Wiese, Maria

[["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.journal","European Journal of Cancer"],["dc.bibliographiccitation.lastpage","8"],["dc.bibliographiccitation.volume","81"],["dc.contributor.author","Karremann, Michael"],["dc.contributor.author","Krämer, Nadja"],["dc.contributor.author","Hoffmann, Marion"],["dc.contributor.author","Wiese, Maria"],["dc.contributor.author","Beilken, Andreas"],["dc.contributor.author","Corbacioglu, Selim"],["dc.contributor.author","Dilloo, Dagmar"],["dc.contributor.author","Hernaiz Driever, Pablo"],["dc.contributor.author","Scheurlen, Wolfram"],["dc.contributor.author","Kulozik, Andreas"],["dc.contributor.author","Gielen, Gerrit H."],["dc.contributor.author","von Bueren, André"],["dc.contributor.author","Dürken, Matthias"],["dc.contributor.author","Kramm, Christof M."],["dc.date.accessioned","2018-10-10T07:47:12Z"],["dc.date.available","2018-10-10T07:47:12Z"],["dc.date.issued","2017"],["dc.description.abstract","Temozolomide (TMZ) is widely used in high-grade glioma (HGG). There is a major concern of treatment-induced secondary haematological malignancies (SHMs). Due to the poor overall survival of HGG patients, the true incidence is yet elusive. Thus, the aim of this study was to determine the risk of SHMs following TMZ in paediatric HGG. We analysed 487 patients from the HIT-HGG database of the German-speaking Society of Pediatric Oncology and Hematology with follow up beyond 1 year. The incidence of SHM was 7.7 ± 3.2% at 10 years. No SHM occurred in 194 patients after first-line TMZ therapy, but four out of 131 patients treated with TMZ for relapse following first-line multiagent chemotherapy experienced SHM (20% at 10 years; p = 0.041). SHMs occurred in two out of 162 patients who underwent multiagent chemotherapy without TMZ (4.1% at 10 years). Gender, patient age and acute haematological toxicity during treatment did not affect the incidence of SHMs. Data of our cohort do not indicate an increased risk of SHM following TMZ treatment when compared to previous chemotherapy regimen. However, if TMZ is administered as a second-line treatment following conventional chemotherapy regimen, the risk might be disproportionately increasing."],["dc.fs.pkfprnr","58469"],["dc.identifier.doi","10.1016/j.ejca.2017.04.023"],["dc.identifier.fs","633320"],["dc.identifier.pmid","28586748"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/15921"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.eissn","1879-0852"],["dc.title","Haematological malignancies following temozolomide treatment for paediatric high-grade glioma"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["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.artnumber","vdac077"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Neuro-Oncology Advances"],["dc.bibliographiccitation.volume","4"],["dc.contributor.author","Gielen, Gerrit H"],["dc.contributor.author","Baugh, Joshua N"],["dc.contributor.author","van Vuurden, Dannis G"],["dc.contributor.author","Veldhuijzen van Zanten, Sophie E M"],["dc.contributor.author","Hargrave, Darren"],["dc.contributor.author","Massimino, Maura"],["dc.contributor.author","Biassoni, Veronica"],["dc.contributor.author","Morales la Madrid, Andres"],["dc.contributor.author","Karremann, Michael"],["dc.contributor.author","Wiese, Maria"],["dc.contributor.author","Kramm, Christof M"],["dc.date.accessioned","2022-07-01T07:35:03Z"],["dc.date.available","2022-07-01T07:35:03Z"],["dc.date.issued","2022"],["dc.description.abstract","Abstract Background The WHO Classification of Tumors of the Central Nervous System has undergone major restructuring. Molecularly defined diagnostic criteria were introduced in 2016 (revised 4th edition) and expanded in 2021 (5th edition) to incorporate further essential diagnostic molecular parameters. We investigated potential differences between specialists in perception of these molecularly defined subtypes for pediatric high-grade gliomas (pedHGG). Methods We designed a 22-question survey studying the impact of the revised 4th edition of the WHO classification on pedHGG. Data were collected and statistically analyzed to examine the spectrum of viewpoints and possible differences between neuro-oncologists and neuropathologists. Results 465 participants from 53 countries were included; 187 pediatric neuro-oncologists (40%), 160 neuropathologists (34%), and 118 additional experts (26%). Neuro-oncologists reported issues with the introduction of molecularly defined tumor types, as well as the abolishment or renaming of established tumor entities, while neuropathologists did not to the same extent. Both groups indicated less relevant or insufficient diagnostic definitions were available in 2016. Reported issues were classified and assessed in the 2021 WHO classification and a substantial improvement was perceived. However, issues of high clinical relevance remain to be addressed, including the definition of clinical phenotypes for diffuse intrinsic pontine glioma and gliomatosis cerebri. Conclusions Within the WHO classification of pediatric brain tumors, such as pedHGG, rapid changes in molecular characterization have been introduced. This study highlights the ongoing need for cross talk between pathologist and oncologist to advance the classification of pedHGG subtypes and ensure biological relevance and clinical impact."