Wulf, Gerald G.

[["dc.bibliographiccitation.firstpage","6"],["dc.bibliographiccitation.journal","Onkologie"],["dc.bibliographiccitation.lastpage","11"],["dc.bibliographiccitation.volume","34 Suppl 5"],["dc.contributor.author","Borchmann, Peter"],["dc.contributor.author","Gökbuget, Nicola"],["dc.contributor.author","Wulf, Gerald"],["dc.contributor.author","Trümper, Lorenz"],["dc.date.accessioned","2019-07-09T11:53:49Z"],["dc.date.available","2019-07-09T11:53:49Z"],["dc.date.issued","2011"],["dc.identifier.doi","10.1159/000329907"],["dc.identifier.fs","585646"],["dc.identifier.pmid","21921661"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/8061"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60503"],["dc.language.iso","de"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1423-0240"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.mesh","Adolescent"],["dc.subject.mesh","Adult"],["dc.subject.mesh","Age Factors"],["dc.subject.mesh","Antibodies, Bispecific"],["dc.subject.mesh","Antibodies, Monoclonal, Murine-Derived"],["dc.subject.mesh","Antineoplastic Combined Chemotherapy Protocols"],["dc.subject.mesh","Child"],["dc.subject.mesh","Child, Preschool"],["dc.subject.mesh","Clinical Trials as Topic"],["dc.subject.mesh","Combined Modality Therapy"],["dc.subject.mesh","Drug Resistance, Neoplasm"],["dc.subject.mesh","Female"],["dc.subject.mesh","Hematopoietic Stem Cell Transplantation"],["dc.subject.mesh","Hodgkin Disease"],["dc.subject.mesh","Humans"],["dc.subject.mesh","Lymphoma, Non-Hodgkin"],["dc.subject.mesh","Male"],["dc.subject.mesh","Neoplasm Staging"],["dc.subject.mesh","Precursor Cell Lymphoblastic Leukemia-Lymphoma"],["dc.subject.mesh","Prognosis"],["dc.subject.mesh","Remission Induction"],["dc.subject.mesh","Survival Rate"],["dc.subject.mesh","Young Adult"],["dc.title","Lymphatic neoplasias in young patients"],["dc.title.translated","Lymphatische Neoplasien bei jungen Patienten"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","e28"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","The Lancet Haematology"],["dc.bibliographiccitation.lastpage","e39"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Beelen, Dietrich Wilhelm"],["dc.contributor.author","Trenschel, Rudolf"],["dc.contributor.author","Stelljes, Matthias"],["dc.contributor.author","Groth, Christoph"],["dc.contributor.author","Masszi, Tamás"],["dc.contributor.author","Reményi, Péter"],["dc.contributor.author","Wagner-Drouet, Eva-Maria"],["dc.contributor.author","Hauptrock, Beate"],["dc.contributor.author","Dreger, Peter"],["dc.contributor.author","Luft, Thomas"],["dc.contributor.author","Bethge, Wolfgang"],["dc.contributor.author","Vogel, Wichard"],["dc.contributor.author","Ciceri, Fabio"],["dc.contributor.author","Peccatori, Jacopo"],["dc.contributor.author","Stölzel, Friedrich"],["dc.contributor.author","Schetelig, Johannes"],["dc.contributor.author","Junghanß, Christian"],["dc.contributor.author","Grosse-Thie, Christina"],["dc.contributor.author","Michallet, Mauricette"],["dc.contributor.author","Labussiere-Wallet, Hélène"],["dc.contributor.author","Schaefer-Eckart, Kerstin"],["dc.contributor.author","Dressler, Sabine"],["dc.contributor.author","Grigoleit, Goetz Ulrich"],["dc.contributor.author","Mielke, Stephan"],["dc.contributor.author","Scheid, Christof"],["dc.contributor.author","Holtick, Udo"],["dc.contributor.author","Patriarca, Francesca"],["dc.contributor.author","Medeot, Marta"],["dc.contributor.author","Rambaldi, Alessandro"],["dc.contributor.author","Micò, Maria Caterina"],["dc.contributor.author","Niederwieser, Dietger"],["dc.contributor.author","Franke, Georg-Nikolaus"],["dc.contributor.author","Hilgendorf, Inken"],["dc.contributor.author","Winkelmann, Nils Rudolf"],["dc.contributor.author","Russo, Domenico"],["dc.contributor.author","Socié, Gérard"],["dc.contributor.author","Peffault de Latour, Régis"],["dc.contributor.author","Holler, Ernst"],["dc.contributor.author","Wolff, Daniel"],["dc.contributor.author","Glass, Bertram"],["dc.contributor.author","Casper, Jochen"],["dc.contributor.author","Wulf, Gerald"],["dc.contributor.author","Menzel, Helge"],["dc.contributor.author","Basara, Nadezda"],["dc.contributor.author","Bieniaszewska, Maria"],["dc.contributor.author","Stuhler, Gernot"],["dc.contributor.author","Verbeek, Mareike"],["dc.contributor.author","Grass, Sandra"],["dc.contributor.author","Iori, Anna