Kube, Dieter

[["dc.bibliographiccitation.firstpage","1147"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","International Journal of Cancer"],["dc.bibliographiccitation.lastpage","1158"],["dc.bibliographiccitation.volume","140"],["dc.contributor.author","Feist, Maren"],["dc.contributor.author","Kemper, Judith"],["dc.contributor.author","Taruttis, Franziska"],["dc.contributor.author","Rehberg, Thorsten"],["dc.contributor.author","Engelmann, Julia C."],["dc.contributor.author","Gronwald, Wolfram"],["dc.contributor.author","Hummel, Michael"],["dc.contributor.author","Spang, Rainer"],["dc.contributor.author","Kube, Dieter"],["dc.date.accessioned","2018-11-07T10:27:05Z"],["dc.date.available","2018-11-07T10:27:05Z"],["dc.date.issued","2017"],["dc.description.abstract","A network of autocrine and paracrine signals defines B cell homeostasis and is thought to be involved in transformation processes. Investigating interactions of these microenvironmental factors and their relation to proto-oncogenes as c-Myc (MYC) is fundamental to understand the biology of B cell lymphoma. Therefore, B cells with conditional MYC expression were stimulated with CD40L, insulin-like growth factor 1, alpha-IgM, Interleukin-10 (IL10) and CpG alone or in combination. The impact of forty different interventions on cell proliferation was investigated in MYC deprived cells and calculated by linear regression. Combination of CpG and IL10 led to a strong synergistic activation of cell proliferation (S-phase/doubling of total cell number) comparable to cells with high MYC expression. A synergistic up-regulation of CDK4, CDK6 and CCND3 expression by IL10 and CpG treatment was causal for this proliferative effect as shown by qRT-PCR analysis and inhibition of the CDK4/6 complex by PD0332991. Furthermore, treatment of stimulated MYC deprived cells with MLN120b, ACHP, Pyridone 6 or Ruxolitinib showed that IL10/CpG induced proliferation and CDK4 expression were JAK/STAT3 and IKK/NF-jB dependent. This was further supported by STAT3 and p65/RELA knockdown experiments, showing strongest effects on cell proliferation and CDK4 expression after double knockdown. Additionally, chromatin immunoprecipitation revealed a dual binding of STAT3 and p65 to the proximal promotor of CDK4 after IL10/CpG treatment. Therefore, the observed synergism of IL10R and TLR9 signalling was able to induce proliferation in a comparable way as aberrant MYC and might play a role in B cell homeostasis or transformation."],["dc.description.sponsorship","BMBF network eBio \"MMML-MycSys\" [BMBF-FKZ 0316166E, 0316166G, 0316166F]"],["dc.identifier.doi","10.1002/ijc.30444"],["dc.identifier.isi","000393976100017"],["dc.identifier.pmid","27668411"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/43179"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","1097-0215"],["dc.relation.issn","0020-7136"],["dc.title","Synergy of interleukin 10 and toll-like receptor 9 signalling in B cell proliferation: Implications for lymphoma pathogenesis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","1514"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Nature communications"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Feist, Maren"],["dc.contributor.author","Schwarzfischer, Philipp"],["dc.contributor.author","Heinrich, Paul"],["dc.contributor.author","Sun, Xueni"],["dc.contributor.author","Kemper, Judith"],["dc.contributor.author","von Bonin, Frederike"],["dc.contributor.author","Perez-Rubio, Paula"],["dc.contributor.author","Taruttis, Franziska"],["dc.contributor.author","Rehberg, Thorsten"],["dc.contributor.author","Dettmer, Katja"],["dc.contributor.author","Gronwald, Wolfram"],["dc.contributor.author","Reinders, Jörg"],["dc.contributor.author","Engelmann, Julia C."],["dc.contributor.author","Dudek, Jan"],["dc.contributor.author","Klapper, Wolfram"],["dc.contributor.author","Trümper, Lorenz"],["dc.contributor.author","Spang, Rainer"],["dc.contributor.author","Oefner, Peter J."],["dc.contributor.author","Kube, Dieter"],["dc.date.accessioned","2019-07-09T11:45:23Z"],["dc.date.available","2019-07-09T11:45:23Z"],["dc.date.issued","2018"],["dc.description.abstract","Knowledge of stromal factors that have a role in the transcriptional regulation of metabolic pathways aside from c-Myc is fundamental to improvements in lymphoma therapy. Using a MYC-inducible human B-cell line, we observed the cooperative activation of STAT3 and NF-κB by IL10 and CpG stimulation. We show that IL10 + CpG-mediated cell proliferation of MYClow cells depends on glutaminolysis. By 13C- and 15N-tracing of glutamine metabolism and metabolite rescue experiments, we demonstrate that GOT2 provides aspartate and nucleotides to cells with activated or aberrant Jak/STAT and NF-κB signaling. A model of GOT2 transcriptional regulation is proposed, in which the cooperative