von Bueren, André O.

[["dc.bibliographiccitation.firstpage","137"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Acta Neuropathologica"],["dc.bibliographiccitation.lastpage","149"],["dc.bibliographiccitation.volume","128"],["dc.contributor.author","Pietsch, Torsten"],["dc.contributor.author","Schmidt, Rene"],["dc.contributor.author","Remke, Marc"],["dc.contributor.author","Korshunov, Andrey"],["dc.contributor.author","Hovestadt, Volker"],["dc.contributor.author","Jones, David T. W."],["dc.contributor.author","Felsberg, Joerg"],["dc.contributor.author","Kaulich, Kerstin"],["dc.contributor.author","Goschzik, Tobias"],["dc.contributor.author","Kool, Marcel"],["dc.contributor.author","Northcott, Paul A."],["dc.contributor.author","von Hoff, Katja"],["dc.contributor.author","von Bueren, Andre Oscar"],["dc.contributor.author","Friedrich, Carsten"],["dc.contributor.author","Mynarek, Martin"],["dc.contributor.author","Skladny, Heyko"],["dc.contributor.author","Fleischhack, Gudrun"],["dc.contributor.author","Taylor, Michael D."],["dc.contributor.author","Cremer, Friedrich"],["dc.contributor.author","Lichter, Peter"],["dc.contributor.author","Faldum, Andreas"],["dc.contributor.author","Reifenberger, Guido"],["dc.contributor.author","Rutkowski, Stefan"],["dc.contributor.author","Pfister, Stefan M."],["dc.date.accessioned","2018-11-07T09:38:16Z"],["dc.date.available","2018-11-07T09:38:16Z"],["dc.date.issued","2014"],["dc.description.abstract","This study aimed to prospectively evaluate clinical, histopathological and molecular variables for outcome prediction in medulloblastoma patients. Patients from the HIT2000 cooperative clinical trial were prospectively enrolled based on the availability of sufficient tumor material and complete clinical information. This revealed a cohort of 184 patients (median age 7.6 years), which was randomly split at a 2:1 ratio into a training (n = 127), and a test (n = 57) dataset in order to build and test a risk score for this population. Independent validation was performed in a non-overlapping cohort (n = 83). All samples were subjected to thorough histopathological investigation, CTNNB1 mutation analysis, quantitative PCR, MLPA and FISH analyses for cytogenetic variables, and methylome analysis. By univariable analysis, clinical factors (M-stage), histopathological variables (large cell component, endothelial proliferation, synaptophysin pattern), and molecular features (chromosome 6q status, MYC amplification, subgrouping) were found to be prognostic. Molecular consensus subgrouping (WNT, SHH, Group 3, Group 4) was validated as an independent feature to stratify patients into different risk groups. When comparing methods for the identification of WNT-driven medulloblastoma, this study identified CTNNB1 sequencing and methylation profiling to most reliably identify these patients. After removing patients with particularly favorable (CTNNB1 mutation, extensive nodularity) or unfavorable (MYC amplification) markers, a risk score for the remaining \"intermediate molecular risk\" population dependent on age, M-stage, pattern of synaptophysin expression, and MYCN copy-number status was identified, with speckled synaptophysin expression indicating worse outcome. Test and independent validation of the score confirmed significant discrimination of patients by risk profile. Methylation subgrouping and CTNNB1 mutation status represent robust tools for the risk stratification of medulloblastoma. A simple clinico-pathological risk score was identified, which was confirmed in a test set and by independent clinical validation."],["dc.identifier.doi","10.1007/s00401-014-1276-0"],["dc.identifier.isi","000338195600011"],["dc.identifier.pmid","24791927"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/10264"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/33033"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","1432-0533"],["dc.relation.issn","0001-6322"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Prognostic significance of clinical, histopathological, and molecular characteristics of medulloblastomas in the prospective HIT2000 multicenter clinical trial