Hoffmann, Marion

[["dc.bibliographiccitation.firstpage","2328"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Cancer Research"],["dc.bibliographiccitation.lastpage","2338"],["dc.bibliographiccitation.volume","70"],["dc.contributor.author","Hoffmann, Marion"],["dc.contributor.author","Schirmer, Markus Anton"],["dc.contributor.author","Tzvetkov, Mladen Vassilev"],["dc.contributor.author","Kreuz, Markus"],["dc.contributor.author","Ziepert, Marita"],["dc.contributor.author","Wojnowski, Leszek"],["dc.contributor.author","Kube, Dieter"],["dc.contributor.author","Pfreundschuh, Michael"],["dc.contributor.author","Truemper, Lorenz H."],["dc.contributor.author","Loeffler, Markus"],["dc.contributor.author","Brockmoeller, Juergen"],["dc.date.accessioned","2018-11-07T08:45:02Z"],["dc.date.available","2018-11-07T08:45:02Z"],["dc.date.issued","2010"],["dc.description.abstract","NAD(P)H oxidase is a major endogenous source of reactive oxygen species (ROS). ROS may not only be involved in carcinogenesis but also in efficacy of chemotherapeutic agents like doxorubicin. By a comprehensive genotyping approach covering 48 genetic polymorphisms (single-nucleotide polymorphisms) in five subunits of phagocytic NAD(P) H oxidase, we asked whether they affect gene expression, enzymatic activity, and outcome of CHO(E) P chemotherapy. A highly consistent effect was observed for the CYBA 640A>G variant. In peripheral blood granulocytes of 125 healthy volunteers, the G allele of 640A>G was associated with lower NAD(P) H oxidase activity (P = 0.006). Moreover, the G allele was associated with lower mRNA and protein expression (both P = 0.02). Of clinical importance, the outcome of patients suffering from non-Hodgkin lymphoma and treated with CHO(E) P regimen was dependent on the CYBA 640A>G polymorphism. In an exploratory study (n = 401), carriers of 640GG had an event-free survival (EFS) risk ratio of 1.95 [95% confidence interval (95% CI), 1.31-2.90; P = 0.001] compared with 640AA. In a confirmatory set (n = 477), the risk ratios were 1.53 (1.04-2.25, P = 0.03). The complete set of 878 patients showed a relative risk of 1.72 (1.30-2.26) and 1.59 (1.14-2.21) for EFS and overall survival, respectively. Further molecular-biological experiments showed lower expression and reduced stability of transcripts with the G allele in lymphoblastoid cell lines. Transfection of allele-specific plasmids into HEK293 cells elicited lower activity for the G allele in a luciferase reporter gene construct. Thus, CYBA 640A>G was shown to be a functional polymorphism with possible consequences for patients receiving CHO(E) P chemotherapy and might have further implications for other ROS-mediated modalities. Cancer Res; 70(6); 2328-38. (C) 2010 AACR."],["dc.identifier.doi","10.1158/0008-5472.CAN-09-2388"],["dc.identifier.isi","000278485900020"],["dc.identifier.pmid","20215507"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/20334"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Assoc Cancer Research"],["dc.relation.issn","0008-5472"],["dc.title","A Functional Polymorphism in the NAD(P)H Oxidase Subunit CYBA Is Related to Gene Expression, Enzyme Activity, and Outcome in Non-Hodgkin Lymphoma"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","JDDG Journal der Deutschen Dermatologischen Gesellschaft"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Haenssle, Holger Andreas"],["dc.contributor.author","Hoffmann, S."],["dc.contributor.author","Buhl, Timo"],["dc.contributor.author","Emmert, Steffen"],["dc.contributor.author","Schoen, Michael Peter"],["dc.contributor.author","Rosenberger, Albert"],["dc.date.accessioned","2018-11-07T09:36:15Z"],["dc.date.available","2018-11-07T09:36:15Z"],["dc.date.issued","2014"],["dc.format.extent","15"],["dc.identifier.isi","000340532500037"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/32571"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.publisher.place","Hoboken"],["dc.relation.issn","1610-0387"],["dc.relation.issn","1610-0379"],["dc.title","Determination of Patient Characteristics