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  • BSZ  (55)
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  • 1
    UID:
    (DE-627)1391411684
    Format: 107 S. , Ill., graph. Darst.
    Note: dt. Zusammenfassung , Heidelberg, Univ., Diss., 2009
    Language: English
    Keywords: Hochschulschrift
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  • 2
    UID:
    (DE-627)174587867X
    Format: 14
    ISSN: 1949-2553
    Content: https://doi.org/10.18632/oncotarget.10692 Eric W. Prince, Ilango Balakrishnan, Monil Shah, Jean M. Mulcahy Levy, Andrea M. Griesinger, Irina Alimova, Peter S. Harris, Diane K. Birks, Andrew M....
    Note: Gesehen am 29.01.2021
    In: OncoTarget, [S.l.] : Impact Journals LLC, 2010, 7(2016), 33, Seite 53881-53894, 1949-2553
    In: volume:7
    In: year:2016
    In: number:33
    In: pages:53881-53894
    In: extent:14
    Language: English
    URL: Volltext  (lizenzpflichtig)
    URL: Volltext  (lizenzpflichtig)
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  • 3
    UID:
    (DE-627)1662806620
    Format: 14
    ISSN: 1432-0533
    Content: Medulloblastomas are the most common malignant brain tumors in children. Several large-scale genomic studies have detailed their heterogeneity, defining multiple subtypes with unique molecular profiles and clinical behavior. Increased expression of the miR-183~96~182 cluster of microRNAs has been noted in several subgroups, including the most clinically aggressive subgroup associated with genetic amplification of MYC. To understand the contribution of miR-183~96~182 to the pathogenesis of this aggressive subtype of medulloblastoma, we analyzed global gene expression and proteomic changes that occur upon modulation of miRNAs in this cluster individually and as a group in MYC-amplified medulloblastoma cells. Knockdown of the full miR-183~96~182 cluster results in enrichment of genes associated with apoptosis and dysregulation of the PI3K/AKT/mTOR signaling axis. Conversely, there is a relative enrichment of pathways associated with migration, metastasis and epithelial to mesenchymal transition, as well as pathways associated with dysfunction of DNA repair in cells with preserved miR-183 cluster expression. Immunocytochemistry and FACS analysis confirm induction of apoptosis upon knockdown of the miR-183 cluster. Importantly, cell-based migration and invasion assays verify the positive regulation of cell motility/migration by the miR-183 cluster, which is largely mediated by miR-182. We show that the effects on cell migration induced by the miR-183 cluster are coupled to the PI3K/AKT/mTOR pathway through differential regulation of AKT1 and AKT2 isoforms. Furthermore, we show that rapamycin inhibits cell motility/migration in medulloblastoma cells and phenocopies miR-183 cluster knockdown. Thus, the miR-183 cluster regulates multiple biological programs that converge to support the maintenance and metastatic potential of medulloblastoma.
    Note: Gesehen am 04.04.2019
    In: Acta neuropathologica, Berlin : Springer, 1961, 123(2012), 4, Seite 539-552, 1432-0533
    In: volume:123
    In: year:2012
    In: number:4
    In: pages:539-552
    In: extent:14
    Language: English
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  • 4
    UID:
    (DE-627)1578020735
    Format: 9 , Illustrationen
    ISSN: 1573-7373
    Content: Little is known about frequency, association with clinical characteristics, and prognostic impact of DNA copy number alterations (CNA) on survival in central primitive neuroectodermal tumors (CNS-PNET) and tumors of the pineal region. Searches of MEDLINE, Pubmed, and EMBASE—after the original description of comparative genomic hybridization in 1992 and July 2010—identified 15 case series of patients with CNS-PNET and tumors of the pineal region whose tumors were investigated for genome-wide CNA. One additional case study was identified from contact with experts. Individual patient data were extracted from publications or obtained from investigators, and CNAs were converted to a digitized format suitable for data mining and subgroup identification. Summary profiles for genomic imbalances were generated from case-specific data. Overall survival (OS) was estimated using the Kaplan-Meier method, and by univariable and multivariable Cox regression models. In their overall CNA profiles, low grade tumors of the pineal region clearly diverged from CNS-PNET and pineoblastoma. At a median follow-up of 89 months, 7-year OS rates of CNS-PNET, pineoblastoma, and low grade tumors of the pineal region were 22.9 ± 6, 0 ± 0, and 87.5 ± 12 %, respectively. Multivariable analysis revealed that histology (CNS-PNET), age (≤2.5 years), and possibly recurrent CNAs were associated with unfavorable OS. DNA copy number profiling suggests a close relationship between CNS-PNET and pineoblastoma. Low grade tumors of the pineal region differed from CNS-PNET and pineoblastoma. Due to their high biological and clinical variability, a coordinated prospective validation in future studies is necessary to establish robust risk factors.
