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1
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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Slack, R. S., I. S. Skerjanc, B. Lach, J. Craig, K. Jardine und M. W. McBurney. „Cells differentiating into neuroectoderm undergo apoptosis in the absence of functional retinoblastoma family proteins.“ Journal of Cell Biology 129, Nr. 3 (01.05.1995): 779–88. http://dx.doi.org/10.1083/jcb.129.3.779.
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The retinoblastoma (RB) protein is present at low levels in early mouse embryos and in pluripotent P19 embryonal carcinoma cells; however, the levels of RB rise dramatically in neuroectoderm formed both in embryos and in differentiating cultures of P19 cells. To investigate the effect of inactivating RB and related proteins p107 and p130, we transfected P19 cells with genes encoding mutated versions of the adenovirus E1A protein that bind RB and related proteins. When these E1A-expressing P19 cells were induced to differentiate into neuroectoderm, there was a striking rise in the expression of c-fos and extensive cell death. The ultrastructural and biochemical characteristics of the dying cells were indicative of apoptosis. The dying cells were those committed to the neural lineages because neurons and astrocytes were lost from differentiating cultures. Cell death was dependent on the ability of the E1A protein to bind RB and related proteins. Our results suggest that proteins of the RB family are essential for the development of the neural lineages and that the absence of functional RB activity triggers apoptosis of differentiating neuroectodermal cells.
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Rhinn, M., A. Dierich, W. Shawlot, R. R. Behringer, M. Le Meur und S. L. Ang. „Sequential roles for Otx2 in visceral endoderm and neuroectoderm for forebrain and midbrain induction and specification“. Development 125, Nr. 5 (01.03.1998): 845–56. http://dx.doi.org/10.1242/dev.125.5.845.
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The homeobox gene Otx2 is a mouse cognate of the Drosophila orthodenticle gene, which is required for development of the brain, rostral to rhombomere three. We have investigated the mechanisms involved in this neural function and specifically the requirement for Otx2 in the visceral endoderm and the neuroectoderm using chimeric analysis in mice and explant recombination assay. Analyses of chimeric embryos composed of more than 90% of Otx2−/− ES cells identified an essential function for Otx2 in the visceral endoderm for induction of the forebrain and midbrain. The chimeric studies also demonstrated that an anterior neural plate can form without expressing Otx2. However, in the absence of Otx2, expression of important regulatory genes, such as Hesx1/Rpx, Six3, Pax2, Wnt1 and En, fail to be initiated or maintained in the neural plate. Using explant-recombination assay, we could further demonstrate that Otx2 is required in the neuroectodem for expression of En. Altogether, these results demonstrate that Otx2 is first required in the visceral endoderm for the induction, and subsequently in the neuroectoderm for the specification of forebrain and midbrain territories.
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Baleato-González, Sandra, Maria Gabriela Tirapu-de-Sagrario, Elena Pintos-Martínez und Roberto García-Figueiras. „Scrotal Peripheral Primitive Neuroectodermal Tumor“. Current Urology 12, Nr. 1 (2018): 50–53. http://dx.doi.org/10.1159/000447231.
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The peripheral primitive neuroectodermal tumor (pPNET) is a rare malignant tumor originating from neuroectoderm that usually occurs in children or adolescent and is frequently located in the extremities, chest cavity, pelvic cavity and chest wall. We present a rare case of an 84-year-old man with a history of pPNET in the scrotal sac, to our knowledge not previously published in the literature. The presence of a large irreducible mass in the inguinal sac forced to exclude a tumor. Ultrasound and MRI are very useful modalities to assess the location of the mass, its dependency from any organ and the tumoral internal structure. Molecular imaging with the detection of EWS-FLI1 fusion transcripts is useful for the diagnosis and differential diagnosis of Ewing sarcoma/pPNETs.
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Regal, Joshua, Maria Guerra-Garcia, Vaibhav Jain, Vidyalakshmi Chandramohan, David Ashley, Simon Gregory, Eric Thompson, Giselle Lopez und Zachary Reitman. „LGG-13. GANGLIOGLIOMA DEEP TRANSCRIPTOMICS REVEALS A CD34+ PRIMITIVE NEUROECTODERM NEURAL PRECURSOR-LIKE POPULATION“. Neuro-Oncology 25, Supplement_1 (01.06.2023): i58. http://dx.doi.org/10.1093/neuonc/noad073.223.
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Abstract Gangliogliomas are glioneuronal brain tumors that typically present in childhood or early adulthood. Though most often low-grade, new insights are needed to refine glioneuronal tumor classification and to identify therapeutic approaches, particularly for unresectable, high-grade, and/or recurrent disease. Gangliogliomas often possess a rare population of immature astrocyte-appearing CD34+ cells. CD34 is expressed in neuroectoderm neural precursor cells during embryogenesis. Neural cell CD34 expression is usually lost prior to birth. We hypothesized that CD34+ ganglioglioma cells represent tumor precursor/stem cells and closely resemble ganglioglioma cells of origin. To test this, we evaluated five gangliogliomas with single nucleus RNA-seq, cellular indexing of transcriptomes and epitopes by sequencing, and/or spatially-resolved RNA-seq. Developmental trajectory analyses uncovered a neoplastic cellular hierarchy, with CD34+PAX6+SOX2+MSI1+PECAM1-VWF-DCN-COL1A2- cells being the most primordial and precursor to neuron-like and macroglia-like neoplastic cell states. Gene regulatory network inference of CD34+ ganglioglioma cells indicated TCF7L2/MEIS1-PAX6 and SOX2-mediated transcriptional programming, similar to that found during neuroectodermal/neural development in utero. Spatially-resolved transcriptomics revealed a neuroectoderm neural precursor-like tumor cell niche relatively devoid of vascular and immune cells. We used these high-resolution results to deconvolute clinically-annotated transcriptomic data, confirming that CD34+ neural precursor-like cell-associated gene programs associate with gangliogliomas compared to other brain tumors. Together, these deep transcriptomic approaches characterized a ganglioglioma cellular hierarchy - identifying CD34+ neuroectoderm neural precursor-like tumor-initiating cells, corresponding regulatory transcriptional programs, cell signaling pathways, and associated immune cell states. These findings may facilitate improved ganglioglioma tumor classification, diagnosis, and therapeutic investigations.
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Kim, K. J., B. W. Jang, S. K. Lee, B. K. Kim und S. L. Nam. „A case of peripheral primitive neuroectodermal tumor of the ovary“. International Journal of Gynecologic Cancer 14, Nr. 2 (2004): 370–72. http://dx.doi.org/10.1136/ijgc-00009577-200403000-00027.
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Peripheral primitive neuroectodermal tumor (PNET) belongs to the PNET/Ewing's sarcoma family. PNET is a small round cell tumor of putative neuroectoderm origin and is the second most common sarcoma among children and young adults. It may occur anywhere in the body and within any age group; however, it is most likely to occur in the bone and soft tissues. There have been a small number of case reports of PNET arising in the ovary. We presented a case of PNET arising in the right ovary of an 18-year-old woman. The tumor was metastased to the lymph nodes of the pelvis and para-aorta at surgical staging. We had persecuted Taxol/carboplatin chemotherapy, pelvic cavity radiotherapy, and Vincristine/Actinomycink, Cyclophosphamide/Doxorubicin (VACA). She died after 10 months due to septic shock.
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Matsuzaki, M., und K. Saigo. „hedgehog signaling independent of engrailed and wingless required for post-S1 neuroblast formation in Drosophila CNS“. Development 122, Nr. 11 (01.11.1996): 3567–75. http://dx.doi.org/10.1242/dev.122.11.3567.