cohort"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","64564"],["dc.bibliographiccitation.issue","38"],["dc.bibliographiccitation.journal","Oncotarget"],["dc.bibliographiccitation.lastpage","64578"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","El-Ayadi, Moatasem"],["dc.contributor.author","Ansari, Marc"],["dc.contributor.author","Sturm, Dominik"],["dc.contributor.author","Gielen, Gerrit H."],["dc.contributor.author","Warmuth-Metz, Monika"],["dc.contributor.author","Kramm, Christof M."],["dc.contributor.author","von Bueren, Andre O."],["dc.date.accessioned","2021-06-01T10:48:31Z"],["dc.date.available","2021-06-01T10:48:31Z"],["dc.date.issued","2017"],["dc.identifier.doi","10.18632/oncotarget.18478"],["dc.identifier.eissn","1949-2553"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17005"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/85962"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.notes.intern","Merged from goescholar"],["dc.relation.eissn","1949-2553"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","High-grade glioma in very young children: a rare and particular patient population"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","174"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Acta Neuropathologica Communications"],["dc.bibliographiccitation.volume","2"],["dc.contributor.author","Zhukova, Nataliya"],["dc.contributor.author","Ramaswamy, Vijay"],["dc.contributor.author","Remke, Marc"],["dc.contributor.author","Martin, Dianna C."],["dc.contributor.author","Castelo-Branco, Pedro"],["dc.contributor.author","Zhang, Cindy H."],["dc.contributor.author","Fraser, Michael"],["dc.contributor.author","Tse, Ken"],["dc.contributor.author","Poon, Raymond"],["dc.contributor.author","Shih, David JH"],["dc.contributor.author","Baskin, Berivan"],["dc.contributor.author","Ray, Peter N."],["dc.contributor.author","Bouffet, Eric"],["dc.contributor.author","Dirks, Peter"],["dc.contributor.author","von Bueren, Andre O."],["dc.contributor.author","Pfaff, Elke"],["dc.contributor.author","Korshunov, Andrey"],["dc.contributor.author","Jones, David T.W."],["dc.contributor.author","Northcott, Paul A."],["dc.contributor.author","Kool, Marcel"],["dc.contributor.author","Pugh, Trevor J."],["dc.contributor.author","Pomeroy, Scott L."],["dc.contributor.author","Cho, Yoon-Jae"],["dc.contributor.author","Pietsch, Torsten"],["dc.contributor.author","Gessi, Marco"],["dc.contributor.author","Rutkowski, Stefan"],["dc.contributor.author","Bognár, Laszlo"],["dc.contributor.author","Cho, Byung-Kyu"],["dc.contributor.author","Eberhart, Charles G."],["dc.contributor.author","Conter, Cecile F."],["dc.contributor.author","Fouladi, Maryam"],["dc.contributor.author","French, Pim J."],["dc.contributor.author","Grajkowska, Wieslawa A."],["dc.contributor.author","Gupta, Nalin"],["dc.contributor.author","Hauser, Peter"],["dc.contributor.author","Jabado, Nada"],["dc.contributor.author","Vasiljevic, Alexandre"],["dc.contributor.author","Jung, Shin"],["dc.contributor.author","Kim, Seung-Ki"],["dc.contributor.author","Klekner, Almos"],["dc.contributor.author","Kumabe, Toshihiro"],["dc.contributor.author","Lach, Boleslaw"],["dc.contributor.author","Leonard, Jeffrey R."],["dc.contributor.author","Liau, Linda M."],["dc.contributor.author","Massimi, Luca"],["dc.contributor.author","Pollack, Ian F."],["dc.contributor.author","Ra, Young S."],["dc.contributor.author","Rubin, Joshua B."],["dc.contributor.author","Van Meir, Erwin G."],["dc.contributor.author","Wang, Kyu-Chang"],["dc.contributor.author","Weiss, William A."],["dc.contributor.author","Zitterbart, Karel"],["dc.contributor.author","Bristow, Robert G."],["dc.contributor.author","Alman, Benjamin"],["dc.contributor.author","Hawkins, Cynthia E."],["dc.contributor.author","Malkin, David"],["dc.contributor.author","Clifford, Steven C."],["dc.contributor.author","Pfister, Stefan M."],["dc.contributor.author","Taylor, Michael D."],["dc.contributor.author","Tabori, Uri"],["dc.date.accessioned","2019-07-09T11:40:53Z"],["dc.date.available","2019-07-09T11:40:53Z"],["dc.date.issued","2014"],["dc.description.abstract","TP53 mutations confer subgroup specific poor survival for children with medulloblastoma. We hypothesized that WNT activation which is associated with improved survival for such children abrogates TP53 related radioresistance and can be used to sensitize TP53 mutant tumors for radiation. We examined the subgroup-specific role of TP53 mutations in a cohort of 314 patients treated with radiation. TP53 