    Note: Published online: 7 July 2012 , Gesehen am 27.07.2018
    In: Journal of neuro-oncology, Dordrecht [u.a.] : Springer Science + Business Media B.V, 1983, 109(2012), 2, Seite 415-423, 1573-7373
    In: volume:109
    In: year:2012
    In: number:2
    In: pages:415-423
    In: extent:9
    Language: English
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  • 5
    UID:
    (DE-627)158168259X
    Format: 11 , Illustrationen
    ISSN: 1525-2191
    Content: Musashi1 (Msi1) is a highly conserved RNA-binding protein that is required during the development of the nervous system. Msi1 has been characterized as a stem cell marker, controlling the balance between self-renewal and differentiation, and has also been implicated in tumorigenesis, being highly expressed in multiple tumor types. We analyzed Msi1 expression in a large cohort of medulloblastoma samples and found that Msi1 is highly expressed in tumor tissue compared with normal cerebellum. Notably, high Msi1 expression levels proved to be a sign of poor prognosis. Msi1 expression was determined to be particularly high in molecular subgroups 3 and 4 of medulloblastoma. We determined that Msi1 is required for tumorigenesis because inhibition of Msi1 expression by small-interfering RNAs reduced the growth of Daoy medulloblastoma cells in xenografts. To characterize the participation of Msi1 in medulloblastoma, we conducted different high-throughput analyses. Ribonucleoprotein immunoprecipitation followed by microarray analysis (RIP-chip) was used to identify mRNA species preferentially associated with Msi1 protein in Daoy cells. We also used cluster analysis to identify genes with similar or opposite expression patterns to Msi1 in our medulloblastoma cohort. A network study identified RAC1, CTGF, SDCBP, SRC, PRL, and SHC1 as major nodes of an Msi1-associated network. Our results suggest that Msi1 functions as a regulator of multiple processes in medulloblastoma formation and could become an important therapeutic target.
    Note: Gesehen am 09.10.2018
    In: The American journal of pathology, New York [u.a.] : Elsevier, 1925, 181(2012), 5, Seite 1762-1772, 1525-2191
    In: volume:181
    In: year:2012
    In: number:5
    In: pages:1762-1772
    In: extent:11
    Language: English
    URL: Volltext  (kostenfrei)
    URL: Volltext  (kostenfrei)
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  • 6
    UID:
    (DE-627)1571906142
    Format: 12
    ISSN: 1432-0533
    Content: The diagnosis of medulloblastoma likely encompasses several distinct entities, with recent evidence for the existence of at least four unique molecular subgroups that exhibit distinct genetic, transcriptional, demographic, and clinical features. Assignment of molecular subgroup through routine profiling of high-quality RNA on expression microarrays is likely impractical in the clinical setting. The planning and execution of medulloblastoma clinical trials that stratify by subgroup, or which are targeted to a specific subgroup requires technologies that can be economically, rapidly, reliably, and reproducibly applied to formalin-fixed paraffin embedded (FFPE) specimens. In the current study, we have developed an assay that accurately measures the expression level of 22 medulloblastoma subgroup-specific signature genes (CodeSet) using nanoString nCounter Technology.
