Hasenkamp, Justin

[["dc.bibliographiccitation.firstpage","536"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Experimental Hematology"],["dc.bibliographiccitation.lastpage","546"],["dc.bibliographiccitation.volume","32"],["dc.contributor.author","Schroers, Roland"],["dc.contributor.author","Hildebrandt, Y."],["dc.contributor.author","Hasenkamp, Justin"],["dc.contributor.author","Glass, Bertram"],["dc.contributor.author","Lieber, A."],["dc.contributor.author","Wulf, Gerald"],["dc.contributor.author","Piesche, Matthias"],["dc.date.accessioned","2018-11-07T10:48:24Z"],["dc.date.available","2018-11-07T10:48:24Z"],["dc.date.issued","2004"],["dc.description.abstract","Objective. Genetic modification of effector lymphocytes, such as T cells and natural killer (NK) cells, is essential for many approaches to gene-based immunotherapy of cancer. However, transduction of lymphocytes has proven difficult by currently available gene transfer methods. Previous studies have shown that chimeric fiber-modified Ad5/F35 adenoviral vectors are able to efficiently transduce hematopoietic cells including immature progenitors. In this study, we examined the gene transfer into T lymphocytes and NK cells using Ad5/F35 compared with conventional Ad5 adenovectors. Methods. Primary T and NK cells were isolated from healthy donors' peripheral blood leukocytes by immunomagnetic selection. Cell lines and primary lymphocytes were transduced with replication-defective Ad5/F35 and Ad5, both containing a GFP reporter gene under the control of a CMV promoter. Transduction efficiencies were monitored by flow cytometry. The function of transduced lymphocytes was assessed by analysis of proliferative responses to mitogenic agents and in mixed leukocyte reactions. Results. Transgene expression was detected in up to 45% of primary CD3+ T lymphocytes and in up to 60% of primary NK cells using Ad5/F35. In contrast, conventional Ad5 transduced less than 8% and 5% of primary T cells and NK cells, respectively. Transduction efficiencies were similar in CD4+ and CD8+ T lymphocytes, and transgene expression could be detected for up to seven days. Activation of T cells significantly enhanced the efficiency of Ad5/F35-mediated gene transfer. Adenoviral transduction of lymphocytes did not result in any impairment of proliferative functions. Conclusion. The results of this study demonstrate that both T lymphocytes and NK cells can be transduced by chimeric Ad5/F35 adenoviral vectors. (C) 2004 International Society for Experimental Hematology. Published by Elsevier Inc."],["dc.identifier.doi","10.1016/j.exphem.2004.03.010"],["dc.identifier.isi","000222175700004"],["dc.identifier.pmid","15183894"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/48183"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation.issn","0301-472X"],["dc.title","Gene transfer into human T lymphocytes and natural killer cells by Ad5/F35 chimeric adenoviral vectors"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Blood"],["dc.bibliographiccitation.volume","110"],["dc.contributor.author","Glass, Bertram"],["dc.contributor.author","Hasenkamp, Justin"],["dc.contributor.author","Dreger, Peter"],["dc.contributor.author","Gramatzki, Martin"],["dc.contributor.author","Schubert, Joerg"],["dc.contributor.author","Wulf, Gerald G."],["dc.contributor.author","Nickelsen, Maike"],["dc.contributor.author","Truemper, Lorenz H."],["dc.contributor.author","Schmitz, Norbert"],["dc.date.accessioned","2018-11-07T10:52:41Z"],["dc.date.available","2018-11-07T10:52:41Z"],["dc.date.issued","2007"],["dc.format.extent","894A"],["dc.identifier.isi","000251100804080"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/49168"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Soc Hematology"],["dc.publisher.place","Washington"],["dc.relation.conference","49th Annual Meeting of the American-Society-of-Hematology"],["dc.relation.eventlocation","Atlanta, GA"],["dc.relation.issn","0006-4971"],["dc.title","Intermediate intensity conditioning followed by allogeneic peripheral blood stem cell transplantion for treatment of high risk relapse of aggressive lymphoma. Interim analysis of the DSHNHL R3 study"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","757"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","The Lancet