Schill, Fabian

[["dc.bibliographiccitation.firstpage","113"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Klinische Pädiatrie"],["dc.bibliographiccitation.lastpage","117"],["dc.bibliographiccitation.volume","228"],["dc.contributor.author","Wiese, M."],["dc.contributor.author","Schill, Fabian"],["dc.contributor.author","Sturm, Dominik"],["dc.contributor.author","Pfister, Stefan M."],["dc.contributor.author","Hulleman, Esther"],["dc.contributor.author","Johnsen, Steven A."],["dc.contributor.author","Kramm, Christof M."],["dc.date.accessioned","2018-11-07T10:14:53Z"],["dc.date.available","2018-11-07T10:14:53Z"],["dc.date.issued","2016"],["dc.description.abstract","Background: Glioblastoma multiforme (GBM) and diffuse intrinsic pontine glioma (DIPG) belong to the most aggressive cancers in children with poor prognosis and limited therapeutic options. Therapeutic targeting of epigenetic proteins may offer new treatment options. Preclinical studies identified Enhancer of Zeste Homolog 2 (EZH2) within polycomb repressor complex 2 (PRC2) as a potential epigenetic anti-tumor target in adult GBM cells but similar inhibition studies in pediatric GBM/DIPG were still missing. Moreover, approximately 30 % of pediatric high grade gliomas (pedHGG) including GBM and DIPG harbor a lysine 27 mutation (K27M) in histone 3.3 (H3.3) which is correlated with poor outcome and was shown to influence EZH2 function. Patients, materials and methods: The present study investigated the correlation of expression of EZH2 and other PRC2 genes (EZH1, SUZ12, EED) with overall survival of pediatric GBM patients and the cytotoxic impact of EZH2 inhibition by the novel agent Tazemetostat in pediatric GBM/DIPG cells harboring either a H3.3 mutation or a H3 wildtype. Results: EZH2 gene expression does not correlate with survival of pedHGG patients, and EZH2 inhibition does not induce significant cytotoxicity in pedHGG cells independently of H3.3 mutations. Discussion and conclusion: We suggest that EZH2 inhibition might not offer an effective single agent treatment option for paedHGG patients. However, the therapeutic efficacy in combination with cytotoxic and/or other epigenetically active agents still has to be elucidated."],["dc.description.sponsorship","Menschen fur Kinder e.V."],["dc.identifier.doi","10.1055/s-0042-105292"],["dc.identifier.isi","000375862800003"],["dc.identifier.pmid","27135271"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40710"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Georg Thieme Verlag Kg"],["dc.relation.issn","1439-3824"],["dc.relation.issn","0300-8630"],["dc.title","No Significant Cytotoxic Effect of the EZH2 Inhibitor Tazemetostat (EPZ-6438) on Pediatric Glioma Cells with Wildtype Histone 3 or Mutated Histone 3.3"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["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"]]

[["dc.bibliographiccitation.firstpage","588"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Letters in Applied Microbiology"],["dc.bibliographiccitation.lastpage","595"],["dc.bibliographiccitation.volume","71"],["dc.contributor.author","Otte, K."],["dc.contributor.author","Kühne, N.M."],["dc.contributor.author","Furrer, A.D."],["dc.contributor.author","Baena Lozada, L.P."],["dc.contributor.author","Lutz, V.T."],["dc.contributor.author","Schilling, T."],["dc.contributor.author","Hertel, R."],["dc.date.accessioned","2021-04-14T08:22:53Z"],["dc.date.available","2021-04-14T08:22:53Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1111/lam.13349"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/80724"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","1472-765X"],["dc.relation.issn","0266-8254"],["dc.title","A CRISPR‐Cas9 tool to explore the genetics of Bacillus subtilis phages"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["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 prüfen"],["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"]]