    Note: Published online: 6 November 2011 , Gesehen am 11.04.2018
    In: Acta neuropathologica, Berlin : Springer, 1961, 123(2012), 4, Seite 615-626, 1432-0533
    In: volume:123
    In: year:2012
    In: number:4
    In: pages:615-626
    In: extent:12
    Language: English
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  • 7
    UID:
    (DE-627)1884860346
    Format: 1 online resource (263 pages)
    Edition: 1st ed.
    ISBN: 9789004681910
    Series Statement: International Technology Education Studies v.19
    Content: Technology Education and Maker Education both value learning through making and agency of learners. In this book the two fields meet through a series of case-studies and thematic, theory-based reflections on these cases-studies to imagine possible futures for Maker Education.
    Content: Intro -- Contents -- Preface -- Figures and Tables -- Figures -- Tables -- Notes on Contributors -- Part 1. The Rise of Maker Education across the World -- 1. Introduction -- Abstract -- Keywords -- 1 Learning from the Maker Movement -- 2 The Rise of Maker Education -- 3 Reasons behind the Rise of Maker Education -- 4 Educational Value: What Do You Learn through Making? -- 4.1 Educational Reformers Valuing Materiality -- 4.2 Key Principles in Maker-Centered Education -- 4.3 What Do They Learn from Making? -- 5 Maker Education and School Subjects -- 6 Maker Education and Environmental Sustainability -- 7 Set-up and Structure of This Book -- Notes -- References -- 2. The Development and Evolution of Maker Education in China -- Abstract -- Keywords -- 1 The Origin of Maker Education in China -- 2 The Development of Maker Education in China -- References -- 3. A Participatory Design Approach to Sustaining Makerspace Initiatives -- Abstract -- Keywords -- 1 Introduction -- 2 Participatory Design -- Principle 1: Collaborative Hands-on Activities Involving Stakeholders -- Principle 2: Working Frontstage and Backstage -- Principle 3: Infrastructuring -- Principle 4: Working Horizontally and Vertically -- 3 Participatory Strategies for Sustainable Makerspaces in Denmark -- 4 The Six Steps towards Sustaining Makerspace Initiatives -- Step 1: Understanding the Complexity of a Makerspace Initiative -- Step 2: Hands-on Introduction to Makerspace Education -- Step 3: Establishing the Grand Narrative of a Makerspace Initiative -- Step 4: Developing the Makerspace Initiative within the Existing Municipality Landscape -- Step 5: Confirmation and Articulation of Management Support for the Makerspace Initiative -- Step 6: Choosing and Purchasing Technologies for the Makerspace -- 5 Concluding Remarks -- References -- Part 2. Case Studies on Maker Education.
    Content: "Book Summary In this book two fields meet, Technology Education with its long history, and Maker Education, a relative new shoot in the educational field. Both focus on learning through making and both value agency and motivation of learners. The purpose of this book is to understand and analyze the kind of informal and formal educational activities that take place under the umbrella of the Maker Movement and then relate this to the field of Technology Education to uncover what researchers, innovators and teachers in this field can learn from the principles, ideas and practices that are central to the Maker Movement and vice versa. The book contains two types of chapters. The first type is case study chapters that span from Mexico, China, Korea, Denmark, the Netherlands to Kenya and from primary to tertiary level, showing a variety of good practices in maker education including both formal and informal contexts. In the subsequent thematic chapters, dedicated authors have used the case studies to reflect on themes such as curriculum reform, social learning, materiality, spatial thinking, informal versus formal learning as well as the sustainability of learning and relate what is happening in Maker Education with Technology Education to imagine possible futures for Maker Education"--
    Note: Description based on publisher supplied metadata and other sources
    Additional Edition: 9789004681903
    Additional Edition: Erscheint auch als Druck-Ausgabe 9789004681903
    Language: English
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  • 8
    UID:
    (DE-627)1577613732
    Format: 8
    ISSN: 1432-0533
    Content: Medulloblastoma, a small blue cell malignancy of the cerebellum, is a major cause of morbidity and mortality in pediatric oncology. Current mechanisms for clinical prognostication and stratification include clinical factors (age, presence of metastases, and extent of resection) as well as histological subgrouping (classic, desmoplastic, and large cell/anaplastic histology). Transcriptional profiling studies of medulloblastoma cohorts from several research groups around the globe have suggested the existence of multiple distinct molecular subgroups that differ in their demographics, transcriptomes, somatic genetic events, and clinical outcomes. Variations in the number, composition, and nature of the subgroups between studies brought about a consensus conference in Boston in the fall of 2010. Discussants at the conference came to a consensus that the evidence supported the existence of four main subgroups of medulloblastoma (Wnt, Shh, Group 3, and Group 4). Participants outlined the demographic, transcriptional, genetic, and clinical differences between the four subgroups. While it is anticipated that the molecular classification of medulloblastoma will continue to evolve and diversify in the future as larger cohorts are studied at greater depth, herein we outline the current consensus nomenclature, and the differences between the medulloblastoma subgroups.