phosphorylation of STAT3 and direct joint binding of STAT3 and p65/NF-κB to the proximal GOT2 promoter are important. Furthermore, high aberrant GOT2 expression is prognostic in diffuse large B-cell lymphoma underscoring the current findings and importance of stromal factors in lymphoma biology."],["dc.identifier.doi","10.1038/s41467-018-03803-x"],["dc.identifier.pmid","29666362"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15191"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59220"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","2041-1723"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.ddc","610"],["dc.title","Cooperative STAT/NF-κB signaling regulates lymphoma metabolic reprogramming and aberrant GOT2 expression."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","53"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","BioTechniques"],["dc.bibliographiccitation.lastpage","61"],["dc.bibliographiccitation.volume","62"],["dc.contributor.author","Taruttis, Franziska"],["dc.contributor.author","Feist, Maren"],["dc.contributor.author","Schwarzfischer, Phillip"],["dc.contributor.author","Gronwald, Wolfram"],["dc.contributor.author","Kube, Dieter"],["dc.contributor.author","Spang, Rainer"],["dc.contributor.author","Engelmann, Julia C."],["dc.date.accessioned","2018-11-07T10:27:58Z"],["dc.date.available","2018-11-07T10:27:58Z"],["dc.date.issued","2017"],["dc.description.abstract","Gene expression measurements are typically performed on a fixed-weight aliquot of RNA, which assumes that the total number of transcripts per cell stays nearly constant across all conditions. In cases where this assumption does not hold (e.g., when comparing cell types with different cell sizes) the expression data provide a distorted view of cellular events. Assuming constant numbers of total transcripts, increases in expression of some RNAs must be compensated for by decreases in expression of others. Therefore, we propose calibrating gene expression data to an external reference point, the number of cells in the sample, using whole-cell spike-ins. In a systematic dilution experiment, we mixed varying numbers of human cells with fixed numbers of Drosophila melanogaster cells and scaled the expression levels of the human genes relative to those of the Drosophila genes. This approach restored the original gene expression ratios generated by the dilutions. We then used Drosophila whole-cell spike-ins to uncover non-symmetric gene expression changes, in this case much larger numbers of induced than repressed genes, under perturbations of the human cell line P493-6. Drosophila whole-cell spike-ins are an experimentally and computationally easy and low-priced method to derive mRNA fold changes of absolute abundances from RNA sequencing (RNA-Seq) and quantitative real-time PCR (qPCR) data."],["dc.identifier.doi","10.2144/000114514"],["dc.identifier.isi","000393884800003"],["dc.identifier.pmid","28193148"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/43328"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Biotechniques Office"],["dc.relation.issn","1940-9818"],["dc.relation.issn","0736-6205"],["dc.title","External calibration with Drosophila whole-cell spike-ins delivers absolute mRNA fold changes from human RNA-Seq and qPCR data"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","EJC SUPPLEMENTS"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Schrader, Alexandra"],["dc.contributor.author","Bentink, Stefan"],["dc.contributor.author","Spang, Rainer"],["dc.contributor.author","Lenze, Dido"],["dc.contributor.author","Hummel, Michael"],["dc.contributor.author","Kuo, M."],["dc.contributor.author","Murray, P."],["dc.contributor.author","Truemper, Lorenz H."],["dc.contributor.author","Kube, Dieter"],["dc.contributor.author","Vockerodt, Martina"],["dc.date.accessioned","2018-11-07T08:42:32Z"],["dc.date.available","2018-11-07T08:42:32Z"],["dc.date.issued","2010"],["dc.format.extent","107"],["dc.identifier.isi","000288603100400"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/19723"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Pergamon-elsevier Science Ltd"],["dc.publisher.place","Oxford"],["dc.relation.conference","21st Meeting of the European-Association-for-Cancer-Research"],["dc.relation.eventlocation","Oslo, NORWAY"],["dc.relation.issn","1359-6349"],["dc.title","A c-Myc induced gene expression signature in human germinal center B cells predicts subtypes of aggressive non-Hodgkin Lymphoma"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","571"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Molecular Oncology"],["dc.bibliographiccitation.lastpage","589"],["dc.bibliographiccitation.volume","14"],["dc.contributor.author","Arlt, Annekatrin"],["dc.contributor.author","Bonin, Frederike"],["dc.contributor.author","Rehberg, Thorsten"],["dc.contributor.author","Perez‐Rubio, Paula"],["dc.contributor.author","Engelmann, Julia