wild-type or mutant human medulloblastoma cell-lines and normal neural stem cells were used to test radioresistance of TP53 mutations and the radiosensitizing effect of WNT activation on tumors and the developing brain. Children with WNT/TP53 mutant medulloblastoma had higher 5-year survival than those with SHH/TP53 mutant tumours (100% and 36.6% ± 8.7%, respectively (p < 0.001)). Introduction of TP53 mutation into medulloblastoma cells induced radioresistance (survival fractions at 2Gy (SF2) of 89% ± 2% vs. 57.4% ± 1.8% (p < 0.01)). In contrast, β-catenin mutation sensitized TP53 mutant cells to radiation (p < 0.05). Lithium, an activator of the WNT pathway, sensitized TP53 mutant medulloblastoma to radiation (SF2 of 43.5% ± 1.5% in lithium treated cells vs. 56.6 ± 3% (p < 0.01)) accompanied by increased number of γH2AX foci. Normal neural stem cells were protected from lithium induced radiation damage (SF2 of 33% ± 8% for lithium treated cells vs. 27% ± 3% for untreated controls (p = 0.05). Poor survival of patients with TP53 mutant medulloblastoma may be related to radiation resistance. Since constitutive activation of the WNT pathway by lithium sensitizes TP53 mutant medulloblastoma cells and protect normal neural stem cells from radiation, this oral drug may represent an attractive novel therapy for high-risk medulloblastomas."],["dc.identifier.doi","10.1186/s40478-014-0174-y"],["dc.identifier.fs","610476"],["dc.identifier.pmid","25539912"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/11459"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58290"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","WNT activation by lithium abrogates TP53 mutation associated radiation resistance in medulloblastoma"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e0121592"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Pietschmann, Sophie"],["dc.contributor.author","von Bueren, Andre Oscar"],["dc.contributor.author","Kerber, Michael Josef"],["dc.contributor.author","Baumert, Brigitta G."],["dc.contributor.author","Kortmann, Rolf Dieter"],["dc.contributor.author","Mueller, Klaus"],["dc.date.accessioned","2018-11-07T09:58:35Z"],["dc.date.available","2018-11-07T09:58:35Z"],["dc.date.issued","2015"],["dc.description.abstract","Purpose To determine the characteristics, treatments and outcomes of patients with glioblastoma multiforme (GBM) or gliosarcoma (GS) and metastases outside of the central nervous system (CNS). Methods PubMed and Web of Science searches for peer-reviewed articles pertaining to GBM/GS patients with metastatic dissemination were conducted using the keywords gliosarcoma, glioblastoma, GBM, metastasis, metastases and metastatic. Additionally, we performed hand search following the references from the selected papers. Cases with metastases to the CNS were excluded and evaluated in a separate study. Results 109 articles published between 1928 and 2013 were eligible. They reported on 150 patients. We observed a remarkable increase in the number of cases per decade over time. Median overall survival from diagnosis of metastasis (OSM+) was 6.0 +/- 0.8 months and median overall survival from initial diagnosis (OSID) 13 +/- 2.4 months. On univariate analyses, gender, age, the histological subtype, the time interval between initial diagnosis and diagnosis of metastasis and pulmonary involvement did not influence OSM+. We did not observe any substantial treatment progress. A comparison of the present cohort with 84 GBM/GS patients with exclusive CNS dissemination suggests that metastases outside the CNS are related to a slightly more favorable outcome. Conclusions The occurrence of extra-CNS metastasis from GBM/GS is associated with a dismal prognosis, however it seems to compare slightly favorable to CNS dissemination. Crucial treatment progress has not been achieved over recent decades. A central registry should be considered to consecutively gain more information about the ideal therapeutic approach."