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The hedgehog gene product, secreted from engrailed-expressing neuroectoderm, is required for the formation of post-S1 neuroblasts in rows 2, 5 and 6. The hedgehog protein functions not only as a paracrine but also as an autocrine factor and its transient action on the neuroectoderm 1–2 hours (at 18 degrees C) prior to neuroblast delamination is necessary and sufficient to form normal neuroblasts. In contrast to epidermal development, hedgehog expression required for neuroblast formation is regulated by neither engrailed nor wingless. hedgehog and wingless bestow composite positional cues on the neuroectodermal regions for S2-S4 neuroblasts at virtually the same time and, consequently, post-S1 neuroblasts in different rows can acquire different positional values along the anterior-posterior axis. The average number of proneural cells for each of three eagle-positive S4-S5 neuroblasts was found to be 5–9, the same for S1 NBs. As with wingless (Chu-LaGraff et al., Neuron 15, 1041–1051, 1995), huckebein expression in putative proneural regions for certain post-S1 neuroblasts is under the control of hedgehog. hedgehog and wingless are involved in separate, parallel pathways and loss of either is compensated for by the other in NB 7–3 formation. NBs 6–4 and 7–3, arising from the engrailed domain, were also found to be specified by the differential expression of two homeobox genes, gooseberry-distal and engrailed.
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Jussen, David, Janina von Hilchen und Rolf Urbach. „Genetic regulation and function of epidermal growth factor receptor signalling in patterning of the embryonic Drosophila brain“. Open Biology 6, Nr. 12 (Dezember 2016): 160202. http://dx.doi.org/10.1098/rsob.160202.
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The specification of distinct neural cell types in central nervous system development crucially depends on positional cues conferred to neural stem cells in the neuroectoderm. Here, we investigate the regulation and function of the epidermal growth factor receptor (EGFR) signalling pathway in early development of the Drosophila brain. We find that localized EGFR signalling in the brain neuroectoderm relies on a neuromere-specific deployment of activating (Spitz, Vein) and inhibiting (Argos) ligands. Activated EGFR controls the spatially restricted expression of all dorsoventral (DV) patterning genes in a gene- and neuromere-specific manner. Further, we reveal a novel role of DV genes— ventral nervous system defective ( vnd ), intermediate neuroblast defective (ind), Nkx6 —in regulating the expression of vein and argos , which feed back on EGFR, indicating that EGFR signalling stands not strictly atop the DV patterning genes. Within this network of genetic interactions, Vnd acts as a positive EGFR feedback regulator. Further, we show that EGFR signalling becomes dependent on single-minded -expressing midline cells in the posterior brain (tritocerebrum), but remains midline-independent in the anterior brain (deuto- and protocerebrum). Finally, we demonstrate that activated EGFR controls the proper formation of brain neuroblasts by regulating the number, survival and proneural gene expression of neuroectodermal progenitor cells. These data demonstrate that EGFR signalling is crucially important for patterning and early neurogenesis of the brain.
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Hardy, R. J., und V. L. Friedrich. „Oligodendrocyte progenitors are generated throughout the embryonic mouse brain, but differentiate in restricted foci“. Development 122, Nr. 7 (01.07.1996): 2059–69. http://dx.doi.org/10.1242/dev.122.7.2059.
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Recent evidence from studies mapping the expression of putative oligodendrocyte progenitor specific mRNAs has suggested that oligodendrocyte progenitors arise during embryogenesis, in specific foci of the neuroectoderm. In order to test this hypothesis, we have assayed different regions of the embryonic central nervous system for their ability to generate oligodendrocytes following transplantation into neonatal cerebrum. To allow identification of donor-derived oligodendrocytes in wild-type host brain, we used the MbetaP transgenic mouse, which expresses lacZ in oligodendrocytes, as donor tissue. We found that tissue fragments derived from several levels of the anterior-posterior axis of the neural tube at E14.5 and E12.5, chosen to include (hindbrain, cervical and lumbar spinal cord), or exclude (dorsal telencephalon) putative foci of oligodendrocyte progenitors, all produced oligodendrocytes following transplantation. In addition, these same regions taken from E10.5, prior to the appearance of putative oligodendrocyte progenitor markers, also all yielded oligodendrocytes on transplantation. This indicates that precursor cells that can generate oligodendrocytes are widespread throughout the neuroectoderm as early as E10.5. We have also used the oligodendrocyte lineage-specific glycolipid antibodies O4, R-mAb and O1 to identify those regions of the developing brain that first support the differentiation of oligodendrocytes from their progenitor cells. We found that the first oligodendrocytes arise in prenatal brain at E14.5, in a restricted zone adjacent to the midline of the medulla. These cells are mitotically inactive, differentiated oligodendrocytes and, using light and electron microscopy, we show that they become functional, myelin-bearing oligodendrocytes. We have mapped the subsequent appearance of differentiated oligodendrocytes in the prenatal brain and show that they appear in a restricted, tract-specific manner. Our results suggest that oligodendrocytes are generated from neuroectodermal cells positioned throughout the rostrocaudal axis of the neural tube, rather than at restricted locations of the neuroectoderm. By contrast, the differentiation of such cells into oligodendrocytes does occur in a restricted manner, consistent with local regulation of oligodendrocyte progenitor differentiation.
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Kuratani, S. C., und G. Eichele. „Rhombomere transplantation repatterns the segmental organization of cranial nerves and reveals cell-autonomous expression of a homeodomain protein“. Development 117, Nr. 1 (01.01.1993): 105–17. http://dx.doi.org/10.1242/dev.117.1.105.
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The developing vertebrate hindbrain consists of segmental units known as rhombomeres. Hindbrain neuroectoderm expresses 3′ Hox 1 and 2 cluster genes in characteristic patterns whose anterior limit of expression coincides with rhombomere boundaries. One particular Hox gene, referred to as Ghox 2.9, is initially expressed throughout the hindbrain up to the anterior border of rhombomere 4 (r4). Later, Ghox 2.9 is strongly upregulated in r4 and Ghox 2.9 protein is found in all neuroectodermal cells of r4 and in the hyoid crest cell population derived from this rhombomere. Using a polyclonal antibody, Ghox 2.9 was immunolocalized after transplanting r4 within the hindbrain. Wherever r4 was transplanted, Ghox 2.9 expression was cell-autonomous, both in the neuroectoderm of the graft and in the hyoid crest cell population originating from the graft. In all vertebrates, rhombomeres and cranial nerves (nerves V, VII+VIII, IX, X) exhibit a stereotypic relationship: nerve V arises at the level of r2, nerve VII+VIII at r4 and nerves IX-X extend caudal to r6. To examine how rhombomere transplantation affects this pattern, operated embryos were stained with monoclonal antibodies E/C8 (for visualization of the PNS and of even-numbered rhombomeres) and HNK-1 (to detect crest cells and odd-numbered rhombomeres). Upon transplantation, rhombomeres did not change E/C8 or HNK-1 expression or their ability to produce crest cells. For example, transplanted r4 generated a lateral stream of crest cells irrespective of the site into which it was grafted. Moreover, later in development, ectopic r4 formed an additional cranial nerve root. In contrast, transplantation of r3 (lacks crest cells) into the region of r7 led to inhibition of nerve root formation in the host. These findings emphasize that in contrast to spinal nerve segmentation, which entirely depends on the pattern of somites, cranial nerve patterning is brought about by factors intrinsic to rhombomeres and to the attached neural crest cell populations. The patterns of the neuroectoderm and of the PNS are specified early in hindbrain development and cannot be influenced by tissue transplantation. The observed cell-autonomous expression of Ghox 2.9 (and possibly also of other Hox genes) provides further evidence for the view that Hox gene expression underlies, at least in part, the segmental specification within the hindbrain neuroectoderm.