C."],["dc.contributor.author","Limm, Katharina"],["dc.contributor.author","Reinke, Sarah"],["dc.contributor.author","Dullin, Christian"],["dc.contributor.author","Sun, Xueni"],["dc.contributor.author","Specht, Rieke"],["dc.contributor.author","Maulhardt, Markus"],["dc.contributor.author","Linke, Franziska"],["dc.contributor.author","Bunt, Gertrude"],["dc.contributor.author","Klapper, Wolfram"],["dc.contributor.author","Vockerodt, Martina"],["dc.contributor.author","Wilting, Jörg"],["dc.contributor.author","Pukrop, Tobias"],["dc.contributor.author","Dettmer, Katja"],["dc.contributor.author","Gronwald, Wolfram"],["dc.contributor.author","Oefner, Peter J."],["dc.contributor.author","Spang, Rainer"],["dc.contributor.author","Kube, Dieter"],["dc.date.accessioned","2021-04-14T08:27:44Z"],["dc.date.available","2021-04-14T08:27:44Z"],["dc.date.issued","2020"],["dc.description.abstract","Macrophages (Mφ) are abundantly present in the tumor microenvironment and may predict outcome in solid tumors and defined lymphoma subtypes. Mφ heterogeneity, the mechanisms of their recruitment, and their differentiation into lymphoma‐promoting, alternatively activated M2‐like phenotypes are still not fully understood. Therefore, further functional studies are required to understand biological mechanisms associated with human tumor‐associated Mφ (TAM). Here, we show that the global mRNA expression and protein abundance of human Mφ differentiated in Hodgkin lymphoma (HL)‐conditioned medium (CM) differ from those of Mφ educated by conditioned media from diffuse large B‐cell lymphoma (DLBCL) cells or, classically, by macrophage colony‐stimulating factor (M‐CSF). Conditioned media from HL cells support TAM differentiation through upregulation of surface antigens such as CD40, CD163, CD206, and PD‐L1. In particular, RNA and cell surface protein expression of mannose receptor 1 (MRC1)/CD206 significantly exceed the levels induced by classical M‐CSF stimulation in M2‐like Mφ; this is regulated by interleukin 13 to a large extent. Functionally, high CD206 enhances mannose‐dependent endocytosis and uptake of type I collagen. Together with high matrix metalloprotease9 secretion, HL‐TAMs appear to be active modulators of the tumor matrix. Preclinical in ovo models show that co‐cultures of HL cells with monocytes or Mφ support dissemination of lymphoma cells via lymphatic vessels, while tumor size and vessel destruction are decreased in comparison with lymphoma‐only tumors. Immunohistology of human HL tissues reveals a fraction of cases feature large numbers of CD206‐positive cells, with high MRC1 expression being characteristic of HL‐stage IV. In summary, the lymphoma‐TAM interaction contributes to matrix‐remodeling and lymphoma cell dissemination."],["dc.description.abstract","The study highlights the ability of Hodgkin lymphoma cells to attract and to differentiate monocytes into M2‐like Mφ and the role of IL13 in regulating CD206 but also that CD206 contributes to the remodeling of the tumor microenvironment via take up glycoconjugates as well as type‐I collagen and immunosuppression by PD‐L1 upregulation. image"],["dc.description.sponsorship","Stiftung der Georg‐August‐Universität"],["dc.description.sponsorship","Wilhelm‐Sander‐Stiftung"],["dc.description.sponsorship","Deutsche Krebshilfe http://dx.doi.org/10.13039/501100005972"],["dc.description.sponsorship","Bundesministerium für Bildung und Forschung http://dx.doi.org/10.13039/501100002347"],["dc.description.sponsorship","Interreg"],["dc.identifier.doi","10.1002/1878-0261.12616"],["dc.identifier.eissn","1878-0261"],["dc.identifier.issn","1574-7891"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17183"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/82387"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.notes.intern","Merged from goescholar"],["dc.relation.eissn","1878-0261"],["dc.relation.issn","1574-7891"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","High CD206 levels in Hodgkin lymphoma‐educated macrophages are linked to matrix‐remodeling and lymphoma dissemination"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2231"],["dc.bibliographiccitation.issue","16"],["dc.bibliographiccitation.journal","Bioinformatics"],["dc.bibliographiccitation.lastpage","2238"],["dc.bibliographiccitation.volume","27"],["dc.contributor.author","Maneck, Matthias"],["dc.contributor.author","Schrader, Alexandra"],["dc.contributor.author","Kube, Dieter"],["dc.contributor.author","Spang, Rainer"],["dc.date.accessioned","2018-11-07T08:53:14Z"],["dc.date.available","2018-11-07T08:53:14Z"],["dc.date.issued","2011"],["dc.description.abstract","Motivation: In biomedical research transcriptomic, proteomic or metabolomic profiles of patient samples are often combined