Paola"],["dc.contributor.author","Finke, Juergen"],["dc.contributor.author","Benedetti, Fabio"],["dc.contributor.author","Pichlmeier, Uwe"],["dc.contributor.author","Hemmelmann, Claudia"],["dc.contributor.author","Tribanek, Michael"],["dc.contributor.author","Klein, Anja"],["dc.contributor.author","Mylius, Heidrun Anke"],["dc.contributor.author","Baumgart, Joachim"],["dc.contributor.author","Dzierzak-Mietla, Monika"],["dc.contributor.author","Markiewicz, Miroslaw"],["dc.date.accessioned","2020-12-10T15:22:09Z"],["dc.date.available","2020-12-10T15:22:09Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1016/S2352-3026(19)30157-7"],["dc.identifier.issn","2352-3026"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/73288"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Treosulfan or busulfan plus fludarabine as conditioning treatment before allogeneic haemopoietic stem cell transplantation for older patients with acute myeloid leukaemia or myelodysplastic syndrome (MC-FludT.14/L): a randomised, non-inferiority, phase 3 trial"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","179"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Bone Marrow Transplantation"],["dc.bibliographiccitation.lastpage","180"],["dc.bibliographiccitation.volume","36"],["dc.contributor.author","Wulf, Gerald G."],["dc.contributor.author","Sadowski, B."],["dc.contributor.author","von Bonin, Frederike"],["dc.contributor.author","Glass, Bertram"],["dc.contributor.author","Truemper, Lorenz H."],["dc.date.accessioned","2018-11-07T08:55:05Z"],["dc.date.available","2018-11-07T08:55:05Z"],["dc.date.issued","2005"],["dc.identifier.doi","10.1038/sj.bmt.1705019"],["dc.identifier.isi","000230244800015"],["dc.identifier.pmid","15937509"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/22824"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","0268-3369"],["dc.title","Bone marrow side population (SP) cells are donor derived after allogeneic stem cell transplantation in humans"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.subtype","letter_note"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Annals of Oncology"],["dc.bibliographiccitation.volume","19"],["dc.contributor.author","Hohloch, Karin"],["dc.contributor.author","Lakhani, Vijai J."],["dc.contributor.author","Sahlmann, Carsten-Oliver"],["dc.contributor.author","Wulf, Gerald"],["dc.contributor.author","Jung, Werner"],["dc.contributor.author","Glass, Bertram"],["dc.contributor.author","Meller, J."],["dc.contributor.author","Truemper, Lorenz H."],["dc.contributor.author","Griesinger, Frank"],["dc.date.accessioned","2018-11-07T11:14:10Z"],["dc.date.available","2018-11-07T11:14:10Z"],["dc.date.issued","2008"],["dc.format.extent","184"],["dc.identifier.isi","000256693500359"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/54064"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.publisher.place","Oxford"],["dc.relation.conference","10th International Conference on Malignant Lymphoma"],["dc.relation.eventlocation","Lugano, SWITZERLAND"],["dc.relation.issn","0923-7534"],["dc.title","Tandem HD-chemotherapy and myeloablative radioimmunotherapy with 131I-anti-CD20 rituximab in relapsed and refractory B-cell lymphoma: Final results of a phase II study of the German Rait Study Group"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","467"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Bone Marrow Transplantation"],["dc.bibliographiccitation.lastpage","468"],["dc.bibliographiccitation.volume","48"],["dc.contributor.author","Dicke, C. C."],["dc.contributor.author","Kertesz, Andras"],["dc.contributor.author","Henke, R. P."],["dc.contributor.author","Hasenkamp, J."],["dc.contributor.author","Jung, Werner"],["dc.contributor.author","Truemper, Lorenz H."],["dc.contributor.author","Wulf, Gerald