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Kube, Dieter
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Kube, Dieter
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Kube, Dieter
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Kube, D.
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2010Journal Article [["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"]]Details DOI PMID PMC WOS2007Journal Article [["dc.bibliographiccitation.firstpage","164"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Genes and Immunity"],["dc.bibliographiccitation.lastpage","167"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Kube, Dieter"],["dc.contributor.author","Hua, T-D"],["dc.contributor.author","Kloess, Marita"],["dc.contributor.author","Kulle, Bettina"],["dc.contributor.author","Brockmoeller, Juergen"],["dc.contributor.author","Wojnowski, Leszek"],["dc.contributor.author","Loeffler, Markus"],["dc.contributor.author","Pfreundschuh, Michael"],["dc.contributor.author","Truemper, Lorenz H."],["dc.date.accessioned","2018-11-07T11:04:26Z"],["dc.date.available","2018-11-07T11:04:26Z"],["dc.date.issued","2007"],["dc.description.abstract","The Interleukin 10 (IL-10) gene is highly polymorphic, and the IL-10_(1087AG) (rs1800896) gene variation is the only so far studied intensively in association with certain diseases. Conflicting data have been published about an association of IL-10_(1087AG) gene variation with lower rates of complete remission and lower overall survival (OS) in patients with diffuse large B-cell lymphoma. To further investigate this in malignant lymphoma, we established the IL-10 genotypes in patients from the NHL-B1/B2 studies from the German High-Grade Non-Hodgkin's Lymphoma Study Group. In our study, allele frequencies of lymphoma patients are comparable as in healthy controls. No increase of IL-10_(1087G) alleles was found. In addition we did not find any difference in OS or event-free survival between patients with IL-10_(1087AA) and the other genotypes. Comparable results were obtained for the IL-10 loci at -3538 (A/T), -1354 (A/G), -824 (C/T) and -597 (A/C) (rs1800890, rs1800893, rs1800871 and rs1800872)."],["dc.identifier.doi","10.1038/sj.gene.6364364"],["dc.identifier.isi","000244715500010"],["dc.identifier.pmid","17215862"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/51844"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","1466-4879"],["dc.title","The interleukin-10 gene promoter polymorphism - 1087AG does not correlate with clinical outcome in non-Hodgkin's lymphoma"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS2012Conference Abstract [["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"]]Details WOS2005Conference Abstract [["dc.bibliographiccitation.journal","Annals of Oncology"],["dc.bibliographiccitation.volume","16"],["dc.contributor.author","Kube, Dieter"],["dc.contributor.author","Hua, T."],["dc.contributor.author","Kulle, Bettina"],["dc.contributor.author","Gocht, D."],["dc.contributor.author","Kloess, Marita"],["dc.contributor.author","Brockmoeller, Juergen"],["dc.contributor.author","Wojnowski, Leszek"],["dc.contributor.author","Loeffler, Markus"],["dc.contributor.author","Pfreundschuh, Michael"],["dc.contributor.author","Truemper, Lorenz H."],["dc.date.accessioned","2018-11-07T10:14:54Z"],["dc.date.available","2018-11-07T10:14:54Z"],["dc.date.issued","2005"],["dc.format.extent","77"],["dc.identifier.isi","000233670100135"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40713"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.publisher.place","Oxford"],["dc.relation.conference","9th International Conference on Malignant Lymphoma"],["dc.relation.eventlocation","Lugano, SWITZERLAND"],["dc.relation.issn","0923-7534"],["dc.title","Interleukin-10 gene promoter polymorphisms in aggressive non-Hodgkin lymphoma"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details WOS2012Journal Article [["dc.bibliographiccitation.firstpage","3637"],["dc.bibliographiccitation.issue","13"],["dc.bibliographiccitation.journal","Clinical Cancer Research"],["dc.bibliographiccitation.lastpage","3647"],["dc.bibliographiccitation.volume","18"],["dc.contributor.author","Heemann, Christina"],["dc.contributor.author","Kreuz, Markus"],["dc.contributor.author","Stoller, Irene"],["dc.contributor.author","Schoof, Nils"],["dc.contributor.author","von