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2022"],["dc.identifier.doi","10.1093/noajnl/vdac077"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/112075"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-581"],["dc.relation.eissn","2632-2498"],["dc.rights","CC BY 4.0"],["dc.title","Pediatric high-grade gliomas and the WHO CNS Tumor Classification—Perspectives of pediatric neuro-oncologists and neuropathologists in light of recent updates"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","6770"],["dc.bibliographiccitation.issue","16"],["dc.bibliographiccitation.journal","Oncotarget"],["dc.bibliographiccitation.lastpage","6787"],["dc.bibliographiccitation.volume","5"],["dc.contributor.author","Zatula, Nathalie"],["dc.contributor.author","Wiese, Maria"],["dc.contributor.author","Bunzendahl, Jens"],["dc.contributor.author","Birchmeier, Walter"],["dc.contributor.author","Perske, Christina"],["dc.contributor.author","Bleckmann, Annalen"],["dc.contributor.author","Brembeck, Felix H."],["dc.date.accessioned","2019-07-09T11:42:11Z"],["dc.date.available","2019-07-09T11:42:11Z"],["dc.date.issued","2014-08-30"],["dc.description.abstract","The majority of human breast cancers express estrogen receptor alpha (ER), which is important for therapy with anti-estrogens. Here we describe the role of BCL9-2, a proto-oncogene previously characterized as co-activator of Wnt/ß-catenin signaling, for mammary tumorigenesis in mice and human. ER positive human breast cancers showed overexpression of BCL9-2 and tamoxifen treated patients with high BCL9-2 demonstrated a better survival. BCL9-2 was upregulated during puberty and pregnancy in normal mammary epithelia, but downregulated in the involuted gland. BCL9-2 overexpression in vivo delayed the mammary involution and induced alveolar hyperplasia. Moreover, aged BCL9-2 transgenic mice developed ductal-like mammary tumors with high nuclear ER expression. We found, that primary cell cultures of BCL9-2 breast tumors responded to tamoxifen treatment. Moreover, BCL9-2 regulated the expression of ER and the proliferation of human breast cancer cells independently of ß-catenin. Finally, we describe a novel mechanism, how BCL9-2 regulates ER transcription by interaction with Sp1 through the proximal ESR1 gene promoter. In summary, BCL9-2 induces ER positive breast cancers in vivo, regulates ER expression by a novel ß-catenin independent mechanism in breast cancer cells, and might predict the therapy response to tamoxifen treatment."],["dc.identifier.doi","10.18632/oncotarget.2252"],["dc.identifier.pmid","25149534"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12963"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58610"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1949-2553"],["dc.rights","CC BY 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/3.0"],["dc.subject.mesh","Animals"],["dc.subject.mesh","Breast Neoplasms"],["dc.subject.mesh","Carcinogenesis"],["dc.subject.mesh","DNA-Binding Proteins"],["dc.subject.mesh","Estrogen Receptor alpha"],["dc.subject.mesh","Female"],["dc.subject.mesh","Humans"],["dc.subject.mesh","Mammary Neoplasms, Experimental"],["dc.subject.mesh","Mice"],["dc.subject.mesh","Mice, Transgenic"],["dc.subject.mesh","Tamoxifen"],["dc.subject.mesh","Transcription Factors"],["dc.subject.mesh","Transcriptional Activation"],["dc.subject.mesh","Wnt Signaling Pathway"],["dc.subject.mesh","beta Catenin"],["dc.title","The BCL9-2 proto-oncogene governs estrogen receptor alpha expression in breast tumorigenesis."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1359"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Gastroenterology"],["dc.bibliographiccitation.lastpage","U810"],["dc.bibliographiccitation.volume","141"],["dc.contributor.author","Brembeck, Felix H."],["dc.contributor.author","Wiese, Maria"],["dc.contributor.author","Zatula, Nathalie"],["dc.contributor.author","Grigoryan, Tamara"],["dc.contributor.author","Dai, Yiyang"],["dc.contributor.author","Fritzmann, Johannes"],["dc.contributor.author","Birchmeier, Walter"],["dc.date.accessioned","2018-11-07T08:51:06Z"],["dc.date.available","2018-11-07T08:51:06Z"],["dc.date.issued","2011"],["dc.description.abstract","BACKGROUND & AIMS: The roles of the 2 BCL9 and 2 Pygopus genes in Wnt to beta-catenin signaling are not clear in vertebrates. We examined their expression and function in normal and tumor intestinal epithelia in mice and humans. METHODS: Specific antibodies were generated to characterize the BCL9 and Pygopus proteins in normal intestine and in colon tumors. Targets of BCL9 and Pygopus in colon cancer cells were analyzed using small interfering RNA analysis. Transgenic mice were created that overexpressed BCL9-2 in intestine; these were crossed with APC(Min/+) mice to create BCL9-2; APC(Min/+) mice. RESULTS: BCL9 and Pygopus2 were expressed in all normal intestinal and colon cancer cells. BCL9-2 was detectable only in the villi, not in the crypts of normal intestine. BCL9-2 was up-regulated in adenomas