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2015"],["dc.identifier.doi","10.1371/journal.pone.0121592"],["dc.identifier.isi","000352590300027"],["dc.identifier.pmid","25860797"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/11782"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/37392"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Public Library Science"],["dc.relation.issn","1932-6203"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","An Individual Patient Data Meta-Analysis on Characteristics, Treatments and Outcomes of Glioblastoma/Gliosarcoma Patients with Metastases Outside of the Central Nervous System"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e0178351"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Andreiuolo, Felipe"],["dc.contributor.author","Le Teuff, Gwenael"],["dc.contributor.author","Bayar, Mohamed Amine"],["dc.contributor.author","Kilday, John-Paul"],["dc.contributor.author","Pietsch, Torsten"],["dc.contributor.author","von Bueren, Andre Oscar"],["dc.contributor.author","Witt, Hendrik"],["dc.contributor.author","Korshunov, Andrey"],["dc.contributor.author","Modena, Piergiorgio"],["dc.contributor.author","Pfister, Stefan M."],["dc.contributor.author","Pages, Melanie"],["dc.contributor.author","Castel, David"],["dc.contributor.author","Giangaspero, Felice"],["dc.contributor.author","Chimelli, Leila"],["dc.contributor.author","Varlet, Pascale"],["dc.contributor.author","Rutkowski, Stefan"],["dc.contributor.author","Frappaz, Didier"],["dc.contributor.author","Massimino, Maura"],["dc.contributor.author","Grundy, Richard"],["dc.contributor.author","Grill, Jacques"],["dc.date.accessioned","2018-11-07T10:22:41Z"],["dc.date.available","2018-11-07T10:22:41Z"],["dc.date.issued","2017"],["dc.description.abstract","Purpose Despite multimodal therapy, prognosis of pediatric intracranial ependymomas remains poor with a 5-year survival rate below 70% and frequent late deaths. Experimental design This multicentric European study evaluated putative prognostic biomarkers. Tenascin-C (TNC) immunohistochemical expression and copy number status of 1q25 were retained for a pooled analysis of 5 independent cohorts. The prognostic value of TNC and 1q25 on the overall survival (OS) was assessed using a Cox model adjusted to age at diagnosis, tumor location, WHO grade, extent of resection, radiotherapy and stratified by cohort. Stratification on a predictor that did not satisfy the proportional hazards assumption was considered. Model performance was evaluated and an internal-external cross validation was performed. Results Among complete cases with 5-year median follow-up (n = 470; 131 deaths), TNC and 1q25 gain were significantly associated with age at diagnosis and posterior fossa tumor location. 1q25 status added independent prognostic value for death beyond the classical variables with a hazard ratio (HR) = 2.19 95%CI = [1.29; 3.76] (p = 0.004), while TNC prognostic relation was tumor location-dependent with HR = 2.19 95%CI = [1.29; 3.76] (p = 0.004) in posterior fossa and HR = 0.64 [0.28; 1.48] (p = 0.295) in supratentorial (interaction p value = 0.015). The derived prognostic score identified 3 different robust risk groups. The omission of upfront RT was not associated with OS for good and intermediate prognostic groups while the absence of upfront RT was negatively associated with OS in the poor risk group. Conclusion Integrated TNC expression and 1q25 status are useful to better stratify patients and to eventually adapt treatment regimens in pediatric intracranial ependymoma."],["dc.identifier.doi","10.1371/journal.pone.0178351"],["dc.identifier.isi","000403364600009"],["dc.identifier.pmid","28617804"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14555"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42317"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Public Library Science"],["dc.relation.issn","1932-6203"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Integrating Tenascin-C protein expression and 1q25 copy number status in pediatric intracranial ependymoma prognostication: A new model for risk stratification"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Journal of Neuro-Oncology"],["dc.contributor.author","Veldhuijzen van Zanten, Sophie E. M."],["dc.contributor.author","Baugh, Joshua"],["dc.contributor.author","Chaney, Brooklyn"],["dc.contributor.author","De Jongh, Dennis"],["dc.contributor.author","Sanchez Aliaga, Esther"],["dc.contributor.author","Barkhof, Frederik"],["dc.contributor.author","Noltes, Johan"],["dc.contributor.author","De Wolf, Ruben"],["dc.contributor.author","Van Dijk, Jet"],["dc.contributor.author","Cannarozzo, Antonio"],["dc.contributor.author","Damen-Korbijn, Carin