Kroemer, Heyo Klaus

[["dc.bibliographiccitation.firstpage","1069"],["dc.bibliographiccitation.issue","16"],["dc.bibliographiccitation.journal","European Heart Journal"],["dc.bibliographiccitation.lastpage","1077"],["dc.bibliographiccitation.volume","35"],["dc.contributor.author","Meder, Benjamin"],["dc.contributor.author","Rühle, Frank"],["dc.contributor.author","Weis, Tanja"],["dc.contributor.author","Homuth, Georg"],["dc.contributor.author","Keller, Andreas"],["dc.contributor.author","Franke, Jennifer"],["dc.contributor.author","Peil, Barbara"],["dc.contributor.author","Bermejo, Justo Lorenzo"],["dc.contributor.author","Frese, Karen"],["dc.contributor.author","Huge, Andreas"],["dc.contributor.author","Witten, Anika"],["dc.contributor.author","Vogel, Britta"],["dc.contributor.author","Haas, Jan"],["dc.contributor.author","Völker, Uwe"],["dc.contributor.author","Ernst, Florian"],["dc.contributor.author","Teumer, Alexander"],["dc.contributor.author","Ehlermann, Philipp"],["dc.contributor.author","Zugck, Christian"],["dc.contributor.author","Friedrichs, Frauke"],["dc.contributor.author","Kroemer, Heyo"],["dc.contributor.author","Dörr, Marcus"],["dc.contributor.author","Hoffmann, Wolfgang"],["dc.contributor.author","Maisch, Bernhard"],["dc.contributor.author","Pankuweit, Sabine"],["dc.contributor.author","Ruppert, Volker"],["dc.contributor.author","Scheffold, Thomas"],["dc.contributor.author","Kühl, Uwe"],["dc.contributor.author","Schultheiss, Hans-Peter"],["dc.contributor.author","Kreutz, Reinhold"],["dc.contributor.author","Ertl, Georg"],["dc.contributor.author","Angermann, Christiane"],["dc.contributor.author","Charron, Philippe"],["dc.contributor.author","Villard, Eric"],["dc.contributor.author","Gary, Françoise"],["dc.contributor.author","Isnard, Richard"],["dc.contributor.author","Komajda, Michel"],["dc.contributor.author","Lutz, Matthias"],["dc.contributor.author","Meitinger, Thomas"],["dc.contributor.author","Sinner, Moritz F."],["dc.contributor.author","Wichmann, H.-Erich"],["dc.contributor.author","Krawczak, Michael"],["dc.contributor.author","Ivandic, Boris"],["dc.contributor.author","Weichenhan, Dieter"],["dc.contributor.author","Gelbrich, Goetz"],["dc.contributor.author","El-Mokhtari, Nour-Eddine"],["dc.contributor.author","Schreiber, Stefan"],["dc.contributor.author","Felix, Stephan B."],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Pfeufer, Arne"],["dc.contributor.author","Hübner, Norbert"],["dc.contributor.author","Kääb, Stefan"],["dc.contributor.author","Arbustini, Eloisa"],["dc.contributor.author","Rottbauer, Wolfgang"],["dc.contributor.author","Frey, Norbert"],["dc.contributor.author","Stoll, Monika"],["dc.contributor.author","Katus, Hugo A."],["dc.date.accessioned","2017-09-07T11:46:19Z"],["dc.date.available","2017-09-07T11:46:19Z"],["dc.date.issued","2014"],["dc.description.abstract","Aims Dilated cardiomyopathy (DCM) is one of the leading causes for cardiac transplantations and accounts for up to one-third of all heart failure cases. Since extrinsic and monogenic causes explain only a fraction of all cases, common genetic variants are suspected to contribute to the pathogenesis of DCM, its age of onset, and clinical progression. By a large-scale case-control genome-wide association study we aimed here to identify novel genetic risk loci for DCM. Methods and reuslts Applying a three-staged study design, we analysed more than 4100 DCM cases and 7600 controls. We identified and successfully replicated multiple single nucleotide polymorphism on chromosome 6p21. In the combined analysis, the most significant association signal was obtained for rs9262636 (P = 4.90 x 10(-9)) located in HCG22, which could again be replicated in an independent cohort. Taking advantage of expression quantitative trait loci (eQTL) as molecular phenotypes, we identified rs9262636 as an eQTL for several closely located genes encoding class I and class II major histocompatibility complex heavy chain receptors. Conclusion The present study reveals a novel genetic susceptibility locus that clearly underlines the role of genetically driven, inflammatory processes in the pathogenesis of idiopathic DCM."],["dc.identifier.doi","10.1093/eurheartj/eht251"],["dc.identifier.gro","3142146"],["dc.identifier.isi","000335813500015"],["dc.identifier.pmid","23853074"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/5044"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10 / Funder: Bndesministerium fur Bildung und Forschung' (BMBF)"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.eissn","1522-9645"],["dc.relation.issn","0195-668X"],["dc.title","A genome-wide association study identifies 6p21 as novel risk locus for dilated cardiomyopathy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","308"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Nature Reviews Cardiology"],["dc.bibliographiccitation.lastpage","316"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Voelzke, Henry"],["dc.contributor.author","Schmidt, Carsten O."],["dc.contributor.author","Baumeister, Sebastian E."],["dc.contributor.author","Ittermann, Till"],["dc.contributor.author","Fung, Glenn"],["dc.contributor.author","Krafczyk-Korth, Janina"],["dc.contributor.author","Hoffmann, Wolfgang"],["dc.contributor.author","Schwab, Matthias"],["dc.contributor.author","Schwabedissen, Henriette E. Meyer zu"],["dc.contributor.author","Doerr, Marcus"],["dc.contributor.author","Felix, Stephan B."],["dc.contributor.author","Lieb, Wolfgang"],["dc.contributor.author","Kroemer, Heyo K."],["dc.date.accessioned","2018-11-07T09:24:22Z"],["dc.date.available","2018-11-07T09:24:22Z"],["dc.date.issued","2013"],["dc.description.abstract","The primary goals of personalized medicine are to optimize diagnostic and treatment strategies by tailoring them to the specific characteristics of an individual patient. In this Review, we summarize basic concepts and methods of personalizing cardiovascular medicine. In-depth characterization of study participants and patients in general practice using standardized methods is a pivotal component of study design in personalized medicine. Standardization and quality assurance of clinical data are similarly important, but in daily practice imprecise definitions of clinical variables can reduce power and introduce bias, which limits the validity of the data obtained as well as their potential clinical applicability. Changes in statistical methods with personalized medicine include a shift from dichotomous outcomes towards continuously measured variables, predictive modelling, and individualized medical decisions, subgroup analyses, and data-mining strategies. A variety of approaches to personalized medicine exist in cardiovascular research and clinical practice that might have the potential to individualize diagnostic and therapeutic procedures. For some of the emerging methods, such as data mining, the most-efficient way to use these tools is not yet fully understood. In addition, the predictive models-although promising-are far from mature, and are likely to be greatly improved by using available large-scale data sets."],["dc.identifier.doi","10.1038/nrcardio.2013.35"],["dc.identifier.isi","000319441300007"],["dc.identifier.pmid","23528962"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/29806"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","1759-5010"],["dc.relation.issn","1759-5002"],["dc.title","Personalized cardiovascular medicine: concepts and methodological considerations"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","223"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Neuro-Oncology"],["dc.bibliographiccitation.lastpage","242"],["dc.bibliographiccitation.volume","17"],["dc.contributor.author","Herzog, Susann"],["dc.contributor.author","Fink, Matthias Alexander"],["dc.contributor.author","Weitmann, Kerstin"],["dc.contributor.author","Friedel, Claudius"],["dc.contributor.author","Hadlich, Stefan"],["dc.contributor.author","Langner, Sönke"],["dc.contributor.author","Kindermann, Katharina"],["dc.contributor.author","Holm, Tobias"],["dc.contributor.author","Böhm, Andreas"],["dc.contributor.author","Eskilsson, Eskil"],["dc.contributor.author","Miletic, Hrvoje"],["dc.contributor.author","Hildner, Markus"],["dc.contributor.author","Fritsch, Michael"],["dc.contributor.author","Vogelgesang, Silke"],["dc.contributor.author","Havemann, Christoph"],["dc.contributor.author","Ritter, Christoph Alexander"],["dc.contributor.author","Meyer zu Schwabedissen, Henriette Elisabeth"],["dc.contributor.author","Rauch, Bernhard H."],["dc.contributor.author","Hoffmann, Wolfgang"],["dc.contributor.author","Kroemer, Heyo Klaus"],["dc.contributor.author","Schroeder, Henry"],["dc.contributor.author","Bien-Möller, Sandra"],["dc.date.accessioned","2018-08-20T13:35:21Z"],["dc.date.available","2018-08-20T13:35:21Z"],["dc.date.issued","2015"],["dc.description.abstract","BACKGROUND: The current therapy for glioblastoma multiforme (GBM), the most aggressive and common primary brain tumor of adults, involves surgery and a combined radiochemotherapy that controls tumor progression only for a limited time window. Therefore, the identification of new molecular targets is highly necessary. Inhibition of kinases has become a standard of clinical oncology, and thus the oncogenic kinase Pim1 might represent a promising target for improvement of GBM therapy. METHODS: Expression of Pim1 and associated signaling molecules was analyzed in human GBM samples, and the potential role of this kinase in patients' prognosis was evaluated. Furthermore, we analyzed the in vivo role of Pim1 in GBM cell growth in an orthotopic mouse model and examined the consequences of Pim1 inhibition in vitro to clarify underlying pathways. RESULTS: In comparison with normal brain, a strong upregulation of Pim1 was demonstrated in human GBM samples. Notably, patients with short overall survival showed a significantly higher Pim1 expression compared with GBM patients who lived longer than the median. In vitro experiments with GBM cells and analysis of patients' GBM samples suggest that Pim1 regulation is dependent on epidermal growth factor receptor. Furthermore, inhibition of Pim1 resulted in reduced cell viability accompanied by decreased cell numbers and increased apoptotic cells, as seen by elevated subG1 cell contents and caspase-3 and -9 activation, as well as modulation of several cell cycle or apoptosis regulatory proteins. CONCLUSIONS: Altogether, Pim1 could be a novel therapeutic target, which should be further analyzed to improve the outcome of patients with aggressive GBM."],["dc.identifier.doi","10.1093/neuonc/nou216"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/15446"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.eissn","1522-8517"],["dc.title","Pim1 kinase is upregulated in glioblastoma multiforme and mediates tumor cell survival"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]