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Udolph, G., J. Urban, G. Rusing, K. Luer und G. M. Technau. „Differential effects of EGF receptor signalling on neuroblast lineages along the dorsoventral axis of the Drosophila CNS“. Development 125, Nr. 17 (01.09.1998): 3291–99. http://dx.doi.org/10.1242/dev.125.17.3291.
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The Drosophila ventral nerve cord derives from a stereotype population of about 30 neural stem cells, the neuroblasts, per hemineuromere. Previous experiments provided indications for inductive signals at ventral sites of the neuroectoderm that confer neuroblast identities. Using cell lineage analysis, molecular markers and cell transplantation, we show here that EGF receptor signalling plays an instructive role in CNS patterning and exerts differential effects on dorsoventral subpopulations of neuroblasts. The Drosophila EGF receptor (DER) is capable of cell autonomously specifiying medial and intermediate neuroblast cell fates. DER signalling appears to be most critical for proper development of intermediate neuroblasts and less important for medial neuroblasts. It is not required for lateral neuroblast lineages or for cells to adopt CNS midline cell fate. Thus, dorsoventral patterning of the CNS involves both DER-dependent and -independent regulatory pathways. Furthermore, we discuss the possibility that different phases of DER activation exist during neuroectodermal patterning with an early phase independent of midline-derived signals.
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Harris, Kathryn P., und Ulrich Tepass. „Cdc42 and Par proteins stabilize dynamic adherens junctions in the Drosophila neuroectoderm through regulation of apical endocytosis“. Journal of Cell Biology 183, Nr. 6 (08.12.2008): 1129–43. http://dx.doi.org/10.1083/jcb.200807020.
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Cell rearrangements require dynamic changes in cell–cell contacts to maintain tissue integrity. We investigated the function of Cdc42 in maintaining adherens junctions (AJs) and apical polarity in the Drosophila melanogaster neuroectodermal epithelium. About one third of cells exit the epithelium through ingression and become neuroblasts. Cdc42-compromised embryos lost AJs in the neuroectoderm during neuroblast ingression. In contrast, when neuroblast formation was suppressed, AJs were maintained despite the loss of Cdc42 function. Loss of Cdc42 function caused an increase in the endocytotic uptake of apical proteins, including apical polarity factors such as Crumbs, which are required for AJ stability. In addition, Cdc42 has a second function in regulating endocytotic trafficking, as it is required for the progression of apical cargo from the early to the late endosome. The Par complex acts as an effector for Cdc42 in controlling the endocytosis of apical proteins. This study reveals functional interactions between apical polarity proteins and endocytosis that are critical for stabilizing dynamic basolateral AJs.
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Nagasaka, Susumu, Kenneth K. Tanabe, Janet M. Bruner, Hideyuki Saya, Raymond E. Sawaya und Richard S. Morrison. „Alternative RNA splicing of the hyaluronic acid receptor CD44 in the normal human brain and in brain tumors“. Journal of Neurosurgery 82, Nr. 5 (Mai 1995): 858–63. http://dx.doi.org/10.3171/jns.1995.82.5.0858.
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✓ The cell-surface receptor for hyaluronic acid, CD44, is expressed by both normal and malignant cells. Numerous CD44 isoforms have recently been identified that are derived by alternative ribonucleic acid splicing. The expression of some CD44 isoforms has been shown to be involved in tumor progression and metastatic spread in a rat carcinoma model and in human carcinomas. In the present study, CD44 isoform expression was evaluated by reverse transcriptase—polymerase chain reaction (PCR) analysis in frozen sections derived from three samples of normal brain tissue and from 40 brain tumors, including samples of glioblastoma multiforme, anaplastic astrocytoma, low-grade astrocytoma, cerebral primitive neuroectodermal tumor, medulloblastoma, metastatic colon carcinoma, and metastatic melanoma. Normal brain tissue adjacent to the tumors was also examined in 14 of 18 glioblastomas. In all normal brain and tumor samples, with the exception of metastases from colon carcinoma, PCR analysis demonstrated one prominent product that corresponded to the CD44H hematopoietic form of CD44. Metastases from colon carcinoma demonstrated two prominent PCR amplification products corresponding to CD44H and CD44R1. These results suggest that CD44H is the predominant isoform of this protein in normal human brain tissue and in human neuroectodermal tumors of varying degrees of malignancy. The ability of CD44H to mediate tumor cell motility and invasiveness (in contrast to CD44R1) suggests that the CD44 alternative splicing pattern of neuroectoderm-derived tumors may enhance their local biological aggressiveness and intracerebral spread. The lack of expression of larger molecular weight CD44 variants by primary brain tumors may also partially explain why these tumors rarely metastasize to distant sites.
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Kondziolka, Douglas, und Juan M. Bilbao. „An immunohistochemical study of neuroepithelial (colloid) cysts“. Journal of Neurosurgery 71, Nr. 1 (Juli 1989): 91–97. http://dx.doi.org/10.3171/jns.1989.71.1.0091.
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✓ Monoclonal and polyclonal antisera were used against 12 cases of neuroepithelial (colloid) cysts to determine the specific antigenic profile of the cyst epithelium. Intermediate filament markers (cytokeratin, vimentin, neurofilament, and glial fibrillary acidic protein) and epithelial markers (epithelial membrane antigen and monoclonal antibody lu-5) demonstrated that colloid cyst epithelium has a unique antigenic profile in contrast to that of choroid plexus or glial tissue. Theories raised to explain the etiology of colloid cysts have included derivation from the embryonic paraphysis, detachments of developing neuroepithelium from the tela choroidea, and remnants of respiratory epithelium; a more recent theory suggests that these cysts are products of developing choroid plexus or ependyma. The present study shows that colloid cyst epithelium is distinct from that of choroid plexus or ependyma and therefore does not represent a product of their formation, nor does it represent a form of immature glia. This finding supports the conclusion that colloid cysts in any ventricular location represent a developmental anomaly of primitive neuroectoderm in the embryo, which remains unique from other products of neuroectodermal derivation.
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Nakamura, Takaaki, Akio Kishi, Yoshihiko Nishio, Hiroshi Maegawa, Katsuya Egawa, Norman C. W. Wong, Hideto Kojima et al. „Insulin Production in a Neuroectodermal Tumor that Expresses Islet Factor-1, But Not Pancreatic-Duodenal Homeobox 1“. Journal of Clinical Endocrinology & Metabolism 86, Nr. 4 (01.04.2001): 1795–800. http://dx.doi.org/10.1210/jcem.86.4.7429.
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We studied a 60-yr-old female with a brain tumor who showed severe symptoms of hypoglycemia (plasma glucose, 2.2 mmol/L) and hyperinsulinemia (1.28 nmol/L) after radiotherapy. The cystic brain tumor contained proinsulin and insulin at concentrations of 13.6 and 1.22 nmol/L, respectively. Immunohistochemical studies showed the tumor cells were ectodermal in origin but not endodermal, based on three diagnostic features of neuroectodermal tumors 1) pseudorosette formation noted under light microscopy, 2) finding of a small number of dense core neurosecretory granules on electron microscopy, and 3) positive immunostaining for both neuronal specific enolase and protein gene product 9.5. These cells also expressed the transcription factor, neurogenin-3, NeuroD/β2, and islet factor I, which are believed to be transcription factors in neuroectoderm as well as in pancreatic islet cells, but not pancreatic-duodenal homeobox 1, Pax4, or Nkx2.2. In addition, they did not express glucagon, somatostatin, or glucagon-like peptide-1. Our results show the presence of proinsulin in an ectoderm cell brain tumor that does not express the homeobox gene, pancreatic-duodenal homeobox 1, but expresses other transcription factors, i.e. neurogenin3, NeuroD/β2, and islet factor-1, which are related to insulin gene expression in the brain tumor.
