Chapuy, Björn

[["dc.bibliographiccitation.firstpage","1361"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Haematologica"],["dc.bibliographiccitation.lastpage","1368"],["dc.bibliographiccitation.volume","105"],["dc.contributor.author","Chen, Linfeng"],["dc.contributor.author","Ouyang, Jing"],["dc.contributor.author","Wienand, Kirsty"],["dc.contributor.author","Bojarczuk, Kamil"],["dc.contributor.author","Hao, Yansheng"],["dc.contributor.author","Chapuy, Björn"],["dc.contributor.author","Neuberg, Donna"],["dc.contributor.author","Juszczynski, Przemyslaw"],["dc.contributor.author","Lawton, Lee N."],["dc.contributor.author","Rodig, Scott J."],["dc.contributor.author","Monti, Stefano"],["dc.contributor.author","Shipp, Margaret A."],["dc.date.accessioned","2020-12-10T18:44:18Z"],["dc.date.available","2020-12-10T18:44:18Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.3324/haematol.2019.216218"],["dc.identifier.eissn","1592-8721"],["dc.identifier.issn","0390-6078"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/78403"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.relation.orgunit","Klinik für Hämatologie und Medizinische Onkologie"],["dc.title","CXCR4 upregulation is an indicator of sensitivity to B-cell receptor/PI3K blockade and a potential resistance mechanism in B-cell receptor-dependent diffuse large B-cell lymphomas"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","23"],["dc.bibliographiccitation.journal","Blood"],["dc.bibliographiccitation.volume","126"],["dc.contributor.author","Chapuy, Björn"],["dc.contributor.author","Dunford, Andrew J."],["dc.contributor.author","Stewart, Chip"],["dc.contributor.author","Kamburov, Atanas"],["dc.contributor.author","Kim, Jaegil"],["dc.contributor.author","Roemer, Margaretha G. M."],["dc.contributor.author","Ziepert, Marita"],["dc.contributor.author","Li, Amy Jiayue"],["dc.contributor.author","Lawrence, Mike"],["dc.contributor.author","Hess, Julian"],["dc.contributor.author","Rosenburg, Mara"],["dc.contributor.author","Taylor-Weiner, Amaro N."],["dc.contributor.author","Redd, Robert A."],["dc.contributor.author","Horn, Heike"],["dc.contributor.author","Novak, Anne"],["dc.contributor.author","Cerhan, James R."],["dc.contributor.author","Haberman, Thomas M."],["dc.contributor.author","Feldman, Andrew L."],["dc.contributor.author","Link, Brian K."],["dc.contributor.author","Golub, Todd R."],["dc.contributor.author","Neuberg, Donna S."],["dc.contributor.author","Ott, German"],["dc.contributor.author","Siebert, Reiner"],["dc.contributor.author","Rosenwald, Andreas"],["dc.contributor.author","Wulf, Gerald G."],["dc.contributor.author","Monti, Stefano"],["dc.contributor.author","Rodig, Scott J."],["dc.contributor.author","Loeffler, Markus"],["dc.contributor.author","Pfreundschuh, Michael"],["dc.contributor.author","Truemper, Lorenz H."],["dc.contributor.author","Getz, Gad"],["dc.contributor.author","Shipp, Margaret A."],["dc.date.accessioned","2018-11-07T09:47:44Z"],["dc.date.available","2018-11-07T09:47:44Z"],["dc.date.issued","2015"],["dc.identifier.isi","000368021800179"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/35166"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Soc Hematology"],["dc.publisher.place","Washington"],["dc.relation.conference","57th Annual Meeting of the American-Society-of-Hematology"],["dc.relation.eventlocation","Orlando, FL"],["dc.relation.issn","1528-0020"],["dc.relation.issn","0006-4971"],["dc.title","Comprehensive Analyses of Genetic Features Identify Coordinate Signatures in Diffuse Large B-Cell Lymphoma"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2369"],["dc.bibliographiccitation.issue","26"],["dc.bibliographiccitation.journal","Blood"],["dc.bibliographiccitation.lastpage","2382"],["dc.bibliographiccitation.volume","134"],["dc.contributor.author","Chapuy, Björn"],["dc.contributor.author","Stewart, Chip"],["dc.contributor.author","Dunford, Andrew