Oncology"],["dc.bibliographiccitation.lastpage","766"],["dc.bibliographiccitation.volume","15"],["dc.contributor.author","Glass, Bertram"],["dc.contributor.author","Hasenkamp, Justin"],["dc.contributor.author","Wulf, Gerald"],["dc.contributor.author","Dreger, Peter"],["dc.contributor.author","Pfreundschuh, Michael"],["dc.contributor.author","Gramatzki, Martin"],["dc.contributor.author","Silling, Gerda"],["dc.contributor.author","Wilhelm, Christian"],["dc.contributor.author","Zeis, Matthias"],["dc.contributor.author","Schmitz, Norbert"],["dc.date.accessioned","2021-06-01T10:50:22Z"],["dc.date.available","2021-06-01T10:50:22Z"],["dc.date.issued","2014"],["dc.identifier.doi","10.1016/S1470-2045(14)70161-5"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/86631"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.relation.issn","1470-2045"],["dc.title","Rituximab after lymphoma-directed conditioning and allogeneic stem-cell transplantation for relapsed and refractory aggressive non-Hodgkin lymphoma (DSHNHL R3): an open-label, randomised, phase 2 trial"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","391"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Bone Marrow Transplantation"],["dc.bibliographiccitation.lastpage","397"],["dc.bibliographiccitation.volume","34"],["dc.contributor.author","Glass, Bertram"],["dc.contributor.author","Nickelsen, M."],["dc.contributor.author","Dreger, Peter"],["dc.contributor.author","Claviez, Alexander"],["dc.contributor.author","Hasenkamp, J."],["dc.contributor.author","Wulf, Gerald"],["dc.contributor.author","Truemper, Lorenz H."],["dc.contributor.author","Schmitz, Norbert"],["dc.date.accessioned","2018-11-07T10:45:48Z"],["dc.date.available","2018-11-07T10:45:48Z"],["dc.date.issued","2004"],["dc.description.abstract","In patients with poor-risk relapse of aggressive lymphoma, reduced-intensity conditioning followed by allogeneic PBSCT may have its limitations because of rapid regrowth of the tumor. We tried to address this problem by intermediate-intensity conditioning followed by allogeneic SCT. A total of 21 patients received fludarabine, busulfan and cyclophosphamide prior to allogeneic SCT. In the first 10 patients, GVHD prophylaxis by CD34+ selection of the grafts was employed (group I). The next 11 patients received nonmanipulated grafts and mycophenolat mofetil plus cyclosporinA (group II). In group I, no GVHD was observed. In contrast, patients in group II had a significant risk of acute GVHD (aGVHD) (six patients with grade II-IV acute GVHD). However, in group I, all surviving patients progressed within 9 months. In contrast, eight of nine surviving patients of group II remain in remission after a median observation time of 10.5 months (range 4-22 months). Survival differed significantly between the groups (P = 0.004). Multivariate analysis identified intensive GVHD prophylaxis as important risk factor for survival. These results support the existence of a clinically relevant GVL effect in aggressive lymphoma. T-cell depletion (or CD34 selection) of grafts is not recommended in patients with poor-risk aggressive NHL."],["dc.identifier.doi","10.1038/sj.bmt.1704600"],["dc.identifier.isi","000223351200002"],["dc.identifier.pmid","15273707"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/47591"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation.issn","0268-3369"],["dc.title","Reduced-intensity conditioning prior to allogeneic transplantation of hematopoietic stem cells: the need for T cells early after transplantation to induce a graft-versus-lymphoma effect"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","262B"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Blood"],["dc.bibliographiccitation.lastpage","263B"],["dc.bibliographiccitation.volume","108"],["dc.contributor.author","Borgerding, Andrea"],["dc.contributor.author","Hasenkamp, Justin"],["dc.contributor.author","Chapuy, Björn"],["dc.contributor.author","Truemper, Lorenz H."],["dc.contributor.author","Wulf, Gerald"],["dc.contributor.author","Glass, Bertram"],["dc.date.accessioned","2018-11-07T08:57:39Z"],["dc.date.available","2018-11-07T08:57:39Z"],["dc.date.issued","2006"],["dc.identifier.isi","000242440401404"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/23446"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Soc Hematology"],["dc.publisher.place","Washington"],["dc.relation.conference","48th Annual Meeting of the American-Society-of-Hematology"],["dc.relation.eventlocation","Orlando, FL"],["dc.relation.issn","0006-4971"],["dc.title","Response to re-treatment with rituximab plus salvage-chemotherapy in refractory or relapsed aggressive Non-Hodgkin's lymphoma."],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","213"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Experimental