M."],["dc.contributor.author","Lieverst, Jan A."],["dc.contributor.author","Colditz, Niclas"],["dc.contributor.author","Hoffmann, Marion"],["dc.contributor.author","Warmuth-Metz, Monika"],["dc.contributor.author","Bison, Brigitte"],["dc.contributor.author","Jones, David T. W."],["dc.contributor.author","Sturm, Dominik"],["dc.contributor.author","Gielen, Gerrit H."],["dc.contributor.author","Jones, Chris"],["dc.contributor.author","Hulleman, Esther"],["dc.contributor.author","Calmon, Raphael"],["dc.contributor.author","Castel, David"],["dc.contributor.author","Varlet, Pascale"],["dc.contributor.author","Giraud, Géraldine"],["dc.contributor.author","Slavc, Irene"],["dc.contributor.author","Van Gool, Stefaan"],["dc.contributor.author","Jacobs, Sandra"],["dc.contributor.author","Jadrijevic-Cvrlje, Filip"],["dc.contributor.author","Sumerauer, David"],["dc.contributor.author","Nysom, Karsten"],["dc.contributor.author","Pentikainen, Virve"],["dc.contributor.author","Kivivuori, Sanna-Maria"],["dc.contributor.author","Leblond, Pierre"],["dc.contributor.author","Entz-Werle, Natasha"],["dc.contributor.author","von Bueren, Andre O."],["dc.contributor.author","Kattamis, Antonis"],["dc.contributor.author","Hargrave, Darren R."],["dc.contributor.author","Hauser, Péter"],["dc.contributor.author","Garami, Miklos"],["dc.contributor.author","Thorarinsdottir, Halldora K."],["dc.contributor.author","Pears, Jane"],["dc.contributor.author","Gandola, Lorenza"],["dc.contributor.author","Rutkauskiene, Giedre"],["dc.contributor.author","Janssens, Geert O."],["dc.contributor.author","Torsvik, Ingrid K."],["dc.contributor.author","Perek-Polnik, Marta"],["dc.contributor.author","Gil-da-Costa, Maria J."],["dc.contributor.author","Zheludkova, Olga"],["dc.contributor.author","Shats, Liudmila"],["dc.contributor.author","Deak, Ladislav"],["dc.contributor.author","Kitanovski, Lidija"],["dc.contributor.author","Cruz, Ofelia"],["dc.contributor.author","Morales La Madrid, Andres"],["dc.contributor.author","Holm, Stefan"],["dc.contributor.author","Gerber, Nicolas"],["dc.contributor.author","Kebudi, Rejin"],["dc.contributor.author","Grundy, Richard"],["dc.contributor.author","Lopez-Aguilar, Enrique"],["dc.contributor.author","Zapata-Tarres, Marta"],["dc.contributor.author","Emmerik, John"],["dc.contributor.author","Hayden, Tim"],["dc.contributor.author","Bailey, Simon"],["dc.contributor.author","Biassoni, Veronica"],["dc.contributor.author","Massimino, Maura"],["dc.contributor.author","Grill, Jacques"],["dc.contributor.author","Vandertop, William P."],["dc.contributor.author","Kaspers, Gertjan J. L."],["dc.contributor.author","Fouladi, Maryam"],["dc.contributor.author","Kramm, Christof M."],["dc.contributor.author","van Vuurden, Dannis G."],["dc.date.accessioned","2019-07-09T11:43:15Z"],["dc.date.available","2019-07-09T11:43:15Z"],["dc.date.issued","2017"],["dc.description.abstract","Diffuse intrinsic pontine glioma (DIPG) is a rare and deadly childhood malignancy. After 40 years of mostly single-center, often non-randomized trials with variable patient inclusions, there has been no improvement in survival. It is therefore time for international collaboration in DIPG research, to provide new hope for children, parents and medical professionals fighting DIPG. In a first step towards collaboration, in 2011, a network of biologists and clinicians working in the field of DIPG was established within the European Society for Paediatric Oncology (SIOPE) Brain Tumour Group: the SIOPE DIPG Network. By bringing together biomedical professionals and parents as patient representatives, several collaborative DIPG-related projects have been realized. With help from experts in the fields of information technology, and legal advisors, an international, web-based comprehensive database was developed, The SIOPE DIPG Registry and Imaging Repository, to centrally collect data of DIPG patients. As for April 2016, clinical data as well as MR-scans of 694 patients have been entered into the SIOPE DIPG Registry/Imaging Repository. The median progression free survival is 6.0 months (95% Confidence Interval (CI) 5.6–6.4 months) and the median overall survival is 11.0 months (95% CI 10.5–11.5 months). At two and five years post-diagnosis, 10 and 2% of patients are alive, respectively. The establishment of the SIOPE