo, Filomena Aste Silveira, Luciana Amaral Lemos, Maria Eduarda Amaral Faria, Caroline Guida Babinski und Raquel de Marco Rodrigues de Sousa. „Carcinoma neuroendócrino de grandes células do colo do útero: a propósito um caso“. In 44° Congresso da SGORJ - XXIII Trocando Ideias. Zeppelini Editorial e Comunicação, 2020. http://dx.doi.org/10.5327/jbg-0368-1416-2020130206.

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Introdução: As neoplasias neuroendócrinas (NENs) se originam da neuroectoderme embrionária e exibem perfil imuno-histoquímico consistente, com células glandulares endócrinas. Representam um grupo diverso de neoplasias raras que são mais comumente originadas no trato gastrointestinal, embora possam se originar em qualquer parte do corpo em razão da ampla distribuição do sistema neuroendócrino. O carcinoma neuroendócrino do colo do útero é responsável por aproximadamente 0,5 a 1% dos casos de câncer do colo do útero, dos quais cerca de 12,5% são de células grandes, sendo uma variante histológica agressiva desse tipo de câncer, com sobrevida de cinco anos em 34% dos casos. Relato de Caso: Paciente de 66 anos, com queixa de sangramento uterino anormal. No exame físico: massa exteriorizando por orifício externo de canal cervical, com laudo anatomopatológico indeterminado (leiomiossarcoma?) e posterior estudo imuno-histoquímico: cromogranina, sinaptofisina e CD56 positivos; conclusão: carcinoma neuroendócrino de grandes células. Paciente submetida a tratamento cirúrgico e quimioterapia posterior. No momento, em tratamento radioterápico paliativo em razão de recidiva local, com acometimento regional dos sistemas linfático, vascular e urinário. Conclusão: A origem das NENs cervicais não é clara, não havendo lesão precursora definida. Apesar de melhora no prognóstico com a evolução do seu sistema de classificação (OMS-2003), aliado a intervenção cirúrgica mais agressiva e terapia adjunta, o carcinoma neuroendócrino de grandes células ainda constitui um subtipo mais agressivo, com um curso clínico rápido. A sobrevida e o prognóstico global das NENs cervicais são marcadamente piores, quando comparado ao carcinoma de células escamosas cervical ou adenocarcinoma de fase comparável. À medida que a compreensão molecular e genética das NENs aumenta, a criação de opções terapêuticas direcionadas para esses tumores, independentemente da localização dentro do corpo, torna-se mais uma realidade.

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Pisano, Marina, Gabriella Pagnan, Maria Antonietta Dettori, Sara Cossu, Irene Caffa, Ilaria Sassu, Davide Fabbri et al. „Abstract B202: A new curcumin analogue compound endowed with strong antitumor activity against neuroectoderma‐derived cancers“. In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 15-19, 2009; Boston, MA. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/1535-7163.targ-09-b202.

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Sturm, Dominik, Paul A. Northcott, David T. W. Jones, Andrey Korshunov, Daniel Picard, Peter Lichter, Annie Huang, Stefan M. Pfister und Marcel Kool. „Abstract 3089: (Epi)genetic profiling enables molecular re-classification of CNS-primitive neuroectodermal tumors“. In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-3089.

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Loi, Monica, Arianna Giacomini, Pamela Becherini, Fabio Pastorino und Mirco Ponzoni. „Abstract 5609: Bortezomib enhanced cytotoxic effects of novel sTRAIL-targeted nanocarriers against neuroectodermal tumors .“ In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-5609.

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Ahsan, Sama F., Allison Hanaford, Melanie Weingart, Isabella Taylor, Charles Eberhart und Eric Raabe. „Abstract 5051: MYC-driven models of primitive neuroectodermal tumor are sensitive to inhibitors of glutamine metabolism.“ In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-5051.

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Spuldaro, Patricia, Carolline Paggi Montemezzo, Daniellen Brunetto, Gabriela Simionato, Vitória Loss und Delci Inês Zortea Zanusso. „Anoftalmia bilateral congênita associado à surdez bilateral profunda: Relato de caso“. In II SEVEN INTERNATIONAL MEDICAL AND NURSING CONGRESS. Seven Congress, 2023. http://dx.doi.org/10.56238/iicongressmedicalnursing-069.

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A anoftalmia é uma condição oftalmológica rara caracterizada pela ausência de globo ocular com preservação dos seus anexos, que normalmente está associada a síndromes congênitas e malformações extra oculares. Supõe-se que fisiopatologia está relacionada a defeitos no desenvolvimento do neuroectoderma entre a quarta e a sétima semana da embriogênese. Sua etiologia é complexa e ainda não elucidada, envolvendo fatores genéticos e ambientais. Neste estudo relata-se um caso de um paciente do sexo masculino que apresenta anoftalmia bilateral congênita associado a surdez. Foram utilizados dados coletados do prontuário médico durante as consultas de puericultura em uma Unidade Básica de Saúde. Mãe previamente hígida, pré-natal e parto sem intercorrências, paciente nascido a termo por cesariana, peso adequado para idade. Foi identificado anoftalmia bilateral após resistência à abertura ocular no exame físico. Nas triagens neonatais falhou no teste auditivo e foi diagnosticado posteriormente surdez profunda bilateral. Nos testes genéticos apresentou cariótipo normal 46 XY. Está no processo de colocação de implante coclear e está em uso de expansores da cavidade ocular para futuramente alojar uma prótese, o que vai permitir desenvolvimento adequado da face. A raridade da doença descrita, a escassez de pesquisa nesse âmbito e a falta de métodos diagnósticos mais acurados dificultam o diagnóstico precoce e o manejo adequado dessa e outras patologias, evidenciando a necessidade de expandir o conhecimento médico a respeito das condições congênitas.

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McGrail, Maura A., Staci L. Solin, Jeffrey A. Haltom, Laura E. Schultz, Jeffrey J. Essner und Heather R. Shive. „Abstract 4179: Expression profiling of zebrafish rb1- neuroectodermal-like brain tumors: A new model of CNS PNETs“. In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-4179.

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Seidel, Diana, Nicole Huebener, Tina Mueller, Dörthe Pferdmenges, Anastasia Shibina, Torsten Tonn, Ulrike Koehl, Ruth Esser, Winfried S. Wels und Holger N. Lode. „Abstract 5601: NK cells engineered to express the chimeric receptor scFv(ch14.18)-zeta specifically lyse GD2 expressing neuroectodermal tumors“. In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-5601.

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Falahat, Rana, Eva Williams, Marzenna Wiranowska, Ryan Toomey und Norma Alcantar. „Abstract 3677: Enhanced targeted delivery of paclitaxel to tumor cells of epithelial and neuroectodermal origin using chlorotoxin-chitosan nanodelivery system“. In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-3677.

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Gessi, Marco, Andre' von Bueren, Andras Treszl, Anja zur Muehlen, Stefan Rutkowski und Torsten Pietsch. „Abstract 4702: Chromosome 2p gain andN-Mycamplification predict poor outcome of patients with LIN28 negative supratentorial primitive neuroectodermal tumors of the central nervous system (CNS-PNET)..“ In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-4702.

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Berichte der Organisationen zum Thema "Neuroectoderme"

Raju, Dr Dinesh, Dr Chinnamuthu Murugesan, Dr Sanjaya Kumar Bnakal und Dr N. Chennakeshava. Melanotic neuroectodermal tumour- difficult airway management in an infant. The Association of Anaesthetists of Great Britain and Ireland, Februar 2014. http://dx.doi.org/10.21466/ac.odaapnb.2014.

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