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Isshiki, T., M. Takeichi und A. Nose. „The role of the msh homeobox gene during Drosophila neurogenesis: implication for the dorsoventral specification of the neuroectoderm“. Development 124, Nr. 16 (15.08.1997): 3099–109. http://dx.doi.org/10.1242/dev.124.16.3099.
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Development of the Drosophila central nervous system begins with the delamination of neural and glial precursors, called neuroblasts, from the neuroectoderm. An early and important step in the generation of neural diversity is the specification of individual neuroblasts according to their position. In this study, we describe the genetic analysis of the msh gene which is likely to play a role in this process. The msh/Msx genes are one of the most highly conserved families of homeobox genes. During vertebrate spinal cord development, Msx genes (Msx1-3) are regionally expressed in the dorsal portion of the developing neuroectoderm. Similarly in Drosophila, msh is expressed in two longitudinal bands that correspond to the dorsal half of the neuroectoderm, and subsequently in many dorsal neuroblasts and their progeny. We showed that Drosophila msh loss-of-function mutations led to cell fate alterations of neuroblasts formed in the dorsal aspect of the neuroectoderm, including a possible dorsal-to-ventral fate switch. Conversely, ectopic expression of msh in the entire neuroectoderm severely disrupted the proper development of the midline and ventral neuroblasts. The results provide the first in vivo evidence for the role of the msh/Msx genes in neural development, and support the notion that they may perform phylogenetically conserved functions in the dorsoventral patterning of the neuroectoderm.
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Khoddami, Maliheh, Jeremy Squire, Maria Zielenska und Paul Thorner. „Melanotic Neuroectodermal Tumor of Infancy: A Molecular Genetic Study“. Pediatric and Developmental Pathology 1, Nr. 4 (Juli 1998): 295–99. http://dx.doi.org/10.1007/s100249900042.
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Melanotic neuroectodermal tumor of infancy is a rare but well-recognized entity in pediatric pathology. However, the relationship of this tumor to other pediatric small cell tumors with neuroectodermal features (such as neuroblastoma, Ewing sarcoma/peripheral primitive neuroectodermal tumor, and desmoplastic small round cell tumor) is undetermined. Molecular genetic studies of melanotic neuroectodermal tumor of infancy have not been reported. We studied three typical cases of mela-notic neuroectodermal tumor of infancy in an attempt to link this tumor to other small cell tumors with well-characterized molecular genetic changes. Tests performed included: detection of MYCN gene amplification and deletion of 1p (all 3 cases), and presence of the t(11;22)(q24;q12) and the t(11;22)(p13;q12) translocations (2 of 3 cases). None of these tests yielded positive results. Thus, there is no genetic basis at present to link melanotic neuroectodermal tumor of infancy to neuroblastoma, Ewing sarcoma/peripheral primitive neuroectodermal tumor, or desmoplastic small round cell tumor.
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Martin-Bermudo, M. D., C. Martinez, A. Rodriguez und F. Jimenez. „Distribution and function of the lethal of scute gene product during early neurogenesis in Drosophila“. Development 113, Nr. 2 (01.10.1991): 445–54. http://dx.doi.org/10.1242/dev.113.2.445.
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Genes of the achaete-scute complex (ASC) participate in the formation of the central nervous system in the Drosophila embryo. Previous genetic analyses have indicated that lethal of scute (l'sc) is the most important gene of the complex in that process. We have obtained antibodies against the l'sc protein to study the expression of the gene during early neurogenesis. The protein is found in groups of embryonic neuroectodermal cells, analogous to the proneural clusters that precede the appearance of precursors of peripheral sensory organs in imaginal epithelia. The groups appear in different regions of the neuroectoderm, accompanying the three successive waves of neuroblast segregation. Most neuroblasts delaminate from these clusters and express position-specific levels of l'sc protein. No significant differences have been found between the distribution of l'sc RNA and protein. Phenotypic analysis of a l'sc deficiency has shown that the gene is required for neuroblast commitment, although this requirement is less widespread than the domain of l'sc expression, suggesting a high degree of redundancy in the function of genes that participate in the process of neuroblast segregation. The ASC genes have been postulated to play a role in the control of NB identity, revealed by the generation of a defined lineage of identifiable neurons. However, our study in l'sc mutants of the expression of fushi tarazu, engrailed, and even-skipped, used as markers of neuronal identity, has not provided evidence to support this hypothesis.
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Fekany-Lee, K., E. Gonzalez, V. Miller-Bertoglio und L. Solnica-Krezel. „The homeobox gene bozozok promotes anterior neuroectoderm formation in zebrafish through negative regulation of BMP2/4 and Wnt pathways“. Development 127, Nr. 11 (01.06.2000): 2333–45. http://dx.doi.org/10.1242/dev.127.11.2333.
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The neuroectoderm of the vertebrate gastrula was proposed by Nieuwkoop to be regionalized into forebrain, midbrain, hindbrain and spinal cord by a two-step process. In the activation step, the Spemann gastrula organizer induces neuroectoderm with anterior character, followed by posteriorization by a transforming signal. Recently, simultaneous inhibition of BMP and Wnt signaling was shown to induce head formation in frog embryos. However, how the inhibition of BMP and Wnt signaling pathways specify a properly patterned head, and how they are regulated in vivo, is not understood. Here we demonstrate that the loss of anterior neural fates observed in zebrafish bozozok (boz) mutants occurs during gastrulation due to a reduction and subsequent posteriorization of neuroectoderm. The neural induction defect was correlated with decreased chordino expression and consequent increases in bmp2b/4 expression, and was suppressed by overexpression of BMP antagonists. Whereas expression of anterior neural markers was restored by ectopic BMP inhibition in early boz gastrulae, it was not maintained during later gastrulation. The posteriorization of neuroectoderm in boz was correlated with ectopic dorsal wnt8 expression. Overexpression of a Wnt antagonist rescued formation of the organizer and anterior neural fates in boz mutants. We propose that boz specifies formation of anterior neuroectoderm by regulating BMP and Wnt pathways in a fashion consistent with Nieuwkoop's two-step neural patterning model. boz promotes neural induction by positively regulating organizer-derived chordino and limiting the antineuralizing activity of BMP2b/4 morphogens. In addition, by negative regulation of Wnt signaling, boz promotes organizer formation and limits posteriorization of neuroectoderm in the late gastrula.
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Favarolo, María Belén, Diego R. Revinski, Matías J. Garavaglia und Silvia L. López. „Nodal and churchill1 position the expression of a notch ligand during Xenopus germ layer segregation“. Life Science Alliance 5, Nr. 12 (30.09.2022): e202201693. http://dx.doi.org/10.26508/lsa.202201693.
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In vertebrates, Nodal signaling plays a major role in endomesoderm induction, but germ layer delimitation is poorly understood. In avian embryos, the neural/mesoderm boundary is controlled by the transcription factor CHURCHILL1, presumably through the repressor ZEB2, but there is scarce knowledge about its role in other vertebrates. During amphibian gastrulation, Delta/Notch signaling refines germ layer boundaries in the marginal zone, but it is unknown the place this pathway occupies in the network comprising Churchill1 and Nodal. Here, we show that Xenopus churchill1 is expressed in the presumptive neuroectoderm at mid-blastula transition and during gastrulation, upregulates zeb2, prevents dll1 expression in the neuroectoderm, and favors neuroectoderm over endomesoderm development. Nodal signaling prevents dll1 expression in the endoderm but induces it in the presumptive mesoderm, from where it activates Notch1 and its target gene hes4 in the non-involuting marginal zone. We propose a model where Nodal and Churchill1 position Dll1/Notch1/Hes4 domains in the marginal zone, ensuring the delimitation between mesoderm and neuroectoderm.