Hematology"],["dc.bibliographiccitation.lastpage","221"],["dc.bibliographiccitation.volume","38"],["dc.contributor.author","Borgerding, Andrea"],["dc.contributor.author","Hasenkamp, Justin"],["dc.contributor.author","Engelke, Michael"],["dc.contributor.author","Burkhart, Nina"],["dc.contributor.author","Truemper, Lorenz H."],["dc.contributor.author","Wienands, Juergen"],["dc.contributor.author","Glass, Bertram"],["dc.date.accessioned","2018-11-07T08:45:26Z"],["dc.date.available","2018-11-07T08:45:26Z"],["dc.date.issued","2010"],["dc.description.abstract","Objective. Antibody-dependent cellular cytotoxicity (ADCC) by natural killer (NK) cells is a major effector mechanism of the monoclonal anti-CD20 antibody rituximab in eliminating B-cell lymphomas. Resistance to this treatment occurs, although CD20 antigen is expressed oil the tumor cells. Materials and Methods. A model of ADCC was established by stimulating human hulk NK cells and inhibitory killer immunoglobulin receptor (KIR) - defined NK cells from human leukocyte antigen (HLA)-typed donors. NK-cell activation was triggered via stimulation of the Fc receptor with immunoglobulin G aggregates, rituximab-labeled HLA-defined CD20-positive B-lymphohlast cell lines or CD20-positive B-lymphoma cell lines. The effect of KIR ligation by anti-KIR antibodies anti HLA, the HLA expression density and rituximab concentrations on the efficacy of ADCC were analyzed in granzyme B ELISPOT measuring NK-cell activation anti fluorescein-activated cell sorting cytotoxicity assay. Results. HLA, but not CD20 expression density correlated with NK-cell activity against rituximab-labeled targets. ADCC was increased or decreased following HLA shielding or Kill activation by anti-KIR antibodies, respectively. Herein we show that rituximab-induced ADCC is attenuated upon ligation of Kill by HLA molecules expressed on human B-lymphoma target cells. Moreover, anti-KIR antibodies do not only block KIR/HLA interactions, but display agonistic effects at the KIR, which has to be considered for therapeutical applications. Conclusion. KIR activation and HLA expression density are critical determinants for the efficacy of rituximab treatment. An explanation for the failure of rituximab treatment may be the protection of the tumor cells from ADCC by inhibiting NK-cell function with their surface HLA. (C) 2010 ISEH - Society for Hematology and Stem Cells. Published by Elsevier Inc."],["dc.description.sponsorship","Georg-August University Gottingen, Gottingen, Germany"],["dc.identifier.doi","10.1016/j.exphem.2009.12.007"],["dc.identifier.isi","000275364900006"],["dc.identifier.pmid","20056126"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/20440"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Inc"],["dc.relation.issn","0301-472X"],["dc.title","B-lymphoma cells escape rituximab-triggered elimination by NK cells through increased HLA class I expression"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","15"],["dc.bibliographiccitation.journal","Journal of Clinical Oncology"],["dc.bibliographiccitation.volume","30"],["dc.contributor.author","Glass, Bertram"],["dc.contributor.author","Hasenkamp, Justin"],["dc.contributor.author","Wulf, Gerald"],["dc.contributor.author","Dreger, Peter"],["dc.contributor.author","Pfreundschuh, Michael"],["dc.contributor.author","Gramatzki, Martin"],["dc.contributor.author","Silling, Gerda"],["dc.contributor.author","Wilhelm, Christian"],["dc.contributor.author","Zeis, Matthias"],["dc.contributor.author","Pfeiffer, Sebastian"],["dc.contributor.author","Truemper, Lorenz H."],["dc.contributor.author","Schmitz, Norbert"],["dc.date.accessioned","2018-11-07T09:10:20Z"],["dc.date.available","2018-11-07T09:10:20Z"],["dc.date.issued","2012"],["dc.identifier.isi","000318009803810"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/26463"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Soc Clinical Oncology"],["dc.publisher.place","Alexandria"],["dc.relation.conference","48th Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)"],["dc.relation.eventlocation","Chicago, IL"],["dc.relation.issn","0732-183X"],["dc.title","High-dose chemotherapy followed by allogeneic stem cell transplantation in high-risk relapsed and refractory aggressive non-Hodgkin lymphoma: Results of a prospective study of the German high-grade non-Hodgkin lymphoma study group."],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Blood"],["dc.bibliographiccitation.volume","108"],["dc.contributor.author","Hasenkamp, Justin"],["dc.contributor.author","Borgerding, Andrea"],["dc.contributor.author","Chapuy, Björn"],["dc.contributor.author","Wulf, Gerald"],["dc.contributor.author","Missal, Inga"],["dc.contributor.author","Jung, Wolfram"],["dc.contributor.author","Truemper, Lorenz