with genomic profiles from experiments in cell lines or animal models. Integrating experimental data with patient data is still a challenging task due to the lack of tailored statistical tools. Results: Here we introduce guided clustering, a new data integration strategy that combines experimental and clinical high-throughput data. Guided clustering identifies sets of genes that stand out in experimental data while at the same time display coherent expression in clinical data. We report on two potential applications: The integration of clinical microarray data with (i) genome-wide chromatin immunoprecipitation assays and (ii) with cell perturbation assays. Unlike other analysis strategies, guided clustering does not analyze the two datasets sequentially but instead in a single joint analysis. In a simulation study and in several biological applications, guided clustering performs favorably when compared with sequential analysis approaches."],["dc.identifier.doi","10.1093/bioinformatics/btr363"],["dc.identifier.isi","000293620800009"],["dc.identifier.pmid","21685050"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/22358"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","1367-4803"],["dc.title","Genomic data integration using guided clustering"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","47061"],["dc.bibliographiccitation.issue","30"],["dc.bibliographiccitation.journal","Oncotarget"],["dc.bibliographiccitation.lastpage","47081"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Schrader, Alexandra"],["dc.contributor.author","Meyer, Katharina"],["dc.contributor.author","Walther, Neele"],["dc.contributor.author","Stolz, Ailine"],["dc.contributor.author","Feist, Maren"],["dc.contributor.author","Hand, Elisabeth"],["dc.contributor.author","von Bonin, Frederike"],["dc.contributor.author","Evers, Maurits"],["dc.contributor.author","Kohler, Christian W."],["dc.contributor.author","Shirneshan, Katayoon"],["dc.contributor.author","Vockerodt, Martina"],["dc.contributor.author","Klapper, Wolfram"],["dc.contributor.author","Szczepanowski, Monika"],["dc.contributor.author","Murray, Paul G."],["dc.contributor.author","Bastians, Holger"],["dc.contributor.author","Truemper, Lorenz H."],["dc.contributor.author","Spang, Rainer"],["dc.contributor.author","Kube, Dieter"],["dc.date.accessioned","2018-11-07T10:11:28Z"],["dc.date.available","2018-11-07T10:11:28Z"],["dc.date.issued","2016"],["dc.description.abstract","To discover new regulatory pathways in B lymphoma cells, we performed a combined analysis of experimental, clinical and global gene expression data. We identified a specific cluster of genes that was coherently expressed in primary lymphoma samples and suppressed by activation of the B cell receptor (BCR) through aIgM treatment of lymphoma cells in vitro. This gene cluster, which we called BCR. 1, includes numerous cell cycle regulators. A reduced expression of BCR. 1 genes after BCR activation was observed in different cell lines and also in CD10(+) germinal center B cells. We found that BCR activation led to a delayed entry to and progression of mitosis and defects in metaphase. Cytogenetic changes were detected upon long-term aIgM treatment. Furthermore, an inverse correlation of BCR. 1 genes with c-Myc co-regulated genes in distinct groups of lymphoma patients was observed. Finally, we showed that the BCR. 1 index discriminates activated B cell-like and germinal centre B cell-like diffuse large B cell lymphoma supporting the functional relevance of this new regulatory circuit and the power of guided clustering for biomarker discovery."],["dc.identifier.doi","10.18632/oncotarget.9219"],["dc.identifier.isi","000385413000020"],["dc.identifier.pmid","27166259"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14137"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40052"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Impact Journals Llc"],["dc.relation.issn","1949-2553"],["dc.rights","CC BY 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/3.0"],["dc.title","Identification of a new gene regulatory circuit involving B cell receptor activated signaling using a combined analysis of experimental, clinical and global gene expression data"],["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","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"]]

