Hasenkamp, Justin

[["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","341"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Annals of Hematology"],["dc.bibliographiccitation.lastpage","348"],["dc.bibliographiccitation.volume","89"],["dc.contributor.author","Hasenkamp, Justin"],["dc.contributor.author","Borgerding, Andrea"],["dc.contributor.author","Wulf, Gerald"],["dc.contributor.author","Schmitz, Norbert"],["dc.contributor.author","Truemper, Lorenz H."],["dc.contributor.author","Glass, Bertram"],["dc.date.accessioned","2018-11-07T08:44:18Z"],["dc.date.available","2018-11-07T08:44:18Z"],["dc.date.issued","2010"],["dc.description.abstract","Natural killer (NK) cells contribute to the graft-versus-leukemia effect after allogeneic stem cell transplantation. However, the efficacy of NK cell-mediated tumor cell lysis is limited due to target cell resistance, and target cell-induced apoptosis (TiA) was proposed to contribute to differences in susceptibility to NK cells. Here we analyzed the effects of target cells on the apoptosis of cytokine-activated NK cells in vitro. We found no association of target cell susceptibility and TiA of NK cells in an array of human and murine target-effector cell combinations. Incubation of NK cells with caspase inhibitors blocked TiA incompletely, indicating that TiA is partly based on caspase-independent mechanisms. Modulating NK cell susceptibility against TiA by caspase inhibition did not influence cytotoxic efficacy. Furthermore, we found cytotoxic potential of NK cells to be markedly decreased following first target cell contact. Exhaustion of NK cell activity by first target cell contact was, however, not mediated by TiA. In addition, we found no relevant TiA by lymphoma cell lines against activated murine NK cells. We conclude that TiA represents only a minor factor of target cell resistance against NK cell-mediated cytolysis."],["dc.description.sponsorship","Deutsche Krebshilfe"],["dc.identifier.doi","10.1007/s00277-009-0844-1"],["dc.identifier.isi","000274685400002"],["dc.identifier.pmid","19823823"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?goescholar/4146"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/20165"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0939-5555"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Relevance of target cell-induced apoptosis as mechanism of resistance against natural killer cells"],["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","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.firstpage","283"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Annals of Hematology"],["dc.bibliographiccitation.lastpage","289"],["dc.bibliographiccitation.volume","89"],["dc.contributor.author","Borgerding, Andrea"],["dc.contributor.author","Hasenkamp, Justin"],["dc.contributor.author","Glass, Bertram"],["dc.contributor.author","Wulf, Gerald"],["dc.contributor.author","Truemper, Lorenz H."],["dc.date.accessioned","2018-11-07T08:45:09Z"],["dc.date.available","2018-11-07T08:45:09Z"],["dc.date.issued","2010"],["dc.description.abstract","Neither effective salvage regimens nor the outcome and response to retherapy with rituximab containing chemotherapy have been defined for rituximab pre-treated patients with relapsing aggressive lymphoma. We report here a single-centre retrospective outcome analysis of second-line immunochemotherapy with rituximab. In 28 patients with relapsed or refractory diffuse large B cell lymphomas, first-line immunochemotherapy had induced objective responses in 18 patients. Nine of 28 patients responded to rituximab containing salvage therapy, leading to a median overall survival of 243 days after start of second immunochemotherapy. Long-term disease free survivors (1,260 and 949 days) were restricted to the group of twelve patients that had received allogeneic stem cell transplantation as consolidation therapy. In 21 patients with relapsed mantle cell lymphomas (MCL), 19 patients had reached remissions with first-line therapy. Of those, 16 patients experienced responses to salvage therapy with a median overall survival of 226 days. Noteworthy, none of patients with initial non-responding disease reached a remission with second immunochemotherapy. Seven patients with MCL stayed free from progression after high-dose therapy with autologous or allogeneic stem cell transplantation in two and five cases, respectively. In summary, responses to repeated immunotherapy with rituximab were observed in approximately one third and two thirds of initially responding patients with aggressive B cell lymphoma and mantle cell lymphoma, respectively, but not in primarily refractory disease. Lasting remissions were achieved only by high-dose chemotherapy with stem cell transplantation."],["dc.identifier.doi","10.1007/s00277-009-0820-9"],["dc.identifier.isi","000273785700007"],["dc.identifier.pmid","19727725"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?goescholar/4030"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/20366"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0939-5555"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Rituximab retherapy in patients with relapsed aggressive B cell and mantle cell lymphoma"],["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.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"]]