Bonin, Frederike"],["dc.contributor.author","Ziepert, Marita"],["dc.contributor.author","Loeffler, Markus"],["dc.contributor.author","Jung, Wolfram"],["dc.contributor.author","Pfreundschuh, Michael"],["dc.contributor.author","Truemper, Lorenz H."],["dc.contributor.author","Kube, Dieter"],["dc.date.accessioned","2018-11-07T09:08:22Z"],["dc.date.available","2018-11-07T09:08:22Z"],["dc.date.issued","2012"],["dc.description.abstract","Purpose: Peripheral T-cell non-Hodgkin lymphomas (T-NHL) represent a small but heterogeneous and clinically aggressive subset of NHLs with a poor outcome. Cytokines or their receptors might be associated with the clinical outcome of these lymphomas. Therefore, we tested whether gene variations and serum levels of soluble TNF receptor (TNFR)I (sTNFRI), sTNFRII, interleukin (IL)-10, or sIL-4R are predictive for treatment response in T-NHLs. Experimental Design: Peripheral blood DNA from 117 patients with T-NHL treated in prospective clinical trials was subjected to genotyping analysis. Whenever possible, pretreatment sera were obtained, and circulating levels of sTNFRI, sTNFRII, IL-10, and sIL-4R were determined with a specific capture enzyme-linked immunoassay. Results: Patients characterized by TNFRI-609GG (rs4149570) showed a trend toward better event free survival [EFS; univariate: P = 0.041; multivariate: HR, 1.76; confidence interval (CI), 0.99-3.14 with P = 0.056]. A protective role of IL-10-1087A, -824T, and -597A reported in another study was not confirmed in our cohort. Patients with circulating levels of soluble TNFRII >= 2.16 ng/mL had a 2.07-fold increased relative risk for shorter overall survival (OS; univariate: P = 0.0034; multivariate: HR, 2.07; CI, 0.92-4.70 with P = 0.081) and a 2.49-fold higher risk for shorter EFS (univariate: P = 0.00068; multivariate: HR, 2.49; CI, 1.22-5.08 with P = 0.012). Elevations of circulating levels of sTNFRI, IL-10, and sIL-4R are frequent, but the clinical response in these patients is not significantly different. Conclusions: Our findings suggest a critical role for TNF-TNFR signaling for the clinical outcome of patients with peripheral T-NHLs. Clin Cancer Res; 18(13); 3637-47. (C)2012 AACR."],["dc.identifier.doi","10.1158/1078-0432.CCR-11-3299"],["dc.identifier.isi","000307502600016"],["dc.identifier.pmid","22573350"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/26018"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Assoc Cancer Research"],["dc.relation.issn","1078-0432"],["dc.title","Circulating Levels of TNF Receptor II Are Prognostic for Patients with Peripheral T-cell Non-Hodgkin Lymphoma"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS2014Conference Abstract [["dc.bibliographiccitation.firstpage","407"],["dc.bibliographiccitation.journal","Haematologica"],["dc.bibliographiccitation.lastpage","408"],["dc.bibliographiccitation.volume","99"],["dc.contributor.author","Lopez, C."],["dc.contributor.author","Sungalee, Stephanie"],["dc.contributor.author","Bernhardt, S. H. Stephan H."],["dc.contributor.author","Schlesner, Matthias"],["dc.contributor.author","Murga Penas, Eva M."],["dc.contributor.author","Haake, Andrea"],["dc.contributor.author","Richter, J."],["dc.contributor.author","Ammerpohl, Ole"],["dc.contributor.author","Borkhardt, Arndt"],["dc.contributor.author","Brors, Benedikt"],["dc.contributor.author","Burhardt, B."],["dc.contributor.author","Claviez, Alexander"],["dc.contributor.author","Dreyling, M."],["dc.contributor.author","Ebert, Sandra"],["dc.contributor.author","Eils, J. R."],["dc.contributor.author","Eils, Roland"],["dc.contributor.author","Haas, Siegfried"],["dc.contributor.author","Hansmann, Martin Leo"],["dc.contributor.author","Hezaveh, Kebria"],["dc.contributor.author","Hoell, Jessica I."],["dc.contributor.author","Hoffmann, S."],["dc.contributor.author","Hummel, Michael"],["dc.contributor.author","Karsch, Dennis"],["dc.contributor.author","Klapper, Wolfram"],["dc.contributor.author","Kostezka, U."],["dc.contributor.author","Kreuz, Markus"],["dc.contributor.author","Kube, Dieter"],["dc.contributor.author","Kueppers, Ralf"],["dc.contributor.author","Langenberger, David"],["dc.contributor.author","Lawerenz, Chris"],["dc.contributor.author","Leich, Ellen"],["dc.contributor.author","Lenze, Dido"],["dc.contributor.author","Lichter, Peter"],["dc.contributor.author","Loeffler, Markus"],["dc.contributor.author","Moeller, Peter"],["dc.contributor.author","Radlwimmer, Bernhard"],["dc.contributor.author","Radomski, S."],["dc.contributor.author","Rohde, Manfred"],["dc.contributor.author","Rosenstiel, Philip"],["dc.contributor.author","Rosenwald, Andreas"],["dc.contributor.author","Rosolowski, Maciej"],["dc.contributor.author","Schillhabel, M."],["dc.contributor.author","Schreiber, S."],["dc.contributor.author","Stadler, Peter