in Specific Melanoma Subtypes by means of a Prospective Observational Study"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["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.journal","British Journal of Haematology"],["dc.bibliographiccitation.volume","159"],["dc.contributor.author","Richter, J."],["dc.contributor.author","Schlesner, Matthias"],["dc.contributor.author","Leich, Ellen"],["dc.contributor.author","Burkhardt, Birgit"],["dc.contributor.author","Hoffmann, S."],["dc.contributor.author","Szczepanowski, Monika"],["dc.contributor.author","Kreuz, Markus"],["dc.contributor.author","Lenze, Dido"],["dc.contributor.author","Bernhart, S."],["dc.contributor.author","Rosolowski, Maciej"],["dc.contributor.author","Hoell, Jessica I."],["dc.contributor.author","Lawerenz, Chris"],["dc.contributor.author","Jaeger, Nadine"],["dc.contributor.author","Hutter, Barbara"],["dc.contributor.author","Langerberger, D."],["dc.contributor.author","Ammerpohl, Ole"],["dc.contributor.author","Binder, H."],["dc.contributor.author","Borkhardt, Arndt"],["dc.contributor.author","Brors, Benedikt"],["dc.contributor.author","Claviez, Alexander"],["dc.contributor.author","Pischimarov, Jordan"],["dc.contributor.author","Dreyling, M."],["dc.contributor.author","Eils, Roland"],["dc.contributor.author","Hansmann, M-L"],["dc.contributor.author","Binder, V."],["dc.contributor.author","Hornig, Nadine"],["dc.contributor.author","Klapper, Wolfram"],["dc.contributor.author","Korbel, Jan O."],["dc.contributor.author","Kube, Dieter"],["dc.contributor.author","Kueppers, Ralf"],["dc.contributor.author","Lichter, Peter"],["dc.contributor.author","Loeffler, Markus"],["dc.contributor.author","Moeller, Peter"],["dc.contributor.author","Pott, C."],["dc.contributor.author","Rosenwald, Andreas"],["dc.contributor.author","Schreiber, Sefan"],["dc.contributor.author","Schilhabel, Markus"],["dc.contributor.author","Scholtysik, Rene"],["dc.contributor.author","Stadler, Peter F."],["dc.contributor.author","Trautmann, Heiko"],["dc.contributor.author","Wagener, R."],["dc.contributor.author","Zenz, Thorsten"],["dc.contributor.author","Truemper, Lorenz H."],["dc.contributor.author","Rosenstiel, Philip"],["dc.contributor.author","Hummel, Michael"],["dc.contributor.author","Siebert, Reiner"],["dc.date.accessioned","2018-11-07T09:03:43Z"],["dc.date.available","2018-11-07T09:03:43Z"],["dc.date.issued","2012"],["dc.format.extent","7"],["dc.identifier.isi","000312889800013"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/24954"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.publisher.place","Hoboken"],["dc.relation.conference","4th International Symposium on Childhood, Adolescent and Young Adult Non-Hodgkins Lymphoma"],["dc.relation.eventlocation","New York, NY"],["dc.relation.issn","0007-1048"],["dc.title","Sequencing of pediatric Burkitt lymphoma within the ICGC MMML-Seq project"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["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.firstpage","925"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","JDDG Journal der Deutschen Dermatologischen Gesellschaft"],["dc.bibliographiccitation.lastpage","926"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Hoffmann, S."],["dc.contributor.author","Buhl, Timo"],["dc.contributor.author","Holzkamp, R."],["dc.contributor.author","Samhaber, Kinga T."],["dc.contributor.author","Hellriegel, Simin"],["dc.contributor.author","Jantke, M."],["dc.contributor.author","Schoen, Michael Peter"],["dc.contributor.author","Haenssle, Holger Andreas"],["dc.date.accessioned","2018-11-07T09:20:49Z"],["dc.date.available","2018-11-07T09:20:49Z"],["dc.date.issued","2013"],["dc.identifier.isi","000323202300078"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/28964"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.publisher.place","Hoboken"],["dc.relation.issn","1610-0379"],["dc.title","Results of a prospective Study comprising Interviews and clinical Examination: Multiple atypical Naevi allow for a significantly improved early Diagnosis of