and in almost all colon tumors, with a concomitant increase of Pygopus2, whereas levels of BCL9 were similar between normal and cancer cells. Transgenic overexpression of BCL9-2 in theintestine of BCL9-2; APC(Min/+) mice increased formation of adenomas that progressed to invasive tumors, resulting in reduced survival time. Using small interfering RNA analysis, we found that BCL9s and Pygopus are not targets of Wnt in colon cancer cells, but Wnt signaling correlated with levels of BCL9-2. BCL9-2 regulated expression of beta-catenin-dependent and -independent target genes that have been associated with early stages of intestinal tumorigenesis. CONCLUSIONS: BCL9-2 promotes early phases of intestinal tumor progression in humans and in transgenic mice. BCL9-2 increases the expression of a subset of canonical Wnt target genes but also regulates genes that are required for early stages of tumor progression."],["dc.identifier.doi","10.1053/j.gastro.2011.06.039"],["dc.identifier.isi","000295593700043"],["dc.identifier.pmid","21703997"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/21850"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","W B Saunders Co-elsevier Inc"],["dc.relation.issn","0016-5085"],["dc.title","BCL9-2 Promotes Early Stages of Intestinal Tumor Progression"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Pediatric Blood & Cancer"],["dc.contributor.author","El‐Khouly, Fatma E."],["dc.contributor.author","Adil, Syed M."],["dc.contributor.author","Wiese, Maria"],["dc.contributor.author","Hulleman, Esther"],["dc.contributor.author","Hendrikse, N. Harry"],["dc.contributor.author","Kaspers, Gertjan J.L."],["dc.contributor.author","Kramm, Christof M."],["dc.contributor.author","Veldhuijzen van Zanten, Sophie E.M."],["dc.contributor.author","Vuurden, Dannis G."],["dc.contributor.authorgroup","SIOPE DIPG Network"],["dc.date.accessioned","2021-06-01T09:42:21Z"],["dc.date.available","2021-06-01T09:42:21Z"],["dc.date.issued","2021"],["dc.identifier.doi","10.1002/pbc.29061"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/85228"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.relation.eissn","1545-5017"],["dc.relation.issn","1545-5009"],["dc.title","Complementary and alternative medicine in children with diffuse intrinsic pontine glioma—A SIOPE DIPG Network and Registry study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Cell Death & Disease"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Wiese, Maria"],["dc.contributor.author","Hamdan, Feda H."],["dc.contributor.author","Kubiak, Klaudia"],["dc.contributor.author","Diederichs, Christopher"],["dc.contributor.author","Gielen, Gerrit H."],["dc.contributor.author","Nussbaumer, Gunther"],["dc.contributor.author","Carcaboso, Angel M."],["dc.contributor.author","Hulleman, Esther"],["dc.contributor.author","Johnsen, Steven A."],["dc.contributor.author","Kramm, Christof M."],["dc.date.accessioned","2021-04-14T08:24:30Z"],["dc.date.available","2021-04-14T08:24:30Z"],["dc.date.issued","2020"],["dc.description.sponsorship","Open-Access-Publikationsfonds 2021"],["dc.identifier.doi","10.1038/s41419-020-02800-7"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17777"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/81304"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.notes.intern","Merged from goescholar"],["dc.relation.eissn","2041-4889"],["dc.relation.orgunit","Klinik für Kinder- und Jugendmedizin"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Combined treatment with CBP and BET inhibitors reverses inadvertent activation of detrimental super enhancer programs in DIPG cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","123"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Neuro-Oncology"],["dc.bibliographiccitation.lastpage","131"],["dc.bibliographiccitation.volume","20"],["dc.contributor.author","Karremann, Michael"],["dc.contributor.author","Gielen, Gerrit H"],["dc.contributor.author","Hoffmann, Marion"],["dc.contributor.author","Wiese, Maria"],["dc.contributor.author","Colditz, Niclas"],["dc.contributor.author","Warmuth-Metz, Monika"],["dc.contributor.author","Bison, Brigitte"],["dc.contributor.author","Claviez, Alexander"],["dc.contributor.author","van Vuurden, Dannis G"],["dc.contributor.author","von Bueren, André O"],["dc.contributor.author","Gessi, Marco"],["dc.contributor.author","Kühnle, Ingrid"],["dc.contributor.author","Hans, Volkmar H"],["dc.contributor.author","Benesch, Martin"],["dc.contributor.author","Sturm, Dominik"],["dc.contributor.author","Kortmann, Rolf-Dieter"],["dc.contributor.author","Waha, Andreas"],["dc.contributor.author","Pietsch, Torsten"],["dc.contributor.author","Kramm, Christof M"],["dc.date.accessioned","2020-12-10T18:19:37Z"],["dc.date.available","2020-12-10T18:19:37Z"],["dc.date.issued","2017"],["dc.identifier.doi","10.1093/neuonc/nox149"],["dc.identifier.eissn","1523-5866"],["dc.identifier.issn","1522-8517"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/75312"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Diffuse high-grade gliomas with H3 K27M mutations carry a dismal prognosis independent of tumor location"],["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"]]