J."],["dc.contributor.author","Kim, Jaegil"],["dc.contributor.author","Wienand, Kirsty"],["dc.contributor.author","Kamburov, Atanas"],["dc.contributor.author","Griffin, Gabriel K."],["dc.contributor.author","Chen, Pei-Hsuan"],["dc.contributor.author","Lako, Ana"],["dc.contributor.author","Redd, Robert A."],["dc.contributor.author","Cote, Claire M."],["dc.contributor.author","Ducar, Matthew D."],["dc.contributor.author","Thorner, Aaron R."],["dc.contributor.author","Rodig, Scott J."],["dc.contributor.author","Getz, Gad"],["dc.contributor.author","Shipp, Margaret A."],["dc.date.accessioned","2020-04-03T14:46:27Z"],["dc.date.available","2020-04-03T14:46:27Z"],["dc.date.issued","2019-12-26"],["dc.description.abstract","Primary mediastinal large B-cell lymphomas (PMBLs) are aggressive tumors that typically present as large mediastinal masses in young women. PMBLs share clinical, transcriptional, and molecular features with classical Hodgkin lymphoma (cHL), including constitutive activation of nuclear factor κB (NF-κB), JAK/STAT signaling, and programmed cell death protein 1 (PD-1)-mediated immune evasion. The demonstrated efficacy of PD-1 blockade in relapsed/refractory PMBLs led to recent approval by the US Food and Drug Administration and underscored the importance of characterizing targetable genetic vulnerabilities in this disease. Here, we report a comprehensive analysis of recurrent genetic alterations -somatic mutations, somatic copy number alterations, and structural variants-in a cohort of 37 newly diagnosed PMBLs. We identified a median of 9 genetic drivers per PMBL, including known and newly identified components of the JAK/STAT and NF-κB signaling pathways and frequent B2M alterations that limit major histocompatibility complex class I expression, as in cHL. PMBL also exhibited frequent, newly identified driver mutations in ZNF217 and an additional epigenetic modifier, EZH2. The majority of these alterations were clonal, which supports their role as early drivers. In PMBL, we identified several previously uncharacterized molecular features that may increase sensitivity to PD-1 blockade, including high tumor mutational burden, microsatellite instability, and an apolipoprotein B mRNA editing catalytic polypeptide-like (APOBEC) mutational signature. The shared genetic features between PMBL and cHL provide a framework for analyzing the mechanism of action of PD-1 blockade in these related lymphoid malignancies."],["dc.identifier.doi","10.1182/blood.2019002067"],["dc.identifier.pmid","31697821"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/63691"],["dc.language.iso","en"],["dc.relation.eissn","1528-0020"],["dc.relation.issn","0006-4971"],["dc.relation.issn","1528-0020"],["dc.relation.orgunit","Klinik für Hämatologie und Medizinische Onkologie"],["dc.title","Genomic analyses of PMBL reveal new drivers and mechanisms of sensitivity to PD-1 blockade"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","679"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Nature Medicine"],["dc.bibliographiccitation.lastpage","690"],["dc.bibliographiccitation.volume","24"],["dc.contributor.author","Chapuy, Björn"],["dc.contributor.author","Stewart, Chip"],["dc.contributor.author","Dunford, Andrew J."],["dc.contributor.author","Kim, Jaegil"],["dc.contributor.author","Kamburov, Atanas"],["dc.contributor.author","Redd, Robert A."],["dc.contributor.author","Lawrence, Mike S."],["dc.contributor.author","Roemer, Margaretha G. M."],["dc.contributor.author","Li, Amy J."],["dc.contributor.author","Ziepert, Marita"],["dc.contributor.author","Staiger, Annette M."],["dc.contributor.author","Wala, Jeremiah A."],["dc.contributor.author","Ducar, Matthew