Melanoma"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","177"],["dc.bibliographiccitation.journal","Radiation Oncology"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Mueller, Klaus"],["dc.contributor.author","Scheithauer, Heike"],["dc.contributor.author","Pietschmann, Sophie"],["dc.contributor.author","Hoffmann, Marion"],["dc.contributor.author","Roessler, Jochen"],["dc.contributor.author","Graf, Norbert"],["dc.contributor.author","Baumert, Brigitta G."],["dc.contributor.author","Christiansen, Hans"],["dc.contributor.author","Kortmann, Rolf-Dieter"],["dc.contributor.author","Kramm, Christof M."],["dc.contributor.author","von Bueren, Andre Oscar"],["dc.date.accessioned","2018-11-07T09:36:38Z"],["dc.date.available","2018-11-07T09:36:38Z"],["dc.date.issued","2014"],["dc.description.abstract","Background and purpose: The aim of the present analysis was to assess the feasibility, toxicity, and the tumor control of reirradiation as a salvage treatment for progressive pediatric non-pontine high-grade gliomas (HGG). Patients and methods: The database of the Reference Center for Radiation Oncology of the German HIT (HIT = German acronym for brain tumor) treatment network for childhood brain tumors was screened for children who were reirradiated for progressive non-pontine HGG. Results: We identified eight patients (WHO grade III: n = 5; WHO grade IV: n = 3) who underwent reirradiation between April 2006 and July 2012. Median age was 13.5 years at primary diagnosis and 14.8 years at first progression. All patients initially underwent surgery (incomplete resection, n = 7; biopsy, n = 1) followed by radiochemotherapy. Relapses occurred inside (n = 2), at the margin (n = 4), and outside of the preirradiated area (n = 2). In all patients, reirradiation was tolerated well without significant acute toxicity. Temporary clinical improvement and tumor regression on magnetic resonance imaging (MRI) following reirradiation was reported (n = 3). However, all patients finally died by disease progression. Median survival time was 26.2 months from initial diagnosis and 11.4 months after first progression. Median time interval between initial radiotherapy and first reirradiation was 9.0 months. In six patients, all macroscopic tumor deposits were reirradiated. In these patients, median progression-free (overall) survival from the start of reirradiation was 2.4 (4.6) months. Conclusion: Our analysis, although based on a limited patient number, suggests that reirradiation of progressive non-pontine HGG is feasible in children. Benefit in terms of quality of life and/or survival needs to be assessed in a prospective and ideally in a randomized manner."],["dc.identifier.doi","10.1186/1748-717X-9-177"],["dc.identifier.isi","000341198300001"],["dc.identifier.pmid","25112658"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/32662"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Biomed Central Ltd"],["dc.relation.issn","1748-717X"],["dc.title","Reirradiation as part of a salvage treatment approach for progressive non-pontine pediatric high-grade gliomas: preliminary experiences from the German HIT-HGG study group"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Neuro-Oncology"],["dc.bibliographiccitation.volume","18"],["dc.contributor.author","Friedrich, Carsten"],["dc.contributor.author","Kuehn, Alexander"],["dc.contributor.author","Zimmermann, Martin"],["dc.contributor.author","Hoffmann, Marion"],["dc.contributor.author","Kuehnle, Ingrid"],["dc.contributor.author","Nowak, Johannes"],["dc.contributor.author","Warmuth-Metz, Monika"],["dc.contributor.author","Pietsch, Torsten"],["dc.contributor.author","Schrappe, Martin"],["dc.contributor.author","Escherich, Gabriele"],["dc.contributor.author","Burkhardt, Birgit"],["dc.contributor.author","Kortmann, Rolf-Dieter"],["dc.contributor.author","von Bueren, Andre Oscar"],["dc.contributor.author","Kramm, Christof