DIPG Network and SIOPE DIPG Registry means a paradigm shift towards collaborative research into DIPG. This is seen as an essential first step towards understanding the disease, improving care and (ultimately) cure for children with DIPG."],["dc.identifier.doi","10.1007/s11060-016-2363-y"],["dc.identifier.pmid","28110411"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14362"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58845"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1573-7373"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Development of the SIOPE DIPG network, registry and imaging repository: a collaborative effort to optimize research into a rare and lethal disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","161"],["dc.bibliographiccitation.journal","Radiation Oncology"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Scholtyssek, Felix"],["dc.contributor.author","Zwiener, Isabella"],["dc.contributor.author","Schlamann, Annika"],["dc.contributor.author","Seidel, Clemens"],["dc.contributor.author","Meixensberger, Juergen"],["dc.contributor.author","Bauer, Manfred"],["dc.contributor.author","Hoffmann, Karl-Titus"],["dc.contributor.author","Combs, Stephanie E."],["dc.contributor.author","von Bueren, Andre Oscar"],["dc.contributor.author","Kortmann, Rolf-Dieter"],["dc.contributor.author","Mueller, Klaus"],["dc.date.accessioned","2018-11-07T09:22:30Z"],["dc.date.available","2018-11-07T09:22:30Z"],["dc.date.issued","2013"],["dc.description.abstract","Purposes: First, to evaluate outcome, the benefit of concurrent chemotherapy and prognostic factors in a cohort of sixty-four high-grade glioma patients who underwent a second course of radiation therapy at progression. Second, to validate a new prognostic score for overall survival after reirradiation of progressive gliomas with an independent patient cohort. Patients and methods: All patients underwent fractionated reirradiation with a median physical dose of 36 Gy. Median planned target volume was 110.4 ml. Thirty-six patients received concurrent chemotherapy consisting in 24/36 cases (67%) of carboplatin and etoposide and in 12/36 cases (33%) of temozolomide. We used the Kaplan Meier method, log rank test and proportional hazards regression analysis for statistical assessment. Results: Median overall survival from the start of reirradiation was 7.7 +/- 0.7 months. Overall survival rates at 6 and 12 months were 60 +/- 6% and 24 +/- 6%, respectively. Despite relatively large target volumes we did not observe any major acute toxicity. Concurrent chemotherapy did not appear to improve outcome. In contrast, female gender, young age, WHO grade III histology, favorable Karnofsky performance score and complete resection of the tumor prior to reirradiation were identified as positive prognostic factors for overall survival. We finally validated a recent suggestion for a prognostic score with our independent but small patient cohort. Our preliminary findings suggest that its ability to discriminate between different prognostic groups is limited. Conclusions: Outcome of our patients was comparable to previous studies. Even in case of large target volumes reirradiation seems to be feasible without observing major toxicity. The benefit of concurrent chemotherapy is still elusive. A reassessment of the prognostic score, tested in this study, using a larger patient cohort is needed."],["dc.identifier.doi","10.1186/1748-717X-8-161"],["dc.identifier.isi","000321565200001"],["dc.identifier.pmid","23822643"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/9136"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/29353"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Biomed Central Ltd"],["dc.relation.issn","1748-717X"],["dc.rights","CC BY 2.