D."],["dc.contributor.author","Leshchiner, Ignaty"],["dc.contributor.author","Rheinbay, Ester"],["dc.contributor.author","Taylor-Weiner, Amaro"],["dc.contributor.author","Coughlin, Caroline A."],["dc.contributor.author","Hess, Julian M."],["dc.contributor.author","Pedamallu, Chandra S."],["dc.contributor.author","Livitz, Dimitri"],["dc.contributor.author","Rosebrock, Daniel"],["dc.contributor.author","Rosenberg, Mara"],["dc.contributor.author","Tracy, Adam A."],["dc.contributor.author","Horn, Heike"],["dc.contributor.author","van Hummelen, Paul"],["dc.contributor.author","Feldman, Andrew L."],["dc.contributor.author","Link, Brian K."],["dc.contributor.author","Novak, Anne J."],["dc.contributor.author","Cerhan, James R."],["dc.contributor.author","Habermann, Thomas M."],["dc.contributor.author","Siebert, Reiner"],["dc.contributor.author","Rosenwald, Andreas"],["dc.contributor.author","Thorner, Aaron R."],["dc.contributor.author","Meyerson, Matthew L."],["dc.contributor.author","Golub, Todd R."],["dc.contributor.author","Beroukhim, Rameen"],["dc.contributor.author","Wulf, Gerald G."],["dc.contributor.author","Ott, German"],["dc.contributor.author","Rodig, Scott J."],["dc.contributor.author","Monti, Stefano"],["dc.contributor.author","Neuberg, Donna S."],["dc.contributor.author","Loeffler, Markus"],["dc.contributor.author","Pfreundschuh, Michael"],["dc.contributor.author","Trümper, Lorenz"],["dc.contributor.author","Getz, Gad"],["dc.contributor.author","Shipp, Margaret A."],["dc.date.accessioned","2020-12-10T18:10:04Z"],["dc.date.available","2020-12-10T18:10:04Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1038/s41591-018-0016-8"],["dc.identifier.eissn","1546-170X"],["dc.identifier.issn","1078-8956"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/73839"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Molecular subtypes of diffuse large B cell lymphoma are associated with distinct pathogenic mechanisms and outcomes"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2203"],["dc.bibliographiccitation.issue","18"],["dc.bibliographiccitation.journal","Blood"],["dc.bibliographiccitation.lastpage","2213"],["dc.bibliographiccitation.volume","127"],["dc.contributor.author","Chapuy, Björn"],["dc.contributor.author","Cheng, Hongwei"],["dc.contributor.author","Watahiki, Akira"],["dc.contributor.author","Ducar, Matthew D."],["dc.contributor.author","Tan, Yuxiang"],["dc.contributor.author","Chen, Linfeng"],["dc.contributor.author","Roemer, Margaretha G. M."],["dc.contributor.author","Ouyang, Jing"],["dc.contributor.author","Christie, Amanda L."],["dc.contributor.author","Zhang, L."],["dc.contributor.author","Gusenleitner, Daniel"],["dc.contributor.author","Abo, Ryan P."],["dc.contributor.author","Farinha, Pedro"],["dc.contributor.author","von Bonin, Frederike"],["dc.contributor.author","Thorner, Aaron R."],["dc.contributor.author","Sun, Heather H."],["dc.contributor.author","Gascoyne, Randy D."],["dc.contributor.author","Pinkus, Geraldine S."],["dc.contributor.author","van Hummelen, Paul"],["dc.contributor.author","Wulf, Gerald G."],["dc.contributor.author","Aster, Jon C."],["dc.contributor.author","Weinstock, David M."],["dc.contributor.author","Monti, Stefano"],["dc.contributor.author","Rodig, Scott J."],["dc.contributor.author","Wang, Y."],["dc.contributor.author","Shipp, Margaret A."],["dc.date.accessioned","2018-11-07T10:14:25Z"],["dc.date.available","2018-11-07T10:14:25Z"],["dc.date.issued","2016"],["dc.description.abstract","Diffuse large B-cell lymphoma (DLBCL) is a heterogeneous disease defined by transcriptional classifications, specific signaling and survival pathways, and multiple low-frequency genetic alterations. Preclinical model systems that capture the genetic and functional heterogeneity of DLBCL are urgently needed. Here, we generated and characterized a panel of large B-cell lymphoma (LBCL) patient-derived xenograft (PDX) models, including 8 that reflect the immunophenotypic, transcriptional, genetic, and functional heterogeneity of primary DLBCL and 1 that is a plasmablastic lymphoma. All LBCL PDX models were subjected to whole-transcriptome sequencing to classify cell of origin and consensus clustering classification (CCC) subtypes. Mutations and chromosomal re-arrangements were evaluated by whole-exome sequencing with an extended bait set. Six of the 8 DLBCL models were activated B-cell (ABC)-type tumors that exhibited ABC-associated mutations such as MYD88, CD79B, CARD11, and PIM1. The remaining 2 DLBCL models were germinal B-cell type, with characteristic alterations of GNA13, CREBBP, and EZH2, and chromosomal translocations involving IgH and either BCL2 or MYC. Only 25% of the DLBCL PDX models harbored inactivating TP53 mutations, whereas 75% exhibited copy number alterations of TP53 or its upstream modifier, CDKN2A, consistent with the reported incidence and type of p53 pathway alterations in primary DLBCL. By CCC criteria, 6 of 8 DLBCL PDX models were B-cell receptor (BCR)-type tumors that exhibited selective surface immunoglobulin expression and sensitivity to entospletinib, a recently developed spleen tyrosine kinase inhibitor. In summary, we have established and characterized faithful PDX models of DLBCL and demonstrated their usefulness in functional analyses of proximal BCR pathway inhibition."],["dc.identifier.doi","10.1182/blood-2015-09-672352"],["dc.identifier.isi","000378333100009"],["dc.identifier.pmid","26773040"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40612"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation.issn","1528-0020"],["dc.relation.issn","0006-4971"],["dc.title","Diffuse large B-cell lymphoma patient-derived xenograft models capture the molecular and biological heterogeneity of the disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","39"],["dc.bibliographiccitation.issue","Supplement 1"],["dc.bibliographiccitation.journal","Blood"],["dc.bibliographiccitation.lastpage","39"],["dc.bibliographiccitation.volume","132"],["dc.contributor.author","Bojarczuk, Kamil"],["dc.contributor.author","Wienand, Kirsty"],["dc.contributor.author","Ryan, Jeremy A."],["dc.contributor.author","Chen, Linfeng"],["dc.contributor.author","Villalobos-Ortiz, Mariana"],["dc.contributor.author","Mandato, Elisa"],["dc.contributor.author","Stachura, Joanna"],["dc.contributor.author","Lawton, Lee N."],["dc.contributor.author","Letai, Anthony"],["dc.contributor.author","Chapuy, Björn"],["dc.contributor.author","Shipp, Margaret A."],["dc.date.accessioned","2020-12-10T18:38:44Z"],["dc.date.available","2020-12-10T18:38:44Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1182/blood-2018-99-113647"],["dc.identifier.eissn","1528-0020"],["dc.identifier.issn","0006-4971"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77423"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Targeted Inhibition of PI3K α/δ Is Synergistic with BCL-2 Blockade in Genetically Defined Subtypes of DLBCL"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","4065"],["dc.bibliographiccitation.issue","23"],["dc.bibliographiccitation.journal","Blood Advances"],["dc.bibliographiccitation.lastpage","4080"],["dc.bibliographiccitation.volume","3"],["dc.contributor.author","Wienand, Kirsty"],["dc.contributor.author","Chapuy, Björn"],["dc.contributor.author","Stewart, Chip"],["dc.contributor.author","Dunford, Andrew J."],["dc.contributor.author","Wu, David"],["dc.contributor.author","Kim, Jaegil"],["dc.contributor.author","Kamburov, Atanas"],["dc.contributor.author","Wood, Timothy R."],["dc.contributor.author","Cader, Fathima Zumla"],["dc.contributor.author","Ducar, Matthew D."],["dc.contributor.author","Thorner, Aaron R."],["dc.contributor.author","Nag, Anwesha"],["dc.contributor.author","Heubeck, Alexander