M."],["dc.date.accessioned","2018-11-07T10:13:06Z"],["dc.date.available","2018-11-07T10:13:06Z"],["dc.date.issued","2016"],["dc.format.extent","55"],["dc.identifier.isi","000379749000210"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40369"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press Inc"],["dc.publisher.place","Cary"],["dc.relation.conference","17th International Symposium on Pediatric Neuro-Oncology (ISPNO)"],["dc.relation.eventlocation","Liverpool, ENGLAND"],["dc.relation.issn","1523-5866"],["dc.relation.issn","1522-8517"],["dc.title","HIGH-GRADE GLIOMA ARISING IN SURVIVORS OF PEDIATRIC ACUTE LYMPHOBLASTIC MALIGNANCIES: A COOPERATIVE ANALYSIS OF THE GERMAN HIT-HGG/-GBM AND ALL-BFM/COALL STUDIES"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Clinical Neuroradiology"],["dc.contributor.author","Hohm, Annika"],["dc.contributor.author","Karremann, Michael"],["dc.contributor.author","Gielen, Gerrit H."],["dc.contributor.author","Pietsch, Torsten"],["dc.contributor.author","Warmuth-Metz, Monika"],["dc.contributor.author","Vandergrift, Lindsey A."],["dc.contributor.author","Bison, Brigitte"],["dc.contributor.author","Stock, Annika"],["dc.contributor.author","Hoffmann, Marion"],["dc.contributor.author","Pham, Mirko"],["dc.contributor.author","Nowak, Johannes"],["dc.date.accessioned","2022-01-11T14:05:23Z"],["dc.date.available","2022-01-11T14:05:23Z"],["dc.date.issued","2021"],["dc.description.abstract","Abstract Purpose Recent research identified histone H3 K27M mutations to be associated with a dismal prognosis in pediatric diffuse midline glioma (pDMG); however, data on detailed MRI characteristics with respect to H3 K27 mutation status and molecular subgroups (H3.1 and H3.3 K27M mutations) are limited. Methods Standardized magnetic resonance imaging (MRI) parameters and epidemiologic data of 68 pDMG patients (age <18 years) were retrospectively reviewed and compared in a) H3 K27M mutant versus H3 K27 wildtype (WT) tumors and b) H3.1 versus H3.3 K27M mutant tumors. Results Intracranial gliomas ( n  = 58) showed heterogeneous phenotypes with isointense to hyperintense signal in T2-weighted images and frequent contrast enhancement. Hemorrhage and necrosis may be present. Comparing H3 K27M mutant to WT tumors, there were significant differences in the following parameters: i) tumor localization ( p  = 0.001), ii) T2 signal intensity ( p  = 0.021), and iii) T1 signal homogeneity ( p  = 0.02). No significant imaging differences were found in any parameter between H3.1 and H3.3 K27M mutant tumors; however, H3.1 mutant tumors occurred at a younger age ( p  = 0.004). Considering spinal gliomas ( n  = 10) there were no significant imaging differences between the analyzed molecular groups. Conclusion With this study, we are the first to provide detailed MR imaging data on H3 K27M mutant pDMG with respect to molecular subgroup status in a large patient cohort. Our findings may support diagnosis and future targeted therapeutic trials of pDMG within the framework of the radiogenomics concept."],["dc.description.abstract","Abstract Purpose Recent research identified histone H3 K27M mutations to be associated with a dismal prognosis in pediatric diffuse midline glioma (pDMG); however, data on detailed MRI characteristics with respect to H3 K27 mutation status and molecular subgroups (H3.1 and H3.3 K27M mutations) are limited. Methods Standardized magnetic resonance imaging (MRI) parameters and epidemiologic data of 68 pDMG patients (age <18 years) were retrospectively reviewed and compared in a) H3 K27M mutant versus H3 K27 wildtype (WT) tumors and b) H3.1 versus H3.3 K27M mutant tumors. Results Intracranial gliomas ( n  = 58) showed heterogeneous phenotypes with isointense to hyperintense signal in T2-weighted images and frequent contrast enhancement. Hemorrhage and necrosis may be present. Comparing H3 K27M mutant to WT tumors, there were significant differences in the following parameters: i) tumor localization ( p  = 0.001), ii) T2 signal intensity ( p  = 0.021), and iii) T1 signal homogeneity ( p  = 0.02). No significant imaging differences were found in any parameter between H3.1 and H3.3 K27M mutant tumors; however, H3.1 