G."],["dc.date.accessioned","2018-11-07T09:27:21Z"],["dc.date.available","2018-11-07T09:27:21Z"],["dc.date.issued","2013"],["dc.identifier.doi","10.1038/bmt.2012.165"],["dc.identifier.isi","000316920100026"],["dc.identifier.pmid","22964591"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/30514"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation.issn","0268-3369"],["dc.title","Retroperitoneal fibrosis as manifestation of chronic GVHD after allogeneic hematopoietic SCT"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","letter_note"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","395"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Clinical Cancer Research"],["dc.bibliographiccitation.lastpage","404"],["dc.bibliographiccitation.volume","22"],["dc.contributor.author","Koch, Raphael"],["dc.contributor.author","Aung, Thiha"],["dc.contributor.author","Vogel, Daniel"],["dc.contributor.author","Chapuy, Björn"],["dc.contributor.author","Wenzel, Dirk"],["dc.contributor.author","Becker, Sabrina"],["dc.contributor.author","Sinzig, Ursula"],["dc.contributor.author","Venkataramani, Vivek"],["dc.contributor.author","von Mach, Tobias"],["dc.contributor.author","Jacob, Ralf"],["dc.contributor.author","Truemper, Lorenz H."],["dc.contributor.author","Wulf, Gerald G."],["dc.date.accessioned","2018-11-07T10:19:22Z"],["dc.date.available","2018-11-07T10:19:22Z"],["dc.date.issued","2016"],["dc.description.abstract","Purpose: Although R-CHOP-based immunochemotherapy cures significant proportions of patients with aggressive B-cell lymphoma, tumor cell susceptibility to chemotherapy varies, with mostly fatal outcome in cases of resistant disease. We and others have shown before that export of cytostatic drugs contributes to drug resistance. Now we provide a novel approach to overcome exosome-mediated drug resistance in aggressive B-cell lymphomas. Experimental Design: We used well-established centrifugation protocols to purify exosomes from DLBCL cell lines and detected anthracyclines using FACS and HPLC. We used shRNA knockdown of ABCA3 to determine ABCA3 dependence of chemotherapy susceptibility and monitored ABCA3 expression after indomethacin treatment using qPCR. Finally, we established an in vivo assay using a chorioallantoic membrane (CAM) assay to determine the synergy of anthracycline and indomethacin treatment. Results: We show increased efficacy of the anthracycline doxorubicin and the anthracenedione pixantrone by suppression of exosomal drug resistance with indomethacin. B-cell lymphoma cells in vitro efficiently extruded doxorubicin and pixantrone, in part compacted in exosomes. Exosomal biogenesis was critically dependent on the expression of the ATP-transporter A3 (ABCA3). Genetic or chemical depletion of ABCA3 augmented intracellular retention of both drugs and shifted the subcellular drug accumulation to prolonged nuclear retention. Indomethacin increased the cytostatic efficacy of both drugs against DLBCL cell lines in vitro and in vivo in a CAM assay. Conclusions: We propose pretreatment with indomethacin toward enhanced antitumor efficacy of anthracyclines and anthracenediones. (C) 2015 AACR."],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft; University Medicine Goettingen"],["dc.identifier.doi","10.1158/1078-0432.CCR-15-0577"],["dc.identifier.isi","000369076500016"],["dc.identifier.pmid","26369630"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/41643"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation.issn","1557-3265"],["dc.relation.issn","1078-0432"],["dc.title","Nuclear Trapping through Inhibition of Exosomal Export by Indomethacin Increases Cytostatic Efficacy of Doxorubicin and Pixantrone"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","362"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Oncology"],["dc.bibliographiccitation.lastpage","370"],["dc.bibliographiccitation.volume","84"],["dc.contributor.author","Overbeck, Tobias R."],["dc.contributor.author","Hupfeld, Timo"],["dc.contributor.author","Krause, Doris"],["dc.contributor.author","Waldmann-Beushausen, Regina"],["dc.contributor.author","Chapuy, Björn"],["dc.contributor.author","Guedenzoph, Bjoern"],["dc.contributor.author","Aung, Thiha"],["dc.contributor.author","Inagaki, Nobuya"],["dc.contributor.author","Schoendube, Friedrich