T."],["dc.contributor.author","Buonopane, Michael J."],["dc.contributor.author","Redd, Robert A."],["dc.contributor.author","Bojarczuk, Kamil"],["dc.contributor.author","Lawton, Lee N."],["dc.contributor.author","Armand, Philippe"],["dc.contributor.author","Rodig, Scott J."],["dc.contributor.author","Fromm, Jonathan R."],["dc.contributor.author","Getz, Gad"],["dc.contributor.author","Shipp, Margaret A."],["dc.date.accessioned","2020-04-03T13:47:43Z"],["dc.date.available","2020-04-03T13:47:43Z"],["dc.date.issued","2019-12-10"],["dc.description.abstract","Classical Hodgkin lymphoma (cHL) is composed of rare malignant Hodgkin Reed-Sternberg (HRS) cells within an extensive, but ineffective, inflammatory/immune cell infiltrate. HRS cells exhibit near-universal somatic copy gains of chromosome 9p/9p24.1, which increase expression of the programmed cell death protein 1 (PD-1) ligands. To define genetic mechanisms of response and resistance to PD-1 blockade and identify complementary treatment targets, we performed whole-exome sequencing of flow cytometry-sorted HRS cells from 23 excisional biopsies of newly diagnosed cHLs, including 8 Epstein-Barr virus-positive (EBV+) tumors. We identified significantly mutated cancer candidate genes (CCGs) as well as somatic copy number alterations and structural variations and characterized their contribution to disease-defining immune evasion mechanisms and nuclear factor κB (NF-κB), JAK/STAT, and PI3K signaling pathways. EBV- cHLs had a higher prevalence of genetic alterations in the NF-κB and major histocompatibility complex class I antigen presentation pathways. In this young cHL cohort (median age, 26 years), we identified a predominant mutational signature of spontaneous deamination of cytosine- phosphate-guanines (\"Aging\"), in addition to apolipoprotein B mRNA editing catalytic polypeptide-like, activation-induced cytidine deaminase, and microsatellite instability (MSI)-associated hypermutation. In particular, the mutational burden in EBV- cHLs was among the highest reported, similar to that of carcinogen-induced tumors. Together, the overall high mutational burden, MSI-associated hypermutation, and newly identified genetic alterations represent additional potential bases for the efficacy of PD-1 blockade in cHL. Of note, recurrent cHL alterations, including B2M, TNFAIP3, STAT6, GNA13, and XPO1 mutations and 2p/2p15, 6p21.32, 6q23.3, and 9p/9p24.1 copy number alterations, were also identified in >20% of primary mediastinal B-cell lymphomas, highlighting shared pathogenetic mechanisms in these diseases."],["dc.identifier.doi","10.1182/bloodadvances.2019001012"],["dc.identifier.pmid","31816062"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/63640"],["dc.language.iso","en"],["dc.relation.eissn","2473-9537"],["dc.relation.issn","2473-9529"],["dc.relation.issn","2473-9537"],["dc.relation.orgunit","Klinik für Hämatologie und Medizinische Onkologie"],["dc.title","Genomic analyses of flow-sorted Hodgkin Reed-Sternberg cells reveal complementary mechanisms of immune evasion"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1559"],["dc.bibliographiccitation.issue","Supplement 1"],["dc.bibliographiccitation.journal","Blood"],["dc.bibliographiccitation.lastpage","1559"],["dc.bibliographiccitation.volume","132"],["dc.contributor.author","Wienand, Kirsty"],["dc.contributor.author","Chapuy, Björn"],["dc.contributor.author","Stewart, Chip"],["dc.contributor.author","Dunford, Andrew"],["dc.contributor.author","Wu, David"],["dc.contributor.author","Kim, Jaegil"],["dc.contributor.author","Kamburov, Atanas"],["dc.contributor.author","Cader, Fathima Zumla"],["dc.contributor.author","Ducar, Matthew D."],["dc.contributor.author","Thorner, Aaron R."],["dc.contributor.author","Heubeck, Alexander T"],["dc.contributor.author","Buonopane, Michael