mutant tumors occurred at a younger age ( p  = 0.004). Considering spinal gliomas ( n  = 10) there were no significant imaging differences between the analyzed molecular groups. Conclusion With this study, we are the first to provide detailed MR imaging data on H3 K27M mutant pDMG with respect to molecular subgroup status in a large patient cohort. Our findings may support diagnosis and future targeted therapeutic trials of pDMG within the framework of the radiogenomics concept."],["dc.identifier.doi","10.1007/s00062-021-01120-3"],["dc.identifier.pii","1120"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/97653"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-507"],["dc.relation.eissn","1869-1447"],["dc.relation.issn","1869-1439"],["dc.title","Magnetic Resonance Imaging Characteristics of Molecular Subgroups in Pediatric H3 K27M Mutant Diffuse Midline Glioma"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","249"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Pharmacogenetics and Genomics"],["dc.bibliographiccitation.lastpage","259"],["dc.bibliographiccitation.volume","19"],["dc.contributor.author","Schirmer, Markus Anton"],["dc.contributor.author","Hoffmann, Arne O."],["dc.contributor.author","Campean, Radu"],["dc.contributor.author","Janke, Joerg H."],["dc.contributor.author","Zidek, Laura M."],["dc.contributor.author","Hoffmann, Marion"],["dc.contributor.author","Kruse, Moritz"],["dc.contributor.author","Sehrt, Daniel"],["dc.contributor.author","Tzvetkov, Mladen Vassilev"],["dc.contributor.author","Rave-Fraenk, Margret"],["dc.contributor.author","Brockmoeller, Juergen"],["dc.date.accessioned","2018-11-07T08:31:23Z"],["dc.date.available","2018-11-07T08:31:23Z"],["dc.date.issued","2009"],["dc.description.abstract","Objectives The transforming growth factor-beta (TGFB) pathway has substantial impact on cellular functions, cell proliferation, and apoptosis. We used bioinformatics, gene expression, and cell biological assays to evaluate the functionality of frequent Inherited germline polymorphisms in the TGFB receptor 1 (TGFBR1). Methods In an exploratory (n=55) and confirmatory (n=106) study, we analyzed the TGFB1 pathway after incubation with TGF beta 1 ligand and after exposure to X-rays in peripheral blood human mononuclear cells. Expression of TGFB pathway genes was assessed by real-time PCR, and cellular viability was analyzed by flow cytometry. A total of six polymorphisms including the deletion variant ( 6A) were identified to tag currently known common genetic variations in TGFBR1 and were analyzed in relation to the phenotypes. Results In accordance with a negative feedback mechanism, incubations with the ligand TGF beta 1 was followed by up-regulation of the intracellular SMAD7 and down-regulation of the SMAD3 mRNA molecules. The TGFBR1 6A deletion variant attenuated the suppression of SMAD3 in response to TGF beta 1 (P=0.02, in both studies). Moreover, cells harboring 6A were more sensitive toward cytotoxic effects of irradiation (P=0.001 after adjustment for age and sex). Cells were particularly prone toward radiation toxicity when carrying, in addition to 6A, the variant allele of rs11568785, which exhibits a strong genetic selection signature. Conclusion The 6A deletion and the linked rs11568785 polymorphisms seem to attenuate TGFB signaling. This should be considered not only for clinical-epidemiological studies on cancer susceptibility but may also be relevant for side effects from drugs or radiotherapy. Pharmacogenetics and Genomics 19:249-259 (C) 2009 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins."],["dc.description.sponsorship","DFG [GRK1034, KFO179]"],["dc.identifier.doi","10.1097/FPC.0b013e32831cb5a7"],["dc.identifier.isi","000264943900001"],["dc.identifier.pmid","19214138"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/17109"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","1744-6872"],["dc.title","Bioinformatic and functional analysis of TGFBR1 polymorphisms"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]