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","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.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"]]

[["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Neuro-Oncology Advances"],["dc.bibliographiccitation.volume","3"],["dc.contributor.author","Baugh, Joshua N"],["dc.contributor.author","Gielen, Gerrit H"],["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","2021-12-01T09:23:15Z"],["dc.date.available","2021-12-01T09:23:15Z"],["dc.date.issued","2021"],["dc.description.abstract","Abstract Background Pediatric neuro-oncology was profoundly changed in the wake of the 2016 revision of the WHO Classification of Tumors of the Central Nervous System. Practitioners were challenged to quickly adapt to a system of tumor classification redefined by molecular diagnostics. Methods We designed a 22-question survey studying the impact of the revised WHO classification on pediatric high-grade glioma. The survey collected basic demographics, general attitudes, issues encountered, and opinions on pediatric subtypes. Participant answers were analyzed along socioeconomic lines utilizing the human development index (HDI) of the United Nations and membership in the group of seven (G7) world economic forum. Results Four hundred and sixty-five participants from 53 countries were included, 187 pediatric neurooncologists (40%), 160 neuropathologists (34%), and 118 other experts (26%). When asked about pediatric high-grade glioma entities, participants from very high development countries preferred treating a patient based on genetic findings. Participants from high and medium development countries indicated using traditional histology and tumor location as mainstays for therapeutic decisions. Non-G7 countries tended to regard the introduction of molecularly characterized tumor entities as a problem for daily routine due to lack of resources. Conclusions Our findings demonstrate an overall greater reliance and favorability to molecular diagnostics among very high development countries. A disparity in resources and access to molecular diagnostics has left some centers unable to classify pediatric high-grade glioma per the WHO classification. The forthcoming edition should strain to abate disparities in molecular diagnostic availability and work toward universal adaptation."],["dc.description.abstract","Abstract Background Pediatric neuro-oncology was profoundly changed in the wake of the 2016 revision of the WHO Classification of Tumors of the Central Nervous System. Practitioners were challenged to quickly adapt to a system of tumor classification redefined by molecular diagnostics. Methods We designed a 22-question survey studying the impact of the revised WHO classification on pediatric high-grade glioma. The survey collected basic demographics, general attitudes, issues encountered, and opinions on pediatric subtypes. Participant answers were analyzed along socioeconomic lines utilizing the human development index (HDI) of the United Nations and membership in the group of seven (G7) world economic forum. Results Four hundred and sixty-five participants from 53 countries were included, 187 pediatric neurooncologists (40%), 160 neuropathologists (34%), and 118 other experts (26%). When asked about pediatric high-grade glioma entities, participants from very high development countries preferred treating a patient based on genetic findings. Participants from high and medium development countries indicated using traditional histology and tumor location as mainstays for therapeutic decisions. Non-G7 countries tended to regard the introduction of molecularly characterized tumor entities as a problem for daily routine due to lack of resources. Conclusions Our findings demonstrate an overall greater reliance and favorability to molecular diagnostics among very high development countries. A disparity in resources and access to molecular diagnostics has left some centers unable to classify pediatric high-grade glioma per the WHO classification. The forthcoming edition should strain to abate disparities in molecular diagnostic availability and work toward universal adaptation."],["dc.identifier.doi","10.1093/noajnl/vdab113"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/94599"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-478"],["dc.relation.eissn","2632-2498"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0/"],["dc.title","Transitioning to molecular diagnostics in pediatric high-grade glioma: experiences with the 2016 WHO classification of CNS tumors"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]