F."],["dc.contributor.author","Szczepanowski, Monika"],["dc.contributor.author","Truemper, Lorenz H."],["dc.contributor.author","Weniger, Marc A."],["dc.contributor.author","Korbel, Jan O."],["dc.contributor.author","Siebert, Reiner"],["dc.date.accessioned","2018-11-07T09:39:05Z"],["dc.date.available","2018-11-07T09:39:05Z"],["dc.date.issued","2014"],["dc.identifier.isi","000342830902054"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/33203"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Ferrata Storti Foundation"],["dc.publisher.place","Pavia"],["dc.relation.conference","19th Congress of the European-Hematology-Association"],["dc.relation.eventlocation","Milan, ITALY"],["dc.relation.issn","0390-6078"],["dc.title","COMPARISON OF CONVENTIONAL CYTOGENETIC ANALYSIS AND WHOLE GENOME SEQUENCING IN GERMINAL-CENTER DERIVED B-CELL LYMPHOMAS IN THE FRAMEWORK OF 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"]]Details WOS2008Journal Article [["dc.bibliographiccitation.firstpage","3777"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Clinical Cancer Research"],["dc.bibliographiccitation.lastpage","3784"],["dc.bibliographiccitation.volume","14"],["dc.contributor.author","Kube, Dieter"],["dc.contributor.author","Hua, Thanh-Duc"],["dc.contributor.author","von Bonin, Frederike"],["dc.contributor.author","Schoof, Nils"],["dc.contributor.author","Zeynalova, Samira"],["dc.contributor.author","Kloess, Marita"],["dc.contributor.author","Gocht, Daniela"],["dc.contributor.author","Potthoff, Bernd"],["dc.contributor.author","Tzvetkov, Mladen"],["dc.contributor.author","Brockmoeller, Juergen"],["dc.contributor.author","Loeffler, Markus"],["dc.contributor.author","Pfreundschuh, Michael"],["dc.contributor.author","Truemper, Lorenz H."],["dc.date.accessioned","2018-11-07T11:13:57Z"],["dc.date.available","2018-11-07T11:13:57Z"],["dc.date.issued","2008"],["dc.description.abstract","Purpose: Current chemotherapy can achieve high response rates in aggressive non-Hodgkin's lymphoma (NHL), but the factors that influence regression and survival remain unknown. The present exploratory study tested the hypothesis whether interleukin-10 (IL-10) polymorphisms predict clinical outcome, leukocytopenia, or infectivity during therapy. IL-10 was chosen because immune alterations area major risk factor for NHL, and IL-10 is a cytokine involved in inflammatory processes associated with clinical outcome. Experimental Design: Five hundred patients with aggressive NHL treated with CHOP/CHOEP were analyzed for IL-10 gene polymorphisms, including distal loci -7400InDel, -6752AT (rs6676671), and -6208CG (rs10494879) in comparison with proximal loci -3538AT (rs1800890), -1087AG (rs1800896), and -597AC (rs1800872) according to the incidence and outcome of the lymphoma. Results: No differences in allele frequencies or haplotypes were found comparing a cohort of patients with aggressive NHL/diffuse large B-cell lymphoma with a healthy control group. Patients with aggressive NHL characterized by IL-10(-7400DelDel) had shorter overall survival periods compared with the other genotypes (P = 0.004). The 3-year rate is 43.4% for IL-10(-7400DelDel) and 73.4% for IL-10(-7400InIn) and IL-10(-7400InDel) together. A significant increased risk for event-free survival is found for carriers of the genotype IL-10(-6752TT-6208CC-3538AA) (P = 0.047). Multivariate analysis of IL-10(-7400) gene variation in relation to overall survival adjusted to international prognostic index revealed a relative risk of 1.9 for carriers of IL-10(-7400DelDel) (P = 0.037). No associations were found analyzing diffuse large B-cell lymphoma patients separately. Conclusion: Our results indicate that IL-10 gene variations could be associated to the clinical course of aggressive NHL, which points out the importance of host factors and respective genetic elements for treatment response."],["dc.identifier.doi","10.1158/1078-0432.CCR-07-5182"],["dc.identifier.isi","000256779100022"],["dc.identifier.pmid","18559596"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/54018"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Assoc Cancer Research"],["dc.relation.issn","1078-0432"],["dc.title","Effect of interleukin-10 gene polymorphisms on clinical outcome of patients with aggressive non-Hodgkin's