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Bullard, Dennis E., und Darell D. Bigner. „Applications of monoclonal antibodies in the diagnosis and treatment of primary brain tumors“. Journal of Neurosurgery 63, Nr. 1 (Juli 1985): 2–16. http://dx.doi.org/10.3171/jns.1985.63.1.0002.
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✓ The development of monoclonal antibodies has resulted in marked expansion in understanding the central nervous system (CNS). This has been especially true in the study of human neuroectodermal tumors where monoclonal antibodies have been used as physiological probes to define and characterize human neuroectodermal tumor-associated antigens. Utilizing monoclonal antibodies, neuroectodermal tumor-associated antigens have been described in four broad categories; biochemically defined markers, shared nervous systemlymphoid cell markers, shared neuroectodermal-oncofetal markers, and putative restricted tumor markers. Preliminary data have demonstrated the ability to localize animal and human tumors in vitro, ex vivo, and in vivo. Early application of monoclonal antibody technology to neuroimmunology and neuro-oncology has resulted in a new awareness of the complex relationships that exist within the CNS. Their specificity and reproducibility may provide the means to qualitatively and quantitatively define the phenotypic heterogeneity of human neuroectodermal tumors. Potentially, monoclonal antibodies, alone or as carriers of radionuclides, drugs, or toxins, may allow successful diagnosis and treatment of human neuroectodermal tumors.
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Darnell, D. K., M. R. Stark und G. C. Schoenwolf. „Timing and cell interactions underlying neural induction in the chick embryo“. Development 126, Nr. 11 (01.06.1999): 2505–14. http://dx.doi.org/10.1242/dev.126.11.2505.
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Previous studies on neural induction have identified regionally localized inducing activities, signaling molecules, potential competence factors and various other features of this important, early differentiation event. In this paper, we have developed an improved model system for analyzing neural induction and patterning using transverse blastoderm isolates obtained from gastrulating chick embryos. We use this model to establish the timing of neural specification and the spatial distribution of perinodal cells having organizer activity. We show that a tissue that acts either as an organizer or as an inducer of an organizer is spatially co-localized with the prospective neuroectoderm immediately rostral to the primitive streak in the early gastrula. As the primitive streak elongates, this tissue with organizing activity and the prospective neuroectoderm rostral to the streak separate. Furthermore, we show that up to and through the mid-primitive streak stage (i.e., stage 3c/3+), the prospective neuroectoderm cannot self-differentiate (i.e., express neural markers and acquire neural plate morphology) in isolation from tissue with organizer activity. Signals from the organizer and from other more caudal regions of the primitive streak act on the rostral prospective neuroectoderm and the latter gains potency (i.e., is specified) by the fully elongated primitive streak stage (i.e., stage 3d). Transverse blastoderm isolates containing non-specified, prospective neuroectoderm provide an improved model system for analyzing early signaling events involved in neuraxis initiation and patterning.
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Suda, Y., J. Nakabayashi, I. Matsuo und S. Aizawa. „Functional equivalency between Otx2 and Otx1 in development of the rostral head“. Development 126, Nr. 4 (15.02.1999): 743–57. http://dx.doi.org/10.1242/dev.126.4.743.
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Mice have two Otx genes, Otx1 and Otx2. Prior to gastrulation, Otx2 is expressed in the epiblast and visceral endoderm. As the primitive streak forms, Otx2 expression is restricted to the anterior parts of all three germ layers. Otx1 expression begins at the 1 to 3 somite stage in the anterior neuroectoderm. Otx2 is also expressed in cephalic mesenchyme. Otx2 homozygous mutants fail to develop structures anterior to rhombomere 3 (r3), and Otx2 heterozygotes exhibit craniofacial defects. Otx1 homozygous mutants do not show apparent defects in early brain development. In Otx1 and Otx2 double heterozygotes, rostral neuroectoderm is induced normally, but development of the mes/diencephalic domain is impaired starting at around the 3 to 6 somite stage, suggesting cooperative interactions between the two genes in brain regionalization. To determine whether Otx1 and Otx2 genes are functionally equivalent, we generated knock-in mice in which Otx2 was replaced by Otx1. In homozygous mutants, gastrulation occurred normally, and rostral neuroectoderm was induced at 7.5 days postcoitus (7.5 dpc), but the rostral brain failed to develop. Anterior structures such as eyes and the anterior neural ridge were lost by 8.5 dpc, but the isthmus and r1 and r2 were formed. In regionalization of the rostral neuroectoderm, the cooperative interaction of Otx2 with Otx1 revealed by the phenotype of Otx2 and Otx1 double heterozygotes was substitutable by Otx1. The otocephalic phenotype indicative of Otx2 haploinsufficiency was also largely restored by knocked-in Otx1. Thus most Otx2 functions were replaceable by Otx1, but the requirement for Otx2 in the anterior neuroectoderm prior to onset of Otx1 expression was not. These data indicate that Otx2 may have evolved new functions required for establishment of anterior neuroectoderm that Otx1 cannot perform.
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Ašmonienė, Virginija, Daina Skiriutė, Inga Gudinavičienė, Šarūnas Tamašauskas, Kęstutis Skauminas, Vytenis Deltuva und Arimantas Tamašauskas. „A Primary Primitive Neuroectodermal Tumor of the Central Nervous System in a 51-year-old Woman: a Case Report and Literature Review“. Medicina 47, Nr. 8 (05.09.2011): 440. http://dx.doi.org/10.3390/medicina47080060.
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Primitive neuroectodermal tumors are a group of rare, aggressive, and highly malignant embryonal tumors of unknown etiology of the central and peripheral nervous systems. It is a term for a group of small round cell tumors thought to be derived from fetal neuroectodermal precursor cells. Primitive neuroectodermal tumor is usually described as a tumor of children younger than 15 years and is very rare in adults. The article presents a short literature review and a rare case of a primary primitive neuroectodermal tumor of the central nervous system diagnosed in a 51-year-old woman.
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Kim, Seok-Hyung, Jimann Shin, Hae-Chul Park, Sang-Yeob Yeo, Sung-Kook Hong, Sangtae Han, Myungchull Rhee, Cheol-Hee Kim, Ajay B. Chitnis und Tae-Lin Huh. „Specification of an anterior neuroectoderm patterning by Frizzled8a-mediated Wnt8b signalling during late gastrulation in zebrafish“. Development 129, Nr. 19 (01.10.2002): 4443–55. http://dx.doi.org/10.1242/dev.129.19.4443.
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Wnts have been shown to provide a posteriorizing signal that has to be repressed in the anterior neuroectoderm for normal anteroposterior (AP) patterning. We have previously identified a zebrafish frizzled8a (fz8a) gene expressed in the presumptive anterior neuroectoderm as well as prechordal plate at the late gastrula stage. We have investigated the role of Fz8a-mediated Wnt8b signalling in anterior brain patterning in zebrafish. We show that in zebrafish embryos: (1) Wnt signalling has at least two different stage-specific posteriorizing activities in the anterior neuroectoderm, one before mid-gastrulation and the other at late gastrulation; (2) Fz8a plays an important role in mediating anterior brain patterning; (3) Wnt8b and Fz8a can functionally interact to transmit posteriorizing signals that determine the fate of the posterior diencephalon and midbrain in late gastrula embryos; and (4) Wnt8b can suppress fz8a expression in the anterior neuroectoderm and potentially affect the level and/or range of Wnt signalling. In conclusion, we suggest that a gradient of Fz8a-mediated Wnt8b signalling may play crucial role in patterning the posterior diencephalon and midbrain regions in the late gastrula.