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.0"],["dc.title","Reirradiation in progressive high-grade gliomas: outcome, role of concurrent chemotherapy, prognostic factors and validation of a new prognostic score with an independent patient cohort"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e94132"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Hoeland, Katrin"],["dc.contributor.author","Boller, Danielle"],["dc.contributor.author","Hagel, Christian"],["dc.contributor.author","Dolski, Silvia"],["dc.contributor.author","Treszl, Andras"],["dc.contributor.author","Pardo, Olivier E."],["dc.contributor.author","Cwiek, Paulina"],["dc.contributor.author","Salm, Fabiana"],["dc.contributor.author","Leni, Zaira"],["dc.contributor.author","Shepherd, Peter R."],["dc.contributor.author","Styp-Rekowska, Beata"],["dc.contributor.author","Djonov, Valentin"],["dc.contributor.author","von Bueren, Andre Oscar"],["dc.contributor.author","Frei, Karl"],["dc.contributor.author","Arcaro, Alexandre"],["dc.date.accessioned","2018-11-07T09:41:19Z"],["dc.date.available","2018-11-07T09:41:19Z"],["dc.date.issued","2014"],["dc.description.abstract","The phosphoinositide 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) pathway is frequently activated in human cancer and plays a crucial role in glioblastoma biology. We were interested in gaining further insight into the potential of targeting PI3K isoforms as a novel anti-tumor approach in glioblastoma. Consistent expression of the PI3K catalytic isoform PI3K p11 alpha was detected in a panel of glioblastoma patient samples. In contrast, PI3K p11 beta expression was only rarely detected in glioblastoma patient samples. The expression of a module comprising the epidermal growth factor receptor (EGFR)/PI3K p110 alpha/phosphorylated ribosomal S6 protein (p-S6) was correlated with shorter patient survival. Inhibition of PI3K p11 alpha activity impaired the anchorage-dependent growth of glioblastoma cells and induced tumor regression in vivo. Inhibition of PI3K p11 alpha or PI3K p110 alpha also led to impaired anchorage-independent growth, a decreased migratory capacity of glioblastoma cells, and reduced the activation of the Akt/mTOR pathway. These effects were selective, because targeting of PI3K p11 delta d did not result in a comparable impairment of glioblastoma tumorigenic properties. Together, our data reveal that drugs targeting PI3K p110a can reduce growth in a subset of glioblastoma tumors characterized by the expression of EGFR/PI3K p110 alpha/p-S6."],["dc.identifier.doi","10.1371/journal.pone.0094132"],["dc.identifier.isi","000334339000080"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/10208"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/33702"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Public Library Science"],["dc.relation.issn","1932-6203"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Targeting Class I-A PI3K Isoforms Selectively Impairs Cell Growth, Survival, and Migration in Glioblastoma"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e101211"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Schlamann, Annika"],["dc.contributor.author","von Bueren, Andre Oscar"],["dc.contributor.author","Hagel, Christian"],["dc.contributor.author","Zwiener, Isabella"],["dc.contributor.author","Seidel, Clemens"],["dc.contributor.author","Kortmann, Rolf-Dieter"],["dc.contributor.author","Mueller, Klaus"],["dc.date.accessioned","2018-11-07T09:37:49Z"],["dc.date.available","2018-11-07T09:37:49Z"],["dc.date.issued","2014"],["dc.description.abstract","Background and Purpose: In 2007, the WHO classification of brain tumors was extended by three new entities of glioneuronal tumors: papillary glioneuronal tumor (PGNT), rosette-forming glioneuronal tumor of the fourth ventricle (RGNT) and glioneuronal tumor with neuropil-like islands (GNTNI). Focusing on clinical characteristics and outcome, the authors performed a comprehensive individual patient data (IPD) meta-analysis of the cases reported in literature until December 2012. Methods: PubMed, Embase and Web of Science were searched for peer-reviewed articles reporting on PGNT, RGNT, and GNTNI using predefined keywords. Results: 95 publications reported on 182 patients (PGNT, 71; GNTNI, 26; RGNT, 85). Median age at diagnosis was 23 years (range 4-75) for PGNT, 27 years (range 6-79) for RGNT, and 40 years (range 2-65) for GNTNI. Ninety-seven percent of PGNT and 69% of GNTNI were located in the supratentorial region, 23% of GNTNI were in the spinal cord, and 80% of RGNT were localized in the posterior fossa. Complete resection was reported in 52 PGNT (73%), 36 RGNT (42%), and 7 GNTNI (27%) patients. Eight PGNT, 3 RGNT, and 12 GNTNI patients were treated with chemo- and/or radiotherapy as the primary postoperative treatment. Follow-up data were available for 132 cases. After a median follow-up time of 1.5 years (range 0.2-25) across all patients, 1.5-year progression-free survival rates were 52 +/- 12% for GNTNI, 86 +/- 5% for PGNT, and 100% for RGNT. The 1.5-year overall-survival were 95 +/- 5%, 98 +/- 2%, and 100%, respectively. Conclusions: The clinical understanding of the three new entities of glioneuronal tumors, PGNT, RGNT and GNTNI, is currently emerging. The present meta-analysis will hopefully contribute to a delineation of their diagnostic, therapeutic, and prognostic profiles. However, the available data do not provide a solid basis to define the optimum treatment approach. Hence, a central register should be established."],["dc.description.sponsorship","German Research Foundation (DFG); Leipzig University"],["dc.identifier.doi","10.1371/journal.pone.0101211"],["dc.identifier.isi","000341253400049"],["dc.identifier.pmid","24991807"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/10485"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/32927"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Public Library Science"],["dc.relation.issn","1932-6203"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","An Individual Patient Data Meta-Analysis on Characteristics and Outcome of Patients with Papillary Glioneuronal Tumor, Rosette Glioneuronal Tumor with Neuropil-Like Islands and Rosette Forming Glioneuronal Tumor of the Fourth Ventricle"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e0148312"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Beyer, Stefanie"],["dc.contributor.author","von Bueren, Andre Oscar"],["dc.contributor.author","Klautke, Gunther"],["dc.contributor.author","Guckenberger, Matthias"],["dc.contributor.author","Kortmann, Rolf-Dieter"],["dc.contributor.author","Pietschmann, Sophie"],["dc.contributor.author","Mueller, Klaus"],["dc.date.accessioned","2018-11-07T10:18:17Z"],["dc.date.available","2018-11-07T10:18:17Z"],["dc.date.issued","2016"],["dc.description.abstract","Our aim was to determine the characteristics, treatments and outcomes of patients with primary spinal glioblastomas (GB) or gliosarcomas (GS) reported in literature until March 2015. PubMed and Web of Science were searched for peer-reviewed articles pertaining to cases of glioblastomas / gliosarcomas with primary spinal origin, using predefined search terms. Furthermore we performed hand searches tracking the references from the selected papers. Eighty-two articles published between 1938 and March 2015 were eligible. They reported on 157 patients. Median age at diagnosis was 22 years. The proportion of patients who received adjuvant chemo-or radiotherapy clearly increased from the time before 1980 until present. Median overall survival from diagnosis was 8.0 +/- 0.9 months. On univariate analysis age influenced overall survival, whereas tumor location, gender and the extent of initial resection did not. Outcomes did not differ between children (< 18 years) and adults. However, the patients who were treated after 1980 achieved longer survival times than the patients treated before. On multivariable analysis only age (< 60 years) and the time period of treatment (>= 1980) were confirmed as positive independent prognostic factors. In conclusion, primary spinal GB / GS mainly affect younger patients and are associated with a dismal prognosis. However, most likely due to the increasing use of adjuvant treatment, modest therapeutic progress has been achieved over recent decades. The characteristics and treatments of primary spinal glioblastomas should be entered into a central registry in order to gain more information about the ideal treatment approach in the future."],["dc.description.sponsorship","German Research Foundation (DFG); University of Leipzig"],["dc.identifier.doi","10.1371/journal.pone.0148312"],["dc.identifier.isi","000370038400029"],["dc.identifier.pmid","26859136"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13132"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/41406"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Public Library Science"],["dc.relation.issn","1932-6203"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","A Systematic Review on the Characteristics, Treatments and Outcomes of the Patients with Primary Spinal Glioblastomas or Gliosarcomas Reported in Literature until March 2015"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]