[["dc.bibliographiccitation.firstpage","1105"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Journal of Proteome Research"],["dc.bibliographiccitation.lastpage","+"],["dc.bibliographiccitation.volume","16"],["dc.contributor.author","Schwarzfischer, Philipp"],["dc.contributor.author","Reinders, Joerg"],["dc.contributor.author","Dettmer, Katja"],["dc.contributor.author","Kleo, Karsten"],["dc.contributor.author","Dimitrova, Lora"],["dc.contributor.author","Hummel, Michael"],["dc.contributor.author","Feist, Maren"],["dc.contributor.author","Kube, Dieter"],["dc.contributor.author","Szczepanowski, Monika"],["dc.contributor.author","Klapper, Wolfram"],["dc.contributor.author","Taruttis, Franziska"],["dc.contributor.author","Engelmann, Julia C."],["dc.contributor.author","Spang, Rainer"],["dc.contributor.author","Gronwald, Wolfram"],["dc.contributor.author","Oefner, Peter J."],["dc.date.accessioned","2018-11-07T10:26:44Z"],["dc.date.available","2018-11-07T10:26:44Z"],["dc.date.issued","2017"],["dc.description.abstract","Burkitt's lymphoma (BL) and diffuse large B-cell lymphoma (DLBCL) are pathologically and clinically distinct subtypes of aggressive non-Hodgkin B-cell lymphoma. To learn more about their biology, we employed metabolomic and proteomic methods to study both established cell lines as well as cryopreserved and formalin-fixed paraffin-embedded (FFPE) tissue sections of BL and DLBCL. Strikingly, NMR analyses revealed DLBCL cell lines to produce and secrete significantly (P-adj = 1.72 X 10(-22)) more pyruvic acid than BL cell lines. This finding could be reproduced by targeted GC/MS analyses of cryopreserved tissue sections of BL and DLBCL cases. Enrichment analysis of an overlapping set of N = 2315 proteins, that had been quantified by nanoLC-SWATH-MS in BL and DLBCL cultured cells and cryosections, supported the observed difference in pyruvic acid content, as glycolysis and pyruvate metabolism were downregulated, while one-carbon metabolism was upregulated in BL compared to DLBCL. Furthermore, 92.1% of the overlapping significant proteins showed the same direction of regulation in cryopreserved and FFPE material. Proteome data are available via ProteomeXchange with identifier PXD004936."],["dc.identifier.doi","10.1021/acs.jproteome.6b00164"],["dc.identifier.isi","000395726200001"],["dc.identifier.pmid","28161958"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/43107"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Amer Chemical Soc"],["dc.relation.issn","1535-3907"],["dc.relation.issn","1535-3893"],["dc.title","Comprehensive Metaboproteomics of Burkitt's and Diffuse Large B-Cell Lymphoma Cell Lines and Primary Tumor Tissues Reveals Distinct Differences in Pyruvate Content and Metabolism"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","E348"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","International Journal of Cancer"],["dc.bibliographiccitation.lastpage","E361"],["dc.bibliographiccitation.volume","131"],["dc.contributor.author","Schrader, Alexandra"],["dc.contributor.author","Bentink, Stefan"],["dc.contributor.author","Spang, Rainer"],["dc.contributor.author","Lenze, Dido"],["dc.contributor.author","Hummel, Michael"],["dc.contributor.author","Kuo, Michael"],["dc.contributor.author","Arrand, John R."],["dc.contributor.author","Murray, Paul G."],["dc.contributor.author","Truemper, Lorenz H."],["dc.contributor.author","Kube, Dieter"],["dc.contributor.author","Vockerodt, Martina"],["dc.date.accessioned","2018-11-07T09:07:11Z"],["dc.date.available","2018-11-07T09:07:11Z"],["dc.date.issued","2012"],["dc.description.abstract","Gene expression profiling has recently enabled the reclassification of aggressive non-Hodgkin lymphomas (aNHL) into distinct subgroups. In Burkitt lymphoma (BL) aberrant c-Myc activity results from IG-MYC translocations. However, MYC aberrations are not limited to BLs and then have a negative prognostic impact. In this study, we investigated to which extent aberrant c-Myc activity plays a functional role in other aNHL and whether it is independent from MYC translocations. Based on a combined microarray analysis of human germinal center (GC) B cells transfected with c-Myc and 220 aNHLs cases, we developed a c-Myc index. This index measures the extent to which lymphomas express c-Myc responsive genes. It comprises genes that are affected in a variety of tumors compared to normal tissue. This supports the view that aberrant c-Myc expression in GC B cells triggers a tumor-like expression pattern. As expected, the c-Myc index is very high in molecular Burkitt lymphoma (mBL), but more importantly also high within other aNHL. It constitutes a negative prognostic marker independent of established risk factors and of the presence of a MYC translocation. Our data provide new insights into the role of c-Myc activity in different lymphomas and raises the question of treatment changes for those patients under risk."],["dc.identifier.doi","10.1002/ijc.26423"],["dc.identifier.isi","000305451300003"],["dc.identifier.pmid","21913186"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/25734"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","0020-7136"],["dc.title","High myc activity is an independent negative prognostic factor for diffuse large B cell lymphomas"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]