J"],["dc.contributor.author","Armand, Philippe"],["dc.contributor.author","Rodig, Scott J"],["dc.contributor.author","Fromm, Jonathan R."],["dc.contributor.author","Getz, Gad"],["dc.contributor.author","Shipp, Margaret A."],["dc.date.accessioned","2020-12-10T18:38:46Z"],["dc.date.available","2020-12-10T18:38:46Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1182/blood-2018-99-118453"],["dc.identifier.eissn","1528-0020"],["dc.identifier.issn","0006-4971"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77433"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Comprehensive Genomic Analysis of Flow-Sorted Hodgkin Reed Sternberg Cells Reveals Additional Genetic Bases of Immune Evasion"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","23"],["dc.bibliographiccitation.journal","Blood"],["dc.bibliographiccitation.volume","126"],["dc.contributor.author","Chapuy, Björn"],["dc.contributor.author","Cheng, Honwei"],["dc.contributor.author","Watahiki, Akira"],["dc.contributor.author","Ducar, Matthew D."],["dc.contributor.author","Gusenleitner, Daniel"],["dc.contributor.author","Chen, Linfeng"],["dc.contributor.author","Roemer, Margaretha G. M."],["dc.contributor.author","Quyang, Jing"],["dc.contributor.author","Christie, Amanda L."],["dc.contributor.author","Zhang, L."],["dc.contributor.author","Tan, Yuxiang"],["dc.contributor.author","Abo, Ryan P."],["dc.contributor.author","Bonin, Frederike"],["dc.contributor.author","Thorner, Aaron R."],["dc.contributor.author","Sun, Heather H."],["dc.contributor.author","Pinkus, Geraldine S."],["dc.contributor.author","van Hummelen, Paul"],["dc.contributor.author","Wulf, Gerald G."],["dc.contributor.author","Aster, Jon C."],["dc.contributor.author","Weinstock, David M."],["dc.contributor.author","Monti, Stefano"],["dc.contributor.author","Rodig, Scott J."],["dc.contributor.author","Wang, Y."],["dc.contributor.author","Shipp, Margaret A."],["dc.date.accessioned","2018-11-07T09:47:39Z"],["dc.date.available","2018-11-07T09:47:39Z"],["dc.date.issued","2015"],["dc.identifier.isi","000368019002254"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/35159"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Soc Hematology"],["dc.publisher.place","Washington"],["dc.relation.conference","57th Annual Meeting of the American-Society-of-Hematology"],["dc.relation.eventlocation","Orlando, FL"],["dc.relation.issn","1528-0020"],["dc.relation.issn","0006-4971"],["dc.title","Diffuse Large B-Cell Lymphoma Patient-Derived Xenograft Models Capture Molecular and Biologic Heterogeneity and Inform Therapy"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1564"],["dc.bibliographiccitation.issue","Supplement 1"],["dc.bibliographiccitation.journal","Blood"],["dc.bibliographiccitation.lastpage","1564"],["dc.bibliographiccitation.volume","132"],["dc.contributor.author","Chapuy, Björn"],["dc.contributor.author","Stewart, Chip"],["dc.contributor.author","Dunford, Andrew"],["dc.contributor.author","Kim, Jaegil"],["dc.contributor.author","Wienand, Kirsty"],["dc.contributor.author","Kamburov, Atanas"],["dc.contributor.author","Griffin, Gabriel Kenneth"],["dc.contributor.author","Cote, Claire McEwen"],["dc.contributor.author","Ducar, Matthew D."],["dc.contributor.author","Thorner, Aaron R."],["dc.contributor.author","Rodig, Scott J"],["dc.contributor.author","Getz, Gad"],["dc.contributor.author","Shipp, Margaret A."],["dc.date.accessioned","2020-12-10T18:38:45Z"],["dc.date.available","2020-12-10T18:38:45Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1182/blood-2018-99-118135"],["dc.identifier.eissn","1528-0020"],["dc.identifier.issn","0006-4971"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77431"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Comprehensive Genomic Analysis of Primary Mediastinal B-Cell Lymphoma"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]