lymphoma: An exploratory study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS2012Journal Article [["dc.bibliographiccitation.firstpage","1316"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Nature Genetics"],["dc.bibliographiccitation.lastpage","1320"],["dc.bibliographiccitation.volume","44"],["dc.contributor.author","Richter, Julia"],["dc.contributor.author","Schlesner, Matthias"],["dc.contributor.author","Hoffmann, Steve"],["dc.contributor.author","Kreuz, Markus"],["dc.contributor.author","Leich, Ellen"],["dc.contributor.author","Burkhardt, Birgit"],["dc.contributor.author","Rosolowski, Maciej"],["dc.contributor.author","Ammerpohl, Ole"],["dc.contributor.author","Wagener, Rabea"],["dc.contributor.author","Bernhart, Stephan H."],["dc.contributor.author","Lenze, Dido"],["dc.contributor.author","Szczepanowski, Monika"],["dc.contributor.author","Paulsen, Maren"],["dc.contributor.author","Lipinski, Simone"],["dc.contributor.author","Russell, Robert B."],["dc.contributor.author","Adam-Klages, Sabine"],["dc.contributor.author","Apic, Gordana"],["dc.contributor.author","Claviez, Alexander"],["dc.contributor.author","Hasenclever, Dirk"],["dc.contributor.author","Hovestadt, Volker"],["dc.contributor.author","Hornig, Nadine"],["dc.contributor.author","Korbel, Jan O."],["dc.contributor.author","Kube, Dieter"],["dc.contributor.author","Langenberger, David"],["dc.contributor.author","Lawerenz, Chris"],["dc.contributor.author","Lisfeld, Jasmin"],["dc.contributor.author","Meyer, Katharina"],["dc.contributor.author","Picelli, Simone"],["dc.contributor.author","Pischimarov, Jordan"],["dc.contributor.author","Radlwimmer, Bernhard"],["dc.contributor.author","Rausch, Tobias"],["dc.contributor.author","Rohde, Marius"],["dc.contributor.author","Schilhabel, Markus"],["dc.contributor.author","Scholtysik, Rene"],["dc.contributor.author","Spang, Rainer"],["dc.contributor.author","Trautmann, Heiko"],["dc.contributor.author","Zenz, Thorsten"],["dc.contributor.author","Borkhardt, Arndt"],["dc.contributor.author","Drexler, Hans G."],["dc.contributor.author","Moeller, Peter"],["dc.contributor.author","MacLeod, Roderick A. F."],["dc.contributor.author","Pott, Christiane"],["dc.contributor.author","Schreiber, Stefan"],["dc.contributor.author","Truemper, Lorenz H."],["dc.contributor.author","Loeffler, Markus"],["dc.contributor.author","Stadler, Peter F."],["dc.contributor.author","Lichter, Peter"],["dc.contributor.author","Eils, Roland"],["dc.contributor.author","Kueppers, Ralf"],["dc.contributor.author","Hummel, Michael"],["dc.contributor.author","Klapper, Wolfram"],["dc.contributor.author","Rosenstiel, Philip"],["dc.contributor.author","Rosenwald, Andreas"],["dc.contributor.author","Brors, Benedikt"],["dc.contributor.author","Siebert, Reiner"],["dc.date.accessioned","2018-11-07T09:02:50Z"],["dc.date.available","2018-11-07T09:02:50Z"],["dc.date.issued","2012"],["dc.description.abstract","Burkitt lymphoma is a mature aggressive B-cell lymphoma derived from germinal center B cells(1). Its cytogenetic hallmark is the Burkitt translocation t(8;14)(q24;q32) and its variants, which juxtapose the MYC oncogene with one of the three immunoglobulin loci(2). Consequently, MYC is deregulated, resulting in massive perturbation of gene expression(3). Nevertheless, MYC deregulation alone seems not to be sufficient to drive Burkitt lymphomagenesis. By whole-genome, whole-exome and transcriptome sequencing of four prototypical Burkitt lymphomas with immunoglobulin gene (IG)-MYC translocation, we identified seven recurrently mutated genes. One of these genes, ID3, mapped to a region of focal homozygous loss in Burkitt lymphoma(4). In an extended cohort, 36 of 53 molecularly defined Burkitt lymphomas (68%) carried potentially damaging mutations of ID3. These were strongly enriched at somatic hypermutation motifs. Only 6 of 47 other B-cell lymphomas with the IG-MYC translocation (13%) carried ID3 mutations. These findings suggest that cooperation between ID3 inactivation and IG-MYC translocation is a hallmark of Burkitt lymphomagenesis."],["dc.identifier.doi","10.1038/ng.2469"],["dc.identifier.isi","000311713200008"],["dc.identifier.pmid","23143595"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/24773"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","1061-4036"],["dc.title","Recurrent mutation of the ID3 gene in Burkitt lymphoma identified by integrated genome, exome and transcriptome sequencing"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS