Tiburcy, Malte

[["dc.bibliographiccitation.firstpage","219"],["dc.bibliographiccitation.lastpage","239"],["dc.contributor.author","Fujita, Buntaro"],["dc.contributor.author","Tiburcy, Malte"],["dc.contributor.author","Ensminger, Stephan"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.editor","Ieda, Masaki"],["dc.contributor.editor","Zimmermann, Wolfram-Hubertus"],["dc.date.accessioned","2019-02-27T13:40:08Z"],["dc.date.available","2019-02-27T13:40:08Z"],["dc.date.issued","2017"],["dc.description.abstract","Heart muscle restoration with in vitro engineered tissue constructs is an exciting and rapidly advancing field. Feasibility, safety, and efficacy data have been obtained in animal models. First clinical trials are on the way to explore the therapeutic utility of cell-free and non-contractile cell-containing grafts. Engineering of contractile patches according to current good manufacturing practice (cGMP) for bona fide myocardial re-muscularization and scalability to address clinical demands remains challenging. Proof-of-concept for solutions to address obvious technical hurdles exists, and it can be anticipated that the first generation of clinically applicable engineered heart muscle (EHM) grafts will become available in the near future. Foreseeable, but likely manageable risks include arrhythmia induction and teratoma formation. Remaining biomedical challenges pertain to the requirement of immune suppression and the strategic approach to optimize immune suppression without subjecting the target patient population to an unacceptable risk. This chapter summarizes the current state of tissue-engineered heart repair with a special emphasis on knowledge gained from in vitro and in vivo studies as well as issues pertaining to transplant immunology and cGMP process development."],["dc.identifier.doi","10.1007/978-3-319-56106-6_10"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/57646"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/185"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.publisher","Springer"],["dc.publisher.place","Cham, Switzerland"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | C04: Fibroblasten-Kardiomyozyten Interaktion im gesunden und erkrankten Herzen: Mechanismen und therapeutische Interventionen bei Kardiofibroblastopathien"],["dc.relation.crisseries","Cardiac and Vascular Biology"],["dc.relation.doi","10.1007/978-3-319-56106-6"],["dc.relation.isbn","978-3-319-56104-2"],["dc.relation.isbn","978-3-319-56106-6"],["dc.relation.ispartof","Cardiac Regeneration"],["dc.relation.ispartofseries","Cardiac and Vascular Biology"],["dc.relation.issn","2509-7830"],["dc.relation.issn","2509-7849"],["dc.relation.workinggroup","RG Tiburcy (Stem Cell Disease Modeling)"],["dc.relation.workinggroup","RG Zimmermann (Engineered Human Myocardium)"],["dc.title","State-of-the-Art in Tissue-Engineered Heart Repair"],["dc.type","book_chapter"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Acta Physiologica"],["dc.bibliographiccitation.volume","216"],["dc.contributor.author","Jatho, Aline"],["dc.contributor.author","Hartmann, S."],["dc.contributor.author","Kittana, Naim"],["dc.contributor.author","Muegge, F."],["dc.contributor.author","Wuertz, Christina"],["dc.contributor.author","Tiburcy, Malte"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Katschinski, Doerthe Magdalena"],["dc.contributor.author","Lutz, S."],["dc.date.accessioned","2018-11-07T10:17:27Z"],["dc.date.available","2018-11-07T10:17:27Z"],["dc.date.issued","2016"],["dc.identifier.isi","000372285400124"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/41230"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.publisher.place","Hoboken"],["dc.relation.issn","1748-1716"],["dc.relation.issn","1748-1708"],["dc.title","RhoA ambivalently controls prominent myofibroblast characteristics by involving distinct signaling routes"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Naunyn-Schmiedeberg s Archives of Pharmacology"],["dc.bibliographiccitation.volume","389"],["dc.contributor.author","Schlick, S."],["dc.contributor.author","Tiburcy, Malte"],["dc.contributor.author","Zeidler, S."],["dc.contributor.author","Lutz, S."],["dc.contributor.author","Wingender, Edgar"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.date.accessioned","2018-11-07T10:19:01Z"],["dc.date.available","2018-11-07T10:19:01Z"],["dc.date.issued","2016"],["dc.format.extent","S12"],["dc.identifier.isi","000398368200040"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/41573"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","New york"],["dc.relation.conference","82nd Annual Meeting of the German-Society-for-Exerimental-and-Clinical-Pharmacology-and-Toxicology (DGPT) / 18th Annual Meeting of the Network-Clinical-Pharmacology-Germany (VKliPha)"],["dc.relation.eventlocation","Berlin, GERMANY"],["dc.relation.issn","1432-1912"],["dc.relation.issn","0028-1298"],["dc.title","Hyaluronic acid deposition determines engineered heart muscle characteristics and can be pharmacologically targeted to enhance function"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","435"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Future Cardiology"],["dc.bibliographiccitation.lastpage","445"],["dc.bibliographiccitation.volume","3"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Tiburcy, Malte"],["dc.contributor.author","Eschenhagen, Thomas"],["dc.date.accessioned","2017-09-07T11:54:28Z"],["dc.date.available","2017-09-07T11:54:28Z"],["dc.date.issued","2011"],["dc.description.abstract","Engineered myocardium may be used to repair myocardial defects. Although not clinically applicable yet, initial studies in rodents have demonstrated the feasibility of tissue engineering based myocardial repair in vivo. In order for restorative treatment to evolve into a functional treatment modality, tissue engineers have to generate human myocardium of sufficient size and with relevant contractile function to replace/repair myocardial defects. This requires the identification of a scalable and ideally autologous cardiomyocyte source as well as the development of strategies to overcome size limitations. We will further address pivotal issues pertaining to the allocation of suitable human cells for myocardial tissue engineering and discuss the translation of present myocardial tissue engineering concepts into preclinical, as well as clinical, trials."],["dc.identifier.doi","10.2217/14796678.3.4.435"],["dc.identifier.gro","3145184"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/2892"],["dc.language.iso","en"],["dc.notes.intern","Crossref Import"],["dc.notes.status","final"],["dc.relation.issn","1479-6678"],["dc.title","Cardiac tissue engineering: a clinical perspective"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Naunyn-Schmiedeberg s Archives of Pharmacology"],["dc.bibliographiccitation.volume","387"],["dc.contributor.author","Tiburcy, Malte"],["dc.contributor.author","Engel, Guenther"],["dc.contributor.author","Sanders, Sonka-Johanna"],["dc.contributor.author","Sowa, Thomas"],["dc.contributor.author","Maier, Lars S."],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.date.accessioned","2018-11-07T09:44:51Z"],["dc.date.available","2018-11-07T09:44:51Z"],["dc.date.issued","2014"],["dc.format.extent","S20"],["dc.identifier.isi","000359538500077"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/34487"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","New york"],["dc.relation.eventlocation","Hannover, GERMANY"],["dc.relation.issn","1432-1912"],["dc.relation.issn","0028-1298"],["dc.title","Ryanodine receptor calcium leak contributes to statin-induced myopathy"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","145"],["dc.bibliographiccitation.journal","Acta Biomaterialia"],["dc.bibliographiccitation.lastpage","159"],["dc.bibliographiccitation.volume","92"],["dc.contributor.author","Goldfracht, Idit"],["dc.contributor.author","Efraim, Yael"],["dc.contributor.author","Shinnawi, Rami"],["dc.contributor.author","Kovalev, Ekaterina"],["dc.contributor.author","Huber, Irit"],["dc.contributor.author","Gepstein, Amira"],["dc.contributor.author","Arbel, Gil"],["dc.contributor.author","Shaheen, Naim"],["dc.contributor.author","Tiburcy, Malte"],["dc.contributor.author","Gepstein, Lior"],["dc.date.accessioned","2021-06-01T10:49:23Z"],["dc.date.available","2021-06-01T10:49:23Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1016/j.actbio.2019.05.016"],["dc.identifier.pmid","31075518"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/86273"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/266"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | C04: Fibroblasten-Kardiomyozyten Interaktion im gesunden und erkrankten Herzen: Mechanismen und therapeutische Interventionen bei Kardiofibroblastopathien"],["dc.relation","SFB 1002 | S01: In vivo und in vitro Krankheitsmodelle"],["dc.relation.issn","1742-7061"],["dc.relation.workinggroup","RG Tiburcy (Stem Cell Disease Modeling)"],["dc.relation.workinggroup","RG Zimmermann (Engineered Human Myocardium)"],["dc.title","Engineered heart tissue models from hiPSC-derived cardiomyocytes and cardiac ECM for disease modeling and drug testing applications"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","8391"],["dc.bibliographiccitation.journal","Nature Communications"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Sharma, Parveen"],["dc.contributor.author","Abbasi, Cynthia"],["dc.contributor.author","Lazic, Savo"],["dc.contributor.author","Teng, Allen C. T."],["dc.contributor.author","Wang, Dingyan"],["dc.contributor.author","Dubois, Nicole"],["dc.contributor.author","Ignatchenko, Vladimir"],["dc.contributor.author","Wong, Victoria"],["dc.contributor.author","Liu, Jun"],["dc.contributor.author","Araki, Toshiyuki"],["dc.contributor.author","Tiburcy, Malte"],["dc.contributor.author","Ackerley, Cameron"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Hamilton, Robert"],["dc.contributor.author","Sun, Yu"],["dc.contributor.author","Liu, Peter P."],["dc.contributor.author","Keller, Gordon"],["dc.contributor.author","Stagljar, Igor"],["dc.contributor.author","Scott, Ian C."],["dc.contributor.author","Kislinger, Thomas"],["dc.contributor.author","Gramolini, Anthony O."],["dc.date.accessioned","2017-09-07T11:43:34Z"],["dc.date.available","2017-09-07T11:43:34Z"],["dc.date.issued","2015"],["dc.description.abstract","Membrane proteins are crucial to heart function and development. Here we combine cationic silica-bead coating with shotgun proteomics to enrich for and identify plasma membrane-associated proteins from primary mouse neonatal and human fetal ventricular cardiomyocytes. We identify Tmem65 as a cardiac-enriched, intercalated disc protein that increases during development in both mouse and human hearts. Functional analysis of Tmem65 both in vitro using lentiviral shRNA-mediated knockdown in mouse cardiomyocytes and in vivo using morpholino-based knockdown in zebrafish show marked alterations in gap junction function and cardiac morphology. Molecular analyses suggest that Tmem65 interaction with connexin 43 (Cx43) is required for correct localization of Cx43 to the intercalated disc, since Tmem65 deletion results in marked internalization of Cx43, a shorter half-life through increased degradation, and loss of Cx43 function. Our data demonstrate that the membrane protein Tmem65 is an intercalated disc protein that interacts with and functionally regulates ventricular Cx43."],["dc.identifier.doi","10.1038/ncomms9391"],["dc.identifier.gro","3141832"],["dc.identifier.isi","000363137100006"],["dc.identifier.pmid","26403541"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1568"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/94"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | C04: Fibroblasten-Kardiomyozyten Interaktion im gesunden und erkrankten Herzen: Mechanismen und therapeutische Interventionen bei Kardiofibroblastopathien"],["dc.relation.issn","2041-1723"],["dc.relation.workinggroup","RG Tiburcy (Stem Cell Disease Modeling)"],["dc.relation.workinggroup","RG Zimmermann (Engineered Human Myocardium)"],["dc.title","Evolutionarily conserved intercalated disc protein Tmem65 regulates cardiac conduction and connexin 43 function"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","79"],["dc.bibliographiccitation.journal","Acta Physiologica"],["dc.bibliographiccitation.lastpage","80"],["dc.bibliographiccitation.volume","213"],["dc.contributor.author","Vogler, Melanie"],["dc.contributor.author","Zieseniss, Anke"],["dc.contributor.author","Hesse, Amke Rena"],["dc.contributor.author","Levent, Elif"],["dc.contributor.author","Tiburcy, Malte"],["dc.contributor.author","Heinze, Eva"],["dc.contributor.author","Burzlaff, Nicolai"],["dc.contributor.author","Schley, Gunnar"],["dc.contributor.author","Eckardt, K. U."],["dc.contributor.author","Willam, Carsten"],["dc.contributor.author","Katschinski, Doerthe Magdalena"],["dc.date.accessioned","2018-11-07T09:59:51Z"],["dc.date.available","2018-11-07T09:59:51Z"],["dc.date.issued","2015"],["dc.identifier.isi","000362554200170"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/37684"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.publisher.place","Hoboken"],["dc.relation.issn","1748-1716"],["dc.relation.issn","1748-1708"],["dc.title","Pre- and post-conditional inhibition of prolyl-4-hydroxylase domain enzymes protects the heart from an ischemic insult"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","39"],["dc.bibliographiccitation.journal","Journal of Molecular and Cellular Cardiology"],["dc.bibliographiccitation.lastpage","54"],["dc.bibliographiccitation.volume","88"],["dc.contributor.author","Ongherth, Anita"],["dc.contributor.author","Pasch, Sebastian"],["dc.contributor.author","Wuertz, Christina M."],["dc.contributor.author","Nowak, Karolin"],["dc.contributor.author","Kittana, Naim"],["dc.contributor.author","Weis, Cleo A."],["dc.contributor.author","Jatho, Aline"],["dc.contributor.author","Vettel, Christiane"],["dc.contributor.author","Tiburcy, Malte"],["dc.contributor.author","Toischer, Karl"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Wieland, Thomas"],["dc.contributor.author","Lutz, Susanne"],["dc.date.accessioned","2017-09-07T11:43:27Z"],["dc.date.available","2017-09-07T11:43:27Z"],["dc.date.issued","2015"],["dc.description.abstract","Cardiac remodeling, a hallmark of heart disease, is associated with intense auto- and paracrine signaling leading to cardiac fibrosis. We hypothesized that the specific mediator of G(q/11)-dependent RhoA activation p63RhoGEF, which is expressed in cardiac fibroblasts, plays a role in the underlying processes. We could show that p63RhoGEF is up-regulated in mouse hearts subjected to transverse aortic constriction (TAC). In an engineered heart muscle model (EHM), p63RhoGEF expression in cardiac fibroblasts increased resting and twitch tensions, and the dominant negative p63 Delta N decreased both. In an engineered connective tissue model (ECT), p63RhoGEF increased tissue stiffness and its knockdown as well as p63 Delta N reduced stiffness. In 2D cultures of neonatal rat cardiac fibroblasts, p63RhoGEF regulated the angiotensin II (Ang II)-dependent RhoA activation, the activation of the serum response factor, and the expression and secretion of the connective tissue growth factor (CTGF). All these processes were inhibited by the knockdown of p63RhoGEF or by p63 Delta N likely based on their negative influence on the actin cytoskeleton. Moreover, we show that p63RhoGEF also regulates CTGF in engineered tissues and correlates with it in the TAC model. Finally, confocal studies revealed a closely related localization of p63RhoGEF and CTGF in the trans-Golgi network. (C) 2015 Published by Elsevier Ltd."],["dc.identifier.doi","10.1016/j.yjmcc.2015.09.009"],["dc.identifier.gro","3141795"],["dc.identifier.isi","000365059300004"],["dc.identifier.pmid","26392029"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1157"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/117"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | C02: RhoGTPasen und ihre Bedeutung für die Last-abhängige Myokardfibrose"],["dc.relation","SFB 1002 | C04: Fibroblasten-Kardiomyozyten Interaktion im gesunden und erkrankten Herzen: Mechanismen und therapeutische Interventionen bei Kardiofibroblastopathien"],["dc.relation.eissn","1095-8584"],["dc.relation.issn","0022-2828"],["dc.relation.workinggroup","RG Hasenfuß (Transition zur Herzinsuffizienz)"],["dc.relation.workinggroup","RG Lutz (G Protein-Coupled Receptor Mediated Signaling)"],["dc.relation.workinggroup","RG Tiburcy (Stem Cell Disease Modeling)"],["dc.relation.workinggroup","RG Toischer (Kardiales Remodeling)"],["dc.relation.workinggroup","RG Zimmermann (Engineered Human Myocardium)"],["dc.title","p63RhoGEF regulates auto- and paracrine signaling in cardiac fibroblasts"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","13"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Basic Research in Cardiology"],["dc.bibliographiccitation.volume","117"],["dc.contributor.author","Haupt, Luis Peter"],["dc.contributor.author","Rebs, Sabine"],["dc.contributor.author","Maurer, Wiebke"],["dc.contributor.author","Hübscher, Daniela"],["dc.contributor.author","Tiburcy, Malte"],["dc.contributor.author","Pabel, Steffen"],["dc.contributor.author","Maus, Andreas"],["dc.contributor.author","Köhne, Steffen"],["dc.contributor.author","Tappu, Rewati"],["dc.contributor.author","Haas, Jan"],["dc.contributor.author","Streckfuss-Bömeke, Katrin"],["dc.date.accessioned","2022-04-01T10:01:09Z"],["dc.date.available","2022-04-01T10:01:09Z"],["dc.date.issued","2022"],["dc.description.abstract","Abstract Cancer therapies with anthracyclines have been shown to induce cardiovascular complications. The aims of this study were to establish an in vitro induced pluripotent stem cell model (iPSC) of anthracycline-induced cardiotoxicity (ACT) from patients with an aggressive form of B-cell lymphoma and to examine whether doxorubicin (DOX)-treated ACT-iPSC cardiomyocytes (CM) can recapitulate the clinical features exhibited by patients, and thus help uncover a DOX-dependent pathomechanism. ACT-iPSC CM generated from individuals with CD20 + B-cell lymphoma who had received high doses of DOX and suffered cardiac dysfunction were studied and compared to control-iPSC CM from cancer survivors without cardiac symptoms. In cellular studies, ACT-iPSC CM were persistently more susceptible to DOX toxicity including augmented disorganized myofilament structure, changed mitochondrial shape, and increased apoptotic events. Consistently, ACT-iPSC CM and cardiac fibroblasts isolated from fibrotic human ACT myocardium exhibited higher DOX-dependent reactive oxygen species. In functional studies, Ca 2+ transient amplitude of ACT-iPSC CM was reduced compared to control cells, and diastolic sarcoplasmic reticulum Ca 2+ leak was DOX-dependently increased. This could be explained by overactive CaMKIIδ in ACT CM. Together with DOX-dependent augmented proarrhythmic cellular triggers and prolonged action potentials in ACT CM, this suggests a cellular link to arrhythmogenic events and contractile dysfunction especially found in ACT engineered human myocardium. CamKIIδ inhibition prevented proarrhythmic triggers in ACT. In contrast, control CM upregulated SERCA2a expression in a DOX-dependent manner, possibly to avoid heart failure conditions. In conclusion, we developed the first human patient-specific stem cell model of DOX-induced cardiac dysfunction from patients with B-cell lymphoma. Our results suggest that DOX-induced stress resulted in arrhythmogenic events associated with contractile dysfunction and finally in heart failure after persistent stress activation in ACT patients."],["dc.identifier.doi","10.1007/s00395-022-00918-7"],["dc.identifier.pii","918"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/105613"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-530"],["dc.relation.eissn","1435-1803"],["dc.relation.issn","0300-8428"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Doxorubicin induces cardiotoxicity in a pluripotent stem cell model of aggressive B cell lymphoma cancer patients"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]