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Satou-Kobayashi, Yumeko, Shuji Takahashi, Yoshikazu Haramoto, Makoto Asashima und Masanori Taira. „Zbtb11 interacts with Otx2 and patterns the anterior neuroectoderm in Xenopus“. PLOS ONE 19, Nr. 7 (31.07.2024): e0293852. http://dx.doi.org/10.1371/journal.pone.0293852.
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The zinc finger and BTB domain-containing 11 gene (zbtb11) is expressed in the Xenopus anterior neuroectoderm, but the molecular nature of the Zbtb11 protein during embryonic development remains to be elucidated. Here, we show the role of Zbtb11 in anterior patterning of the neuroectoderm and the cooperative action with the transcription factor Otx2. Both overexpression and knockdown of zbtb11 caused similar phenotypes: expanded expression of the posterior gene gbx2 in the neural plate, and later microcephaly with reduced eyes, suggesting that a proper level of zbtb11 expression is necessary for normal patterning of the neuroectoderm, including eye formation. Co-immunoprecipitation assays showed that Zbtb11 formed a complex with itself and with a phosphomimetic and repressive form of Otx2, suggesting that Zbtb11 forms a dimer or oligomer and interacts with Otx2 in a phosphorylation-dependent manner. Reporter analysis further showed that Zbtb11 enhanced the activity of the phosphomimetic Otx2 to repress a silencer element of the posterior gene meis3. These data suggest that Zbtb11 coordinates with phosphorylated Otx2 to specify the anterior neuroectoderm by repressing posterior genes.
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Poudel, Shankar, Upama Sangroula und Ashik Rajak. „Primitive Neuroectodermal Tumour of Subcutaneous Tissue Presenting as a Shoulder Lump: A Case Report“. Journal of Nepal Medical Association 60, Nr. 247 (11.03.2022): 303–5. http://dx.doi.org/10.31729/jnma.6266.
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Primitive neuroectodermal tumour is a poorly differentiated small round cell neoplasm that primarily affects children and is very rarely seen in adults. Peripheral primitive neuroectodermal tumours are rare compared to the central type and resemble soft tissue sarcoma. Primitive neuroectodermal tumours involving the subcutaneous tissue are rare and only a few cases involving the subcutaneous tissue of the anterior abdominal wall have been reported. However, no cases involving the subcutaneous tissue of the shoulder region have been reported. We report the case of a peripheral primitive neuroectodermal tumour arising from subcutaneous tissue of the right shoulder in a young adult.
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Zhao, Guoyan, und James B. Skeath. „The Sox-domain containing geneDichaete/fish-hookacts in concert withvndandindto regulate cell fate in theDrosophilaneuroectoderm“. Development 129, Nr. 5 (01.03.2002): 1165–74. http://dx.doi.org/10.1242/dev.129.5.1165.
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In the Drosophila embryonic central nervous system, neural stem cells, called neuroblasts, acquire fates in a position-specific manner. Recent work has identified a set of genes that functions along the dorsoventral axis to enable neuroblasts that develop in different dorsoventral domains to acquire distinct fates. These genes include the evolutionarily conserved transcription factors ventral nerve cord defective and intermediate neuroblasts defective, as well as the Drosophila EGF receptor. We show that the Sox-domain-containing gene Dichaete/fish-hook also plays a crucial role to pattern the neuroectoderm along the DV axis. Dichaete is expressed in the medial and intermediate columns of the neuroectoderm, and mutant analysis indicates that Dichaete regulates cell fate and neuroblast formation in these domains. Molecular epistasis tests, double mutant analysis and dosage-sensitive interactions demonstrate that during these processes, Dichaete functions in parallel with ventral nerve cord defective and intermediate neuroblasts defective, and downstream of EGF receptor signaling to mediate its effect on development. These results identify Dichaete as an important regulator of dorsoventral pattern in the neuroectoderm, and indicate that Dichaete acts in concert with ventral nerve cord defective and intermediate neuroblasts defective to regulate pattern and cell fate in the neuroectoderm.
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Ge, Li, Amy Zhou, John Maksem, Sarah Gennette und Veronica Schimp. „Tumors With Neuroectodermal Differentiation of the Uterus and Ovary: A Series of 12 Cases and Review of the Literature“. American Journal of Clinical Pathology 152, Supplement_1 (11.09.2019): S37—S38. http://dx.doi.org/10.1093/ajcp/aqz113.002.
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Abstract Objectives Primitive neuroectodermal tumors (PNETs) are a group of small round cell tumors most commonly found in the central nervous system, soft tissue, or bone. Such tumors arising in the uterus or ovary are rare. In this study, we describe the clinicopathologic features from a series of gynecological tumors with neuroectodermal differentiation. Methods In a retrospective review, 5 years of departmental archives were searched for gynecological tumors diagnosed at Orlando Health’s Department of Pathology. Clinicopathological information was analyzed, including age at diagnosis, tumor size, depth of invasion, other component, pathologic stage, FIGO stage, immunohistochemical stains, months of follow-up, and current disease status. Results Twelve fully staged tumors with neuroectodermal differentiation were identified. Eleven were of uterine origin and one was of ovarian origin. Ages at diagnosis ranged from 38 to 78 years (median 65). Neuroectodermal component was variable in morphology, including lymphocyte-like small cells in sheets, perivascular pseudorosettes, or cords; larger cells with prominent nucleoli with or without cystic change; and giant cells resembling megakaryocytes. Components other than neuroectodermal differentiation included carcinosarcoma, dedifferentiated endometrioid carcinoma, and high-grade serous carcinoma. Membranous and/or paranuclear dot-like CD99 immunoreactivity were in all cases. Ten patients were deceased due to disease at 1 to 33 months follow-up, while one patient was alive without evidence of disease after 61 months follow-up, possibly due to being able to tolerate a different therapeutic protocol for peripheral PNET. Conclusion Neuroectodermal differentiation may be found as components of other gynecological tumors, especially those with an aggressive phenotype and high-stage disease. The neuroectodermal component comprises a spectrum of cytohistological features. Because of its presentation in the shadow of other components, it may be more common than is generally assumed. Mortality remains high, but recognition of neuroectodermal differentiation in gynecologic tumors might introduce a different therapeutic approach and potentially improve clinical outcomes.
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Shetty, Shravan S., Vidhi Shah und Eshpuniyani Prriya Prriya. „Primitive Neuroectodermal Tumor of Axilla in an Adult: A Rare Entity“. Journal of Clinical Case Studies Reviews & Reports 3, Nr. 2 (30.04.2021): 1–2. http://dx.doi.org/10.47363/jccsr/2020(3)165.
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Primitive neuroectodermal tumors (PNETs) are poorly differentiated small round cell neoplasms which mainly affect children and are not commonly seen in adults. Superficial primitive neuroectodermal tumors are rare and have a favourable prognosis compared to conventional deep seated tumors. We report a case of a 62 year old gentleman with a primitive neuroectodermal tumor arising from the subcutaneous tissue of the right axilla. He was treated with multimodal treatment including surgery and radiotherapy. He is alive and disease free at 2 year follow up.
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Bartholow, Tanner, und Anil Parwani. „Renal Primitive Neuroectodermal Tumors“. Archives of Pathology & Laboratory Medicine 136, Nr. 6 (01.06.2012): 686–90. http://dx.doi.org/10.5858/arpa.2011-0104-rs.
