Now showing 1 - 3 of 3
  • 2015Journal Article Research Paper
    [["dc.bibliographiccitation.firstpage","1480"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","EMBO Molecular Medicine"],["dc.bibliographiccitation.lastpage","1502"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Isernhagen, Antje"],["dc.contributor.author","Malzahn, Doerthe"],["dc.contributor.author","Viktorova, Elena"],["dc.contributor.author","Elsner, Leslie"],["dc.contributor.author","Monecke, Sebastian"],["dc.contributor.author","von Bonin, Frederike"],["dc.contributor.author","Kilisch, Markus"],["dc.contributor.author","Wermuth, Janne Marieke"],["dc.contributor.author","Walther, Neele"],["dc.contributor.author","Balavarca, Yesilda"],["dc.contributor.author","Stahl-Hennig, Christiane"],["dc.contributor.author","Engelke, Michael"],["dc.contributor.author","Walter, Lutz"],["dc.contributor.author","Bickeboeller, Heike"],["dc.contributor.author","Kube, Dieter"],["dc.contributor.author","Wulf, Gerald"],["dc.contributor.author","Dressel, Ralf"],["dc.date.accessioned","2018-11-07T09:49:36Z"],["dc.date.available","2018-11-07T09:49:36Z"],["dc.date.issued","2015"],["dc.description.abstract","The MHC class I chain-related molecule A (MICA) is a highly polymorphic ligand for the activating natural killer (NK)-cell receptor NKG2D. A single nucleotide polymorphism causes a valine to methionine exchange at position 129. Presence of a MICA-129Met allele in patients (n=452) undergoing hematopoietic stem cell transplantation (HSCT) increased the chance of overall survival (hazard ratio [HR]=0.77, P=0.0445) and reduced the risk to die due to acute graft-versus-host disease (aGVHD) (odds ratio [OR]=0.57, P=0.0400) although homozygous carriers had an increased risk to experience this complication (OR=1.92, P=0.0371). Overall survival of MICA-129Val/Val genotype carriers was improved when treated with anti-thymocyte globulin (HR=0.54, P=0.0166). Functionally, the MICA-129Met isoform was characterized by stronger NKG2D signaling, triggering more NK-cell cytotoxicity and interferon- release, and faster co-stimulation of CD8(+) T cells. The MICA-129Met variant also induced a faster and stronger down-regulation of NKG2D on NK and CD8(+) T cells than the MICA-129Val isoform. The reduced cell surface expression of NKG2D in response to engagement by MICA-129Met variants appeared to reduce the severity of aGVHD."],["dc.description.sponsorship","Open-Access Publikationsfonds 2015"],["dc.identifier.doi","10.15252/emmm.201505246"],["dc.identifier.isi","000364320100008"],["dc.identifier.pmid","26483398"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12462"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/35542"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/127"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | C05: Bedeutung von zellulären Immunreaktionen für das kardiale Remodeling und die Therapie der Herzinsuffizienz durch Stammzelltransplantation"],["dc.relation.issn","1757-4684"],["dc.relation.issn","1757-4676"],["dc.relation.workinggroup","RG Dressel"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","The MICA-129 dimorphism affects NKG2D signaling and outcome of hematopoietic stem cell transplantation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]
    Details DOI PMID PMC WOS
  • 2017-04-18Journal Article
    [["dc.bibliographiccitation.firstpage","27300"],["dc.bibliographiccitation.issue","16"],["dc.bibliographiccitation.journal","Oncotarget"],["dc.bibliographiccitation.lastpage","27313"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Wiese, Maria"],["dc.contributor.author","Walther, Neele"],["dc.contributor.author","Diederichs, Christopher"],["dc.contributor.author","Schill, Fabian"],["dc.contributor.author","Monecke, Sebastian"],["dc.contributor.author","Salinas, Gabriella"],["dc.contributor.author","Sturm, Dominik"],["dc.contributor.author","Pfister, Stefan"],["dc.contributor.author","Dressel, Ralf"],["dc.contributor.author","Johnsen, Steven Arthur"],["dc.contributor.author","Kramm, Christof M."],["dc.date.accessioned","2018-10-10T07:29:11Z"],["dc.date.available","2018-10-10T07:29:11Z"],["dc.date.issued","2017-04-18"],["dc.description.abstract","Pediatric high-grade gliomas (pedHGG) belong to the most aggressive cancers in children with a poor prognosis due to a lack of efficient therapeutic strategies. The β-catenin/Wnt-signaling pathway was shown to hold promising potential as a treatment target in adult high-grade gliomas by abrogating tumor cell invasion and the acquisition of stem cell-like characteristics. Since pedHGG differ from their adult counterparts in genetically and biologically we aimed to investigate the effects of β-catenin/Wnt-signaling pathway-inhibition by the β-catenin/CBP antagonist ICG-001 in pedHGG cell lines. In contrast to adult HGG, pedHGG cells displayed minimal detectable canonical Wnt-signaling activity. Nevertheless, low doses of ICG-001 inhibited cell migration/invasion, tumorsphere- and colony formation, proliferation in vitro as well as tumor growth in vivo/ovo, suggesting that ICG-001 affects pedHGG tumor cell characteristics independent of β-catenin/Wnt-signaling. RNA-sequencing analyses support a Wnt/β-catenin-independent effect of ICG-001 on target gene transcription, revealing strong effects on genes involved in cellular metabolic/biosynthetic processes and cell cycle progression. Among these, high mRNA expression of cell cycle regulator JDP2 was found to confer a better prognosis for pedHGG patients. In conclusion, ICG-001 might offer an effective treatment option for pedHGG patients functioning to regulate cell phenotype and gene expression programs in absence of Wnt/β-catenin signaling-activity."],["dc.fs.pkfprnr","86261"],["dc.identifier.doi","10.18632/oncotarget.15934"],["dc.identifier.fs","633047"],["dc.identifier.pmid","28460484"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14424"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/15920"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.relation.eissn","1949-2553"],["dc.rights","CC BY 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/3.0"],["dc.title","The β-catenin/CBP-antagonist ICG-001 inhibits pediatric glioma tumorigenicity in a Wnt-independent manner"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]
    Details DOI PMID PMC
  • 2017Conference Abstract
    [["dc.bibliographiccitation.journal","Neuro-Oncology"],["dc.bibliographiccitation.volume","19"],["dc.contributor.author","Wiese, Maria"],["dc.contributor.author","Walther, Neele"],["dc.contributor.author","Diederichs, Christopher"],["dc.contributor.author","Schill, Fabian"],["dc.contributor.author","Monecke, Sebastian"],["dc.contributor.author","Salinas, Gabriela"],["dc.contributor.author","Sturm, Dominik"],["dc.contributor.author","Dressel, Ralf"],["dc.contributor.author","Pfister, Stefan M."],["dc.contributor.author","Kramm, Christof M."],["dc.date.accessioned","2018-11-07T10:23:19Z"],["dc.date.available","2018-11-07T10:23:19Z"],["dc.date.issued","2017"],["dc.format.extent","25"],["dc.identifier.isi","000402766800102"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42436"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Oxford Univ Press Inc"],["dc.publisher.place","Cary"],["dc.relation.conference","4th Biennial Conference on Pediatric Neuro-Oncology Basic and Translational Research"],["dc.relation.eventlocation","New York, NY"],["dc.relation.issn","1523-5866"],["dc.relation.issn","1522-8517"],["dc.title","THE beta-CATENIN/CBP-ANTAGONIST ICG-001 INHIBITS PEDIATRIC GLIOMA GROWTH IN AWNT-INDEPENDENT MANNER"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]
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