Albert"],["dc.contributor.author","Danner, Bernhard Christoph"],["dc.contributor.author","Truemper, Lorenz H."],["dc.contributor.author","Wulf, Gerald G."],["dc.date.accessioned","2018-11-07T09:29:56Z"],["dc.date.available","2018-11-07T09:29:56Z"],["dc.date.issued","2013"],["dc.description.abstract","Patients with advanced-stage bronchial cancer benefit from systemic cytostatic therapy, in particular from regimens integrating cisplatin and taxanes. However, eventual disease progression leads to a fatal outcome in most cases, originating from tumor cells resisting chemotherapy. We here show that the intracellular ATP-binding cassette transporter A3 (ABCA3), previously recognized as critical for the secretion of surfactant components from type 2 pneumocytes, is expressed in non-small-cell lung cancer (NSCLC) cells. With some heterogeneity in a given specimen, expression levels detected immunohistochemically in primary cancer tissue were highest in adenocarcinomas and lowest in small cell lung cancers. Genetic silencing of ABCA3 in the NSCLC cell line models A549, NCI-H1650 and NCI-H1975 significantly increased tumor cell susceptibility to the cytostatic effects of both cisplatin (in all cell lines) and paclitaxel (in two of three cell lines). Taken together, ABCA3 emerges as a modulator of NSCLC cell susceptibility to cytostatic therapy. Copyright (c) 2013 S. Karger AG, Basel"],["dc.description.sponsorship","Faculty of Medicine, Georg August University Gottingen, Germany"],["dc.identifier.doi","10.1159/000348884"],["dc.identifier.isi","000320219100007"],["dc.identifier.pmid","23689165"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/10826"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/31175"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation.issn","0030-2414"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Intracellular ATP-Binding Cassette Transporter A3 is Expressed in Lung Cancer Cells and Modulates Susceptibility to Cisplatin and Paclitaxel"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","692"],["dc.bibliographiccitation.issue","Supplement 1"],["dc.bibliographiccitation.journal","Blood"],["dc.bibliographiccitation.lastpage","692"],["dc.bibliographiccitation.volume","138"],["dc.contributor.author","Döhner, Hartmut"],["dc.contributor.author","Weber, Daniela"],["dc.contributor.author","Krzykalla, Julia"],["dc.contributor.author","Fiedler, Walter"],["dc.contributor.author","Wulf, Gerald"],["dc.contributor.author","Salih, Helmut R."],["dc.contributor.author","Lübbert, Michael"],["dc.contributor.author","Kühn, Michael W.M."],["dc.contributor.author","Schroeder, Thomas"],["dc.contributor.author","Salwender, Hans"],["dc.contributor.author","Ganser, Arnold"],["dc.date.accessioned","2022-10-04T10:22:06Z"],["dc.date.available","2022-10-04T10:22:06Z"],["dc.date.issued","2021"],["dc.description.abstract","Abstract\n \n BACKGROUND: Midostaurin is a first-generation, type I multi-targeted kinase inhibitor with inhibitory activity against FLT3-ITD and -TKD mutations. Midostaurin is approved by FDA and EMA in combination with intensive induction and consolidation chemotherapy for adult patients with AML exhibiting an activating FLT3 mutation; the EMA label also includes single-agent maintenance therapy following consolidation chemotherapy. We conducted a phase-II trial (AMLSG 16-10) to evaluate midostaurin with induction chemotherapy followed by allogeneic hematopoietic-cell transplantation (HCT) and a one-year midostaurin maintenance therapy in younger and older patients with acute myeloid leukemia (AML) and FLT3 internal tandem duplication (ITD).