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Primitive neuroectodermal tumors exist as a part of the Ewing sarcoma/primitive neuroectodermal tumor family. These tumors most commonly arise in the chest wall and paraspinal regions; cases with a renal origin are rare entities, but have become increasingly reported in recent years. Although such cases occur across a wide age distribution, the average age for a patient with a renal primitive neuroectodermal tumor is the mid- to late 20s, with both males and females susceptible. Histologically, these tumors are characterized by pseudorosettes. Immunohistochemically, CD99 is an important diagnostic marker. Clinically, these are aggressive tumors, with an average 5-year disease-free survival rate of only 45% to 55%. Given that renal primitive neuroectodermal tumor bears many similarities to other renal tumors, it is important to review the histologic features, immunostaining profile, and genetic abnormalities that can be used for its correct diagnosis.
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Eroshkin, Fedor M., Elena A. Fefelova, Denis V. Bredov, Eugeny E. Orlov, Nataliya M. Kolyupanova, Alexander M. Mazur, Alexey S. Sokolov et al. „Mechanical Tensions Regulate Gene Expression in the Xenopus laevis Axial Tissues“. International Journal of Molecular Sciences 25, Nr. 2 (10.01.2024): 870. http://dx.doi.org/10.3390/ijms25020870.
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During gastrulation and neurulation, the chordamesoderm and overlying neuroectoderm of vertebrate embryos converge under the control of a specific genetic programme to the dorsal midline, simultaneously extending along it. However, whether mechanical tensions resulting from these morphogenetic movements play a role in long-range feedback signaling that in turn regulates gene expression in the chordamesoderm and neuroectoderm is unclear. In the present work, by using a model of artificially stretched explants of Xenopus midgastrula embryos and full-transcriptome sequencing, we identified genes with altered expression in response to external mechanical stretching. Importantly, mechanically activated genes appeared to be expressed during normal development in the trunk, i.e., in the stretched region only. By contrast, genes inhibited by mechanical stretching were normally expressed in the anterior neuroectoderm, where mechanical stress is low. These results indicate that mechanical tensions may play the role of a long-range signaling factor that regulates patterning of the embryo, serving as a link coupling morphogenesis and cell differentiation.
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Soulard, Raoulin, Valère Claude, Philippe Camparo, Jean-Philippe Dufau, Patrick Saint-Blancard und Philippe Gros. „Primitive Neuroectodermal Tumor of the Stomach“. Archives of Pathology & Laboratory Medicine 129, Nr. 1 (01.01.2005): 107–10. http://dx.doi.org/10.5858/2005-129-107-pntots.
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Abstract Ewing sarcoma/primitive neuroectodermal tumor is classically a tumor of the soft tissue or bone in children and young adults, but several cases have been described in patients of all ages. Within the last decade, the clinicopathologic spectrum of Ewing sarcoma/primitive neuroectodermal tumor has been markedly expanded by recognition that the tumor may also have a visceral origin. We describe a case of primitive neuroectodermal tumor arising in the stomach of a 66-year-old woman. The neoplasm was excised using a radical surgical procedure. Microscopically, the tumor was made up of solid nests and sheets of round cells. Immunohistochemically, the tumor cells showed immunoreactivity for CD99, S100, neuron-specific enolase, and vimentin. A multiplex real-time polymerase chain reaction assay detected an EWS-ERG fusion. To our knowledge, this is the first description of a primitive neuroectodermal tumor arising in the stomach.
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Kumar, Vijay, Ravi Shankar Goutam, Zobia Umair, Soochul Park, Unjoo Lee und Jaebong Kim. „Foxd4l1.1 Negatively Regulates Chordin Transcription in Neuroectoderm of Xenopus Gastrula“. Cells 10, Nr. 10 (17.10.2021): 2779. http://dx.doi.org/10.3390/cells10102779.
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Inhibition of the bone morphogenetic proteins (BMPs) is the primary step toward neuroectoderm formation in vertebrates. In this process, the Spemann organizer of the dorsal mesoderm plays a decisive role by secreting several extracellular BMP inhibitors such as Chordin (Chrd). Chrd physically interacts with BMP proteins and inhibits BMP signaling, which triggers the expression of neural-specific transcription factors (TFs), including Foxd4l1.1. Thus, Chrd induces in a BMP-inhibited manner and promotes neuroectoderm formation. However, the regulatory feedback mechanism of Foxd4l1.1 on mesodermal genes expression during germ-layer specification has not been fully elucidated. In this study, we investigated the regulatory mechanism of Foxd4l1.1 on chrd (a mesodermal gene). We demonstrate that Foxd4l1.1 inhibits chrd expression during neuroectoderm formation in two ways: First, Foxd4l1.1 directly binds to FRE (Foxd4l1.1 response elements) within the chrd promoter region to inhibit transcription. Second, Foxd4l1.1 physically interacts with Smad2 and Smad3, and this interaction blocks Smad2 and Smad3 binding to activin response elements (AREs) within the chrd promoter. Site-directed mutagenesis of FRE within the chrd(-2250) promoter completely abolished repressor activity of the Foxd4l1.1. RT-PCR and reporter gene assay results indicate that Foxd4l1.1 strongly inhibits mesoderm- and ectoderm-specific marker genes to maintain neural fate. Altogether, these results suggest that Foxd4l1.1 negatively regulates chrd transcription by dual mechanism. Thus, our study demonstrates the existence of precise reciprocal regulation of chrd transcription during neuroectoderm and mesoderm germ-layer specification in Xenopus embryos.
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Martinez-Barbera, Juan Pedro, Massimo Signore, Pietro Pilo Boyl, Eduardo Puelles, Dario Acampora, Robin Gogoi, Frank Schubert, Andrew Lumsden und Antonio Simeone. „Regionalisation of anterior neuroectoderm and its competence in responding to forebrain and midbrain inducing activities depend on mutual antagonism between OTX2 and GBX2“. Development 128, Nr. 23 (01.12.2001): 4789–800. http://dx.doi.org/10.1242/dev.128.23.4789.
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The anterior neural ridge (ANR), and the isthmic organiser (IsO) represent two signalling centres possessing organising properties necessary for forebrain (ANR) as well as midbrain and rostral hindbrain (IsO) development. An important mediator of ANR and IsO organising property is the signalling molecule FGF8. Previous work has indicated that correct positioning of the IsO and Fgf8 expression in this domain is controlled by the transcription factors Otx2 and Gbx2. In order to provide novel insights into the roles of Otx2 and Gbx2, we have studied mutant embryos carrying different dosages of Otx2, Otx1 and Gbx2. Embryos deficient for both OTX2 and GBX2 proteins (hOtx12/hOtx12; Gbx2–/–) show abnormal patterning of the anterior neural tissue, which is evident at the presomite-early somite stage prior to the onset of Fgf8 neuroectodermal expression. Indeed, hOtx12/hOtx12; Gbx2–/– embryos exhibit broad co-expression of early forebrain, midbrain and rostral hindbrain markers such as hOtx1, Gbx2, Pax2, En1 and Wnt1 and subsequently fail to activate forebrain and midbrain-specific gene expression. In this genetic context, Fgf8 is expressed throughout the entire anterior neural plate, thus indicating that its activation is independent of both OTX2 and GBX2 function. Analysis of hOtx12/hOtx12; Gbx2–/– and Otx1+/–; Otx2+/– mutant embryos also suggests that FGF8 cannot repress Otx2 without the participation of GBX2. Finally, we report that embryos carrying a single strong hypomorphic Otx2 allele (Otx2λ) in an Otx2 and Gbx2 null background (Otx2λ/–; Gbx2–/–) recover both the headless phenotype exhibited by Otx2λ/– embryos and forebrain- and midbrain-specific gene expression that is not observed in hOtx12/hOtx12; Gbx2–/– mutants. Together, these data provide novel genetic evidence indicating that OTX2 and GBX2 are required for proper segregation of early regional identities anterior and posterior to the mid-hindbrain boundary (MHB) and for conferring competence to the anterior neuroectoderm in responding to forebrain-, midbrain- and rostral hindbrain-inducing activities.