H."],["dc.contributor.author","Glass, Bertram"],["dc.date.accessioned","2018-11-07T08:57:59Z"],["dc.date.available","2018-11-07T08:57:59Z"],["dc.date.issued","2006"],["dc.format.extent","822A"],["dc.identifier.isi","000242440003693"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/23535"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Soc Hematology"],["dc.publisher.place","Washington"],["dc.relation.conference","48th Annual Meeting of the American-Society-of-Hematology"],["dc.relation.eventlocation","Orlando, FL"],["dc.relation.issn","0006-4971"],["dc.title","Allo-reactive NK cells after HLA-matched allogeneic hematopoietic stem cell transplantation."],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","444"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Scandinavian Journal of Immunology"],["dc.bibliographiccitation.lastpage","449"],["dc.bibliographiccitation.volume","64"],["dc.contributor.author","Hasenkamp, J."],["dc.contributor.author","Borgerding, Andrea"],["dc.contributor.author","Wulf, Gerald"],["dc.contributor.author","Uhrberg, Markus"],["dc.contributor.author","Jung, Werner"],["dc.contributor.author","Dingeldein, S."],["dc.contributor.author","Truemper, Lorenz H."],["dc.contributor.author","Glass, Bertram"],["dc.date.accessioned","2018-11-07T09:14:01Z"],["dc.date.available","2018-11-07T09:14:01Z"],["dc.date.issued","2006"],["dc.description.abstract","Target cell resistance against natural killer (NK) cell-mediated cytotoxicity obstructs NK cell-based immunotherapy of leukaemia. Several mechanisms of resistance have been described. Because of lack of simple assays for analysing these mechanisms, their relative impact on a given effector-target pair is mostly unknown. We here analysed the combination of the Granzyme B (GrB) enzyme-linked immunospot assay (ELISPOT) for the assessment of NK cell reactivity and cytotoxicity assays to estimate target cell escape mechanisms. Target cell recognition failure leads to negative GrB ELISPOT results, whereas target cell resistance shows positive GrB ELISPOT results in the absence of cytotoxicity. We confronted NK cells with the sensitive target cell line K562, and with the resistant cell lines ML2, SupB15 and Raji. ML2 cells sufficiently activated GrB-release whilst being resistant against cytotoxic granules of NK cells. Partial resistance of Raji results from the interaction of HLA class I with inhibitory killer immunglobulin-like receptors (KIR) on the NK cells. Failure of target recognition by HLA class I-KIR interaction, lacking ligands to stimulatory NK cell receptors and partial resistance to cytotoxic granules all contributed to resistance of SupB15. In conclusion, revealing the mechanisms of resistance against NK cell-mediated cytotoxicity may allow improving the results of NK-based immunotherapy."],["dc.identifier.doi","10.1111/j.1365-3083.2006.01803.x"],["dc.identifier.isi","000240529400014"],["dc.identifier.pmid","16970688"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/27303"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation.issn","0300-9475"],["dc.title","Resistance against natural killer cell cytotoxicity: Analysis of mechanisms"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","877"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Bone Marrow Transplantation"],["dc.bibliographiccitation.lastpage","884"],["dc.bibliographiccitation.volume","54"],["dc.contributor.author","Wulf, Gerald"],["dc.contributor.author","Hasenkamp, Justin"],["dc.contributor.author","Jung, Wolfram"],["dc.contributor.author","Wilhelm, Christian"],["dc.contributor.author","Held, Gerhard"],["dc.contributor.author","Nickelsen, Maike"],["dc.contributor.author","Leha, Andreas"],["dc.contributor.author","Pfreundschuh, Michael"],["dc.contributor.author","Schmitz, Norbert"],["dc.contributor.author","Trümper, Lorenz"],["dc.contributor.author","Glass, Bertram"],["dc.date.accessioned","2020-12-10T18:09:41Z"],["dc.date.available","2020-12-10T18:09:41Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1038/s41409-018-0360-9"],["dc.identifier.eissn","1476-5365"],["dc.identifier.issn","0268-3369"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/73726"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Allogeneic stem cell transplantation for patients with relapsed or refractory T-cell lymphoma: efficacy of lymphoma-directed conditioning against advanced disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]