    Note: First online: 02 December 2011 , Gesehen am 16.07.2018
    In: Acta neuropathologica, Berlin : Springer, 1961, 123(2012), 4, Seite 465-472, 1432-0533
    In: volume:123
    In: year:2012
    In: number:4
    In: pages:465-472
    In: extent:8
    Language: English
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  • 9
    UID:
    (DE-627)1582292108
    Format: 12
    ISSN: 1432-0533
    Content: Medulloblastoma is the most common malignant brain tumor in childhood. Molecular studies from several groups around the world demonstrated that medulloblastoma is not one disease but comprises a collection of distinct molecular subgroups. However, all these studies reported on different numbers of subgroups. The current consensus is that there are only four core subgroups, which should be termed WNT, SHH, Group 3 and Group 4. Based on this, we performed a meta-analysis of all molecular and clinical data of 550 medulloblastomas brought together from seven independent studies. All cases were analyzed by gene expression profiling and for most cases SNP or array-CGH data were available. Data are presented for all medulloblastomas together and for each subgroup separately. For validation purposes, we compared the results of this meta-analysis with another large medulloblastoma cohort (n = 402) for which subgroup information was obtained by immunohistochemistry. Results from both cohorts are highly similar and show how distinct the molecular subtypes are with respect to their transcriptome, DNA copy-number aberrations, demographics, and survival. Results from these analyses will form the basis for prospective multi-center studies and will have an impact on how the different subgroups of medulloblastoma will be treated in the future.
    Note: Gesehen am 25.10.2018
    In: Acta neuropathologica, Berlin : Springer, 1961, 123(2012), 4, Seite 473-484, 1432-0533
    In: volume:123
    In: year:2012
    In: number:4
    In: pages:473-484
    In: extent:12
    Language: English
    URL: Volltext  (kostenfrei)
    URL: Volltext  (kostenfrei)
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  • 10
    UID:
    (DE-627)1849777357
    Format: 4
    ISSN: 1536-3678
    Content: Spinal glioblastoma multiforme (GBM) is rare in children. New therapeutic options should be explored given the poor outcomes reported. We describe the case of an infant with spinal GBM whose condition worsened despite radiotherapy and chemotherapy. Immunohistochemical analysis of the tumor sample showed activation of the Raf-MEK-ERK pathway. Targeted pharmacologic therapy with sorafenib plus valproic acid led to decrease in the size of the tumor and improvement of symptoms. We conclude that regulation of the mitogen-activated protein kinase pathway using sorafenib plus valproic acid warrants further investigation for the management of childhood GBM.
    Note: Gesehen am 15.06.2023
    In: Journal of pediatric hematology - oncology, Hagerstown, Md. : Lippincott Williams & Wilkins, 1995, 32(2010), 6 vom: Aug., Seite 511-514, 1536-3678
    In: volume:32
    In: year:2010
    In: number:6
    In: month:08
    In: pages:511-514
    In: extent:4
    Language: English
    URL: Volltext  (lizenzpflichtig)
    URL: Volltext  (lizenzpflichtig)
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