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Bready, Devin, Aram Modrek, Joshua Frenster, Jane Skok und Dimitris Placantonakis. „CBIO-05. SOX2 CHROMATIN ARCHITECTURE AND ENHANCER ACTIVITY IN THE MAINTENANCE AND DEVELOPMENT OF NEURAL STEM CELLS“. Neuro-Oncology 23, Supplement_6 (02.11.2021): vi28. http://dx.doi.org/10.1093/neuonc/noab196.106.
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Abstract Gain of function mutations in isocitrate dehydrogenase I (IDH1) result in the formation of the oncometabolite 2-hydroxyglutarate (2HG) in adult lower grade gliomas. To gain insight into mechanisms of gliomagenesis, our lab previously created a tractable human cellular model of low grade astrocytoma (LGA) using the putative cell-of-origin, human neural stem cells (NSCs), engineered to express mutant IDH1 and knockdown constructs against TP53 and ATRX, the two other genetic changes that accompany the IDH mutation in these tumors. We found that transcription factor (sex determining region Y)-box 2 SOX2, which is essential to NSC multipotency, the ability to differentiate to neuroglial lineages, behaves as a tumor suppressor during glioma initiation. In this context, we showed SOX2 is transcriptionally downregulated to impair NSC multipotency, thus locking NSCs in an undifferentiated state to initiate gliomagenesis. This downregulation occurs secondary to dynamic reorganization of the topologically associating domain (TAD) of SOX2 and the loss of contact with several genomic loci with histone modifications and chromatin accessibility suggestive of being enhancers. Here we show that those putative enhancers acquire enhancer-like features simultaneous to tje TAD organizing in a way that facilitates interaction with the SOX2 promoter during the process of pluripotent stem cell differentiation into neuroectodermal lineages, suggesting a developmental role. Preliminary data suggests that disruption of the SOX2 TAD by preventing binding of the genome organizer CTCF downregulates SOX2 expression in NSCs. Targeted silencing of several regions of a putative enhancer with CRISPRi also downregulates SOX2. In human embryonic stem cells (hESCs), interfering with these CTCF binding sites biases their differentiation away from the neuroectoderm. We are currently performing CRISPRi screen against all putative enhancer loci, teratoma formation assays on hESCs lacking relevant CTCF binding, and CRISPR mediated deletion of putative enhancers. Understanding this developmental process may reveal underlying vulnerabilities in LGA.
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Hemavathy, K., X. Meng und Y. T. Ip. „Differential regulation of gastrulation and neuroectodermal gene expression by Snail in the Drosophila embryo“. Development 124, Nr. 19 (01.10.1997): 3683–91. http://dx.doi.org/10.1242/dev.124.19.3683.
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The initiation of mesoderm differentiation in the Drosophila embryo requires the gene products of twist and snail. In either mutant, the ventral cell invagination during gastrulation is blocked and no mesoderm-derived tissue is formed. One of the functions of Snail is to repress neuroectodermal genes and restrict their expressions to the lateral regions. The derepression of the neuroectodermal genes into the ventral region in snail mutant is a possible cause of defects in gastrulation and in mesoderm differentiation. To investigate such possibility, we analysed a series of snail mutant alleles. We found that different neuroectodermal genes respond differently in various snail mutant background. Due to the differential response of target genes, one of the mutant alleles, V2, that has reduced Snail function showed an intermediate phenotype. In V2 embryos, neuroectodermal genes, such as single-minded and rhomboid, are derepressed while ventral invagination proceeds normally. However, the differentiation of these invaginated cells into mesodermal lineage is disrupted. The results suggest that the establishment of mesodermal cell fate requires the proper restriction of neuroectodermal genes, while the ventral cell movement is independent of the expression patterns of these genes. Together with the data showing that the expression of some ventral genes disappear in snail mutants, we propose that Snail may repress or activate another set of target genes that are required specifically for gastrulation.
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Bostrom, B., und B. L. Mirkin. „Elevation of cerebrospinal fluid catecholamine metabolites in patients with intracranial tumors of neuroectodermal origin.“ Journal of Clinical Oncology 5, Nr. 7 (Juli 1987): 1090–97. http://dx.doi.org/10.1200/jco.1987.5.7.1090.
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The concentrations of homovanillic acid (HVA), hydroxymethoxyphenylethyleneglycol (HMPG), and vanillylmandelic acid (VMA) were determined in lumbar cerebrospinal fluid (CSF) specimens. The study population consisted of the following groups: control subjects with malignancies of nonneuroectodermal origin (mostly leukemia in remission), neuroblastoma (extracranial and intracranial or cranial metastases), brain tumors (neuroectodermal and glial), and retinoblastoma. A significant increase in the CSF concentration of HVA was observed in patients with brain tumors (neuroectodermal), neuroblastoma (intracranial or cranial metastases), and retinoblastoma when compared with age-matched controls. In contrast, HMPG and VMA concentrations did not differ from controls except in patients with neuroblastoma (intracranial or cranial metastases) and brain tumors (neuroectodermal) who had significant elevations in HMPG and VMA, respectively. An inverse correlation was noted between the CSF concentration of HVA and clinical response to therapy. Nonresponding patients exhibited increases in HVA when compared with pretreatment values. These data suggest that the quantitative determination of catecholamine metabolites in lumbar CSF is an effective method for diagnosing intracranial tumors of neuroectodermal origin and assessing their response to therapy.
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Tan, A. P., Thomas S. Jacques, Kshitij Mankad, Gregory James, Owase Jeelani, Olga Slater und Felice D’Arco. „Melanotic neuroectodermal tumour of infancy: A case report and differential diagnosis“. Neuroradiology Journal 31, Nr. 4 (10.11.2017): 434–39. http://dx.doi.org/10.1177/1971400917741770.
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Melanotic neuroectodermal tumour of infancy is an uncommon pigmented neoplasm of neural crest origin. It was first described in 1918 by Krompecher, known as congenital melanocarcinoma at that time. Although it is generally agreed upon that it is a benign entity, it is locally aggressive and has a significant recurrent risk, reported to be between 10–15%. There have also been prior reports of malignant behaviour in these tumours, although extremely rare. The majority of cases of this tumour (about 70%) arise from the maxilla and its occurrence in the cranial vault represents approximately 15.6% of cases. We describe a rare case of melanotic neuroectodermal tumour of infancy, with simultaneous involvement of the cranial vault and petrous temporal bone, in a four-month-old child, complicated by post-surgical pseudo-meningocele. This case illustrates the diagnostic dilemma in differentiating reactive osseous sclerosis from direct tumour infiltration, both of which can occur in the context of melanotic neuroectodermal tumour of infancy. The discussion places emphasis on differential diagnoses and useful radiological features to assist in clinching the diagnosis of melanotic neuroectodermal tumour of infancy.
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Yosra, Yahyaoui. „Primary Primitive Neuroectodermal Tumor of the Parotid: An Unsuspected Diagnosis“. Clinical Oncology Research and Reports 1, Nr. 1 (24.07.2020): 01–03. http://dx.doi.org/10.31579/2693-4787/014.
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Primitive neuroectodermal tumors (PNETs) are extremely rare tumors. These neoplasms can occur at sites outside of the central nervous system. The head and neck location is unsual. We report a case with primitive neuroectodermal tumor (PNET) of the parotid. We analyze through this observation the clinical, histological and therapeutic characteristics of this entity.
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Millichap, J. Gordon. „Brainstem Neuroectodermal Tumors“. Pediatric Neurology Briefs 14, Nr. 11 (01.11.2000): 81. http://dx.doi.org/10.15844/pedneurbriefs-14-11-1.
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