\n METHODS: Patients 18 to 70 years of age with newly diagnosed FLT3-ITD-positive AML were eligible. Primary and key secondary endpoints were event-free (EFS) and overall survival (OS); results were compared to those of a historical control cohort of 415 patients with FLT3-ITD AML. Statistical analysis was performed using a double-robust adjustment with propensity score weighting and covariate adjustment. Major differences in trial design compared to the pivotal CALGB 10603/RATIFY trial were: i) only AML with FLT3-ITD were eligible; ii) AML with FLT3 tyrosine kinase domain mutations (only) and core-binding factor AML were not eligible; iii) older patients 60-70 years of age were eligible; iv) all patients were assigned to allogeneic HCT; v) a one-year maintenance treatment with midostaurin was included also after allogeneic HCT; vi) a continuous dosing schedule of midostaurin was applied with the aim to achieve a better target inhibition.\n Results: The trial accrued 440 patients, including 312 younger (18-60 yrs) and 128 older (61-70 yrs) patients. Complete remission (CR)/CR with incomplete hematologic recovery rate, median EFS and OS of the 440 patients were 74.9%, 13.6 and 36.2 months, respectively. Multivariate analysis of EFS showed a highly significant hazard reduction for an event for patients treated within AMLSG 16-10 trial compared to the historical controls (HR 0.55; 95%-confidence interval [CI], 0.47, 0.65; P<0.001); this effect was significant in the younger (HR 0.59; 95%-CI, 0.49, 0.71; P<0.001) and the older patient cohort (HR 0.42; 95%-CI, 0.30, 0.60; P<0.001). Multivariate analysis also showed a highly significant beneficial effect on OS (HR 0.57; 95%-CI, 0.47, 0.68; P<0.001), again for both age subgroups. Allogeneic HCT in first CR/CRi was performed according to protocol in 199 of 440 (45%) patients (48% and 38% in younger and older patients, respectively), and an additional 60 patients received allogeneic HCT in firstline therapy (n=33 pts. in CR/CRi after salvage therapy and 27 pts. with active disease); the treatment effect of midostaurin remained significant in sensitivity analysis including allogeneic HCT (n=259) as a time-dependent covariate. Addition of midostaurin to chemotherapy was safe in younger and older patients.\n Conclusions: In comparison to a historical control cohort, the addition of midostaurin to intensive therapy led to a significant improvement in EFS and OS in both younger and older adult patients with AML and FLT3-ITD.\n \n Figure: Survival distribution for the primary endpoint event-free survival (EFS) and key secondary endpoint overall survival (OS) according to study population and age group.\n A EFS by cohort and age group (≤60 versus >60 years)\n B OS by cohort and age group (≤60 versus >60 years)\n Figure 1 Figure 1.\n \n \n Disclosures\n Döhner: Astellas: Consultancy, Honoraria, Research Funding; Celgene: Consultancy, Honoraria, Research Funding; AstraZeneca: Consultancy, Honoraria; Astex: Consultancy, Honoraria; Amgen: Consultancy, Honoraria, Research Funding; Agios: Consultancy, Honoraria, Research Funding; Abbvie: Consultancy, Honoraria, Research Funding; GEMoaB: Consultancy, Honoraria; Bristol Myers Squibb: Consultancy, Honoraria, Research Funding; Berlin-Chemie: Consultancy, Honoraria; Helsinn: Consultancy, Honoraria; Janssen: Consultancy, Honoraria; Jazz: Consultancy, Honoraria, Research Funding; Novartis: Consultancy, Honoraria, Research Funding; Oxford Biomedicals: Consultancy, Honoraria; Pfizer: Research Funding; Roche: Consultancy, Honoraria; Gilead: Consultancy, Honoraria; Ulm University Hospital: Current Employment. Fiedler: Servier: Consultancy, Other: Meeting attendance, Preparation of information material; Stemline: Consultancy; Daiichi Sanyko: Consultancy, Other: Meeting attendance, Preparation of information material; Pfizer: Consultancy, Honoraria, Research Funding; Novartis: Honoraria; MorphoSys: Consultancy, Honoraria; Jazz: Consultancy, Honoraria, Other: Meeting attendance, Preparation of information material; Celgene: Consultancy, Honoraria; Ariad/Incyte: Honoraria; Amgen: Consultancy, Honoraria, Other: Meeting attendance, Preparation of information material, Patents & Royalties, Research Funding; Abbvie: Consultancy, Honoraria, Other: Meeting attendance, Preparation of information material. Wulf: Gilead: Consultancy, Honoraria; Novartis: Consultancy, Honoraria; Takeda: Consultancy, Honoraria; Clinigen: Consultancy, Honoraria. Salih: BMS: Honoraria; Celgene: Honoraria; Pfizer: Honoraria; Synimmune GmbH: Honoraria; Novartis: Honoraria. Lübbert: Imago BioSciences: Honoraria; Janssen: Honoraria, Research Funding; Pfizer: Honoraria; Syros: Honoraria; Aristopharm: Research Funding; Cheplapharm: Research Funding; Janssen: Research Funding; Teva: Research Funding; Hexal: Honoraria; Astex: Honoraria; Abbvie: Honoraria. Kühn: Abbvie: Honoraria; Kura Oncology: Honoraria, Research Funding; Pfizer: Honoraria. Schroeder: Abbvie: Honoraria; Astellas: Honoraria; Celgene: Honoraria; Janssen: Honoraria; Jazz: Honoraria; Novartis: Honoraria; Takeda: Honoraria; Pfizer: Honoraria. Salwender: Oncopeptides: Honoraria; GlaxoSmithKline: Honoraria, Other: TRAVEL, ACCOMMODATIONS, EXPENSES; Sanofi: Honoraria, Other: TRAVEL, ACCOMMODATIONS, EXPENSES; Takeda: Honoraria; Amgen: Honoraria, Other: TRAVEL, ACCOMMODATIONS, EXPENSES; Chugai: Honoraria; AbbVie: Honoraria, Other: TRAVEL, ACCOMMODATIONS, EXPENSES; Janssen-Cilag: Honoraria, Other: TRAVEL, ACCOMMODATIONS, EXPENSES; Bristol-Myers Squibb/Celgene: Honoraria, Other: TRAVEL, ACCOMMODATIONS, EXPENSES; Pfizer: Honoraria. Götze: Abbvie: Honoraria; Celgene/BMS: Honoraria, Research Funding. Westermann: Amgen: Consultancy, Honoraria; BMS: Honoraria; Novartis: Consultancy, Honoraria; Stem Cell Line: Consultancy, Honoraria; Abbvie: Consultancy, Honoraria; Pfizer: Consultancy, Honoraria; Sanofi: Consultancy, Honoraria; Astellas: Honoraria. Fransecky: Abbvie: Honoraria, Research Funding; Takeda: Honoraria; Amgen: Honoraria; Novartis: Honoraria; Medac: Honoraria. Mayer: Novartis: Other: Travel support; Celgene: Other: Travel support; Roche: Other: Travel support; Amgen: Other: Travel support; BMS: Other: Travel support; Pfizer: Other: Travel support; Jazz: Other: Travel support; Astellas: Other: Travel support. Hertenstein: Sanofi: Honoraria; Novartis: Honoraria; Celgene: Honoraria; BMS: Honoraria. Tischler: AstraZeneca: Other: Travel support; Novartis: Other: Travel support; Janssen: Honoraria; GSK: Other: Travel support; Sanofi-Aventis: Other: Travel support; Abbvie: Other: Travel support. Paschka: Abbvie: Honoraria, Other: Travel support; Agios: Honoraria, Speakers Bureau; Astellas: Honoraria, Speakers Bureau; Astex: Honoraria; Celgene: Honoraria, Other: Travel support; Jazz: Honoraria; Novartis: Honoraria, Other: Travel support; Otsuka: Honoraria; Pfizer: Honoraria; Sunesis: Honoraria; BMS: Other, Speakers Bureau; Celgene: Honoraria; Janssen: Other; Takeda: Other. Gaidzik: Janssen: Speakers Bureau; Pfizer: Speakers Bureau; Abbvie: Membership on an entity's Board of Directors or advisory committees, Speakers Bureau. Thol: Abbvie: Honoraria; Astellas: Honoraria; BMS/Celgene: Honoraria, Research Funding; Jazz: Honoraria; Novartis: Honoraria; Pfizer: Honoraria. Heuser: Tolremo: Membership on an entity's Board of Directors or advisory committees; Daiichi Sankyo: Membership on an entity's Board of Directors or advisory committees, Research Funding; Bayer Pharma AG: Research Funding; Novartis: Consultancy, Honoraria, Membership on an entity's Board of Directors or advisory committees, Research Funding; Astellas: Research Funding; Jazz: Honoraria, Membership on an entity's Board of Directors or advisory committees, Research Funding; Janssen: Honoraria; BMS/Celgene: Membership on an entity's Board of Directors or advisory committees, Research Funding; Pfizer: Membership on an entity's Board of Directors or advisory committees, Research Funding; Roche: Membership on an entity's Board of Directors or advisory committees, Research Funding; Karyopharm: Research Funding; BergenBio: Research Funding; AbbVie: Membership on an entity's Board of Directors or advisory committees, Research Funding. Schlenk: Astellas: Honoraria, Research Funding, Speakers Bureau; Celgene: Honoraria; Daiichi Sankyo: Honoraria, Research Funding; Hexal: Honoraria; Neovio Biotech: Honoraria; Novartis: Honoraria; Pfizer: Honoraria, Research Funding, Speakers Bureau; Roche: Honoraria, Research Funding; AstraZeneca: Research Funding; Boehringer Ingelheim: Research Funding; Abbvie: Honoraria; Agios: Honoraria. Bullinger: Abbvie: Honoraria, Membership on an entity's Board of Directors or advisory committees; Amgen: Honoraria; Astellas: Honoraria; Bristol-Myers Squibb / Celgene: Honoraria, Membership on an entity's Board of Directors or advisory committees; Bayer: Research Funding; Daiichi Sankyo: Honoraria, Membership on an entity's Board of Directors or advisory committees; Gilead: Membership on an entity's Board of Directors or advisory committees; Hexal: Membership on an entity's Board of Directors or advisory committees; Janssen: Honoraria, Membership on an entity's Board of Directors or advisory committees; Jazz Pharmaceutical: Honoraria, Membership on an entity's Board of Directors or advisory committees, Research Funding; Menarini: Membership on an entity's Board of Directors or advisory committees; Novartis: Honoraria, Membership on an entity's Board of Directors or advisory committees; Pfizer: Honoraria, Membership on an entity's Board of Directors or advisory committees. Döhner: Amgen: Honoraria; BMS/Celgene: Honoraria, Research Funding; Janssen: Honoraria; Jazz: Honoraria; Novartis: Honoraria, Research Funding; Roche: Honoraria; Daiichi Sankyo: Honoraria; Agios: Research Funding; Astex: Research Funding; Astellas: Research Funding. Ganser: Novartis: Honoraria; Jazz Pharmaceuticals: Honoraria; Celgene: Honoraria.\n \n \n OffLabel Disclosure:\n Midostaurin as single-agent maintenance therapy following allogeneic hematopoietic cell transplantation"],["dc.identifier.doi","10.1182/blood-2021-147256"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/114588"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-600"],["dc.relation.eissn","1528-0020"],["dc.relation.issn","0006-4971"],["dc.title","Midostaurin Plus Intensive Chemotherapy for Younger and Older Patients with Acute Myeloid Leukemia and FLT3 Internal Tandem Duplications"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","3169"],["dc.bibliographiccitation.issue","26"],["dc.bibliographiccitation.journal","Blood"],["dc.bibliographiccitation.lastpage","3176"],["dc.bibliographiccitation.volume","128"],["dc.contributor.author","Fuerst, Daniel"],["dc.contributor.author","Neuchel, Christine"],["dc.contributor.author","Niederwieser, Dietger"],["dc.contributor.author","Bunjes, Donald W."],["dc.contributor.author","Gramatzki, Martin"],["dc.contributor.author","Wagner, Eva M."],["dc.contributor.author","Wulf, Gerald"],["dc.contributor.author","Glass, Bertram"],["dc.contributor.author","Pfreundschuh, Michael"],["dc.contributor.author","Einsele, Hermann"],["dc.contributor.author","Arnold, Renate"],["dc.contributor.author","Stuhler, Gernot"],["dc.contributor.author","Schaefer-Eckart, Kerstin"],["dc.contributor.author","Freitag, Sebastian"],["dc.contributor.author","Casper, Jochen"],["dc.contributor.author","Kaufmann, Martin"],["dc.contributor.author","Wattad, Mohammed"],["dc.contributor.author","Hertenstein, Bernd"],["dc.contributor.author","Klein, Stefan"],["dc.contributor.author","Ringhoffer, Mark"],["dc.contributor.author","Mytilineos, Daphne"],["dc.contributor.author","Tsamadou, Chrysanthi"],["dc.contributor.author","Mueller, Carlheinz R."],["dc.contributor.author","Schrezenmeier, Hubert"],["dc.contributor.author","Mytilineos, Joannis"],["dc.date.accessioned","2018-11-07T10:04:20Z"],["dc.date.available","2018-11-07T10:04:20Z"],["dc.date.issued","2016"],["dc.description.abstract","Major histocompatibility complex class I polypeptide-related sequence A (MICA) is a highly polymorphic ligand of the activating NKG2D receptor on natural killer (NK) cells, gamma delta-T cells, and NKT cells. MICA incompatibilities have been associated with an increased graft-versus-host disease (GVHD) incidence, and the MICA-129 (met/val) dimorphism has been shown to influence NKG2D signaling in unrelated hematopoietic stem cell transplantation (uHSCT). We investigated the effect of MICA matching on survival after uHSCT. We sequenced 2172 patients and their respective donors for MICA. All patients and donors were high-resolution HLA-typed and matched for 10/10 (n = 1379), 9/10 (n = 636), or 8/10 (n = 157) HLA alleles. Within each HLA match group, cases matched and mismatched for MICA and MICA-129 were analyzed for the end points overall survival (OS), disease-free survival (DFS), nonrelapse mortality (NRM), relapse-incidence (RI), and GVHD. Mismatches at the MICA locus as well as MICA-129 increased with the number of HLA mismatches (MICA mismatched 10/10, 9.2% [n = 127]; 9/10, 22.3% [n = 142]; 8/10, 38.2% [n = 60]; MICA-129 mismatched 10/10, 3.9% [n = 54]; 9/10, 10.2% [n = 65]; 8/10, 17.2% [n = 27]). Adverse OS was observed in the 10/10 match group if MICA-129 was mismatched (10/10, hazard ratio [HR], 1.77; confidence interval [CI], 1.22-2.57; P = .003). MICA-129 mismatches correlated with a significantly worse outcome for DFS in the 10/10 HLA match group (HR, 1.77; CI, 1.26-2.50; P = .001). Higher rates of aGVHD were seen in MICA-129 mismatched cases. Our results indicate that MICA-129 matching is relevant in uHSCT. Prospective typing of patients and donors in unrelated donor search may identify mismatches for MICA-129, and compatible donor selection may improve outcome for this small but high-risk subgroup."],["dc.identifier.doi","10.1182/blood-2016-05-716357"],["dc.identifier.isi","000392656400020"],["dc.identifier.pmid","27811019"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/38678"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation.issn","1528-0020"],["dc.relation.issn","0006-4971"],["dc.title","Matching for the MICA-129 polymorphism is beneficial in unrelated hematopoietic stem cell transplantation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1127"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Annals of Hematology"],["dc.bibliographiccitation.lastpage","1133"],["dc.bibliographiccitation.volume","96"],["dc.contributor.author","Budde, Holger"],["dc.contributor.author","Papert, Susanne"],["dc.contributor.author","Maas, Jens-Holger"],["dc.contributor.author","Reichardt, Holger Michael"],["dc.contributor.author","Wulf, Gerald"],["dc.contributor.author","Hasenkamp, Justin"],["dc.contributor.author","Riggert, Joachim"],["dc.contributor.author","Legler, Tobias Joerg"],["dc.date.accessioned","2018-11-07T10:22:22Z"],["dc.date.available","2018-11-07T10:22:22Z"],["dc.date.issued","2017"],["dc.description.abstract","Graft-versus-host disease (GvHD) still belongs to the major challenges after allogeneic hematopoietic stem cell transplantation (HSCT). Immune-suppressive therapy against GvHD is a double-edged sword due to risk of infections and relapse. The ability to adapt prophylactic treatment according to the probability of severe GvHD would be an essential advantage for the patients. We analyzed different biomarkers for their potential to predict the development of GvHD in 28 patients who underwent allogeneic HSCT. Blood was taken once directly after hematopoietic engraftment. In this study, patients were monitored for 12 months after HSCT for the occurrence of acute GvHD or acute/chronic GvHD overlap syndrome. Soluble IL-2 receptor and CD4/CD8 T cell ratio were independently associated with the occurrence of GvHD in the observation period. However, the largest area under the receiver operating characteristic curve with 0.90 was observed when a 5-parameter biomarker score based on CD4(+) T cells, CD8(+) T cells, CD19(-) CD21(+) precursor B cells, CD4/CD8 T cell ratio, and soluble IL-2 receptor was used to predict GvHD. In addition, CD8(+) T cell levels above 2.3% of all mononuclear cells after engraftment may predict relapse-free survival at least for 12 months. In summary, we found a new biomarker panel for prediction of GvHD which is featured by established laboratory assays and high statistical significance. In order to introduce the biomarker panel into routine clinical protocols, we suggest performing a larger multi-center study."],["dc.identifier.doi","10.1007/s00277-017-2999-5"],["dc.identifier.isi","000403078900008"],["dc.identifier.pmid","28447161"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42255"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Springer"],["dc.relation.issn","1432-0584"],["dc.relation.issn","0939-5555"],["dc.title","Prediction of graft-versus-host disease: a biomarker panel based on lymphocytes and cytokines"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]