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.artnumber","144"],["dc.bibliographiccitation.journal","Journal of Translational Medicine"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Grabe, Hans Joergen"],["dc.contributor.author","Assel, Heinrich"],["dc.contributor.author","Bahls, Thomas"],["dc.contributor.author","Doerr, Marcus"],["dc.contributor.author","Endlich, Karlhans"],["dc.contributor.author","Endlich, Nicole"],["dc.contributor.author","Erdmann, Pia"],["dc.contributor.author","Ewert, Ralf"],["dc.contributor.author","Felix, Stephan B."],["dc.contributor.author","Fiene, Beate"],["dc.contributor.author","Fischer, Tobias"],["dc.contributor.author","Flessa, Steffen"],["dc.contributor.author","Friedrich, Nele"],["dc.contributor.author","Gadebusch-Bondio, Mariacarla"],["dc.contributor.author","Salazar, Manuela Gesell"],["dc.contributor.author","Hammer, Elke"],["dc.contributor.author","Haring, Robin"],["dc.contributor.author","Havemann, Christoph"],["dc.contributor.author","Hecker, Michael"],["dc.contributor.author","Hoffmann, Wolfgang"],["dc.contributor.author","Holtfreter, Birte"],["dc.contributor.author","Kacprowski, Tim"],["dc.contributor.author","Klein, Kathleen"],["dc.contributor.author","Kocher, Thomas"],["dc.contributor.author","Kock, Holger"],["dc.contributor.author","Krafczyk, Janina"],["dc.contributor.author","Kuhn, Jana"],["dc.contributor.author","Langanke, Martin"],["dc.contributor.author","Lendeckel, Uwe"],["dc.contributor.author","Lerch, Markus M."],["dc.contributor.author","Lieb, Wolfgang"],["dc.contributor.author","Lorbeer, Roberto"],["dc.contributor.author","Mayerle, Julia"],["dc.contributor.author","Meissner, Konrad"],["dc.contributor.author","Schwabedissen, Henriette E. Meyer zu"],["dc.contributor.author","Nauck, Matthias"],["dc.contributor.author","Ott, Konrad"],["dc.contributor.author","Rathmann, Wolfgang"],["dc.contributor.author","Rettig, Rainer"],["dc.contributor.author","Richardt, Claudia"],["dc.contributor.author","Salje, Karen"],["dc.contributor.author","Schminke, Ulf"],["dc.contributor.author","Schulz, Andrea"],["dc.contributor.author","Schwab, Matthias"],["dc.contributor.author","Siegmund, Werner"],["dc.contributor.author","Stracke, Sylvia"],["dc.contributor.author","Suhre, Karsten"],["dc.contributor.author","Ueffing, Marius"],["dc.contributor.author","Ungerer, Saskia"],["dc.contributor.author","Voelker, Uwe"],["dc.contributor.author","Voelzke, Henry"],["dc.contributor.author","Wallaschofski, Henri"],["dc.contributor.author","Werner, Vivian"],["dc.contributor.author","Zygmunt, Marek T."],["dc.contributor.author","Kroemer, Heyo K."],["dc.date.accessioned","2018-11-07T09:39:59Z"],["dc.date.available","2018-11-07T09:39:59Z"],["dc.date.issued","2014"],["dc.description.abstract","Background: Individualized Medicine aims at providing optimal treatment for an individual patient at a given time based on his specific genetic and molecular characteristics. This requires excellent clinical stratification of patients as well as the availability of genomic data and biomarkers as prerequisites for the development of novel diagnostic tools and therapeutic strategies. The University Medicine Greifswald, Germany, has launched the \"Greifswald Approach to Individualized Medicine\" (GANI_MED) project to address major challenges of Individualized Medicine. Herein, we describe the implementation of the scientific and clinical infrastructure that allows future translation of findings relevant to Individualized Medicine into clinical practice. Methods/design: Clinical patient cohorts (N > 5,000) with an emphasis on metabolic and cardiovascular diseases are being established following a standardized protocol for the assessment of medical history, laboratory biomarkers, and the collection of various biosamples for bio-banking purposes. A multi-omics based biomarker assessment including genome-wide genotyping, transcriptome, metabolome, and proteome analyses complements the multi-level approach of GANI_MED. Comparisons with the general background population as characterized by our Study of Health in Pomerania (SHIP) are performed. A central data management structure has been implemented to capture and integrate all relevant clinical data for research purposes. Ethical research projects on informed consent procedures, reporting of incidental findings, and economic evaluations were launched in parallel."],["dc.identifier.doi","10.1186/1479-5876-12-144"],["dc.identifier.isi","000338469800002"],["dc.identifier.pmid","24886498"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/10153"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/33415"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation.issn","1479-5876"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Cohort profile: Greifswald approach to individualized medicine (GANI_MED)"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","617"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","BMC Cancer"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Oberstadt, Moritz C."],["dc.contributor.author","Bien-Möller, Sandra"],["dc.contributor.author","Weitmann, Kerstin"],["dc.contributor.author","Herzog, Susann"],["dc.contributor.author","Hentschel, Katharina"],["dc.contributor.author","Rimmbach, Christian"],["dc.contributor.author","Vogelgesang, Silke"],["dc.contributor.author","Balz, Ellen"],["dc.contributor.author","Fink, Matthias"],["dc.contributor.author","Michael, Heike"],["dc.contributor.author","Zeden, Jan-Philip"],["dc.contributor.author","Bruckmüller, Henrike"],["dc.contributor.author","Werk, Anneke N."],["dc.contributor.author","Cascorbi, Ingolf"],["dc.contributor.author","Hoffmann, Wolfgang"],["dc.contributor.author","Rosskopf, Dieter"],["dc.contributor.author","Schroeder, Henry W.S."],["dc.contributor.author","Kroemer, Heyo K."],["dc.date.accessioned","2019-07-09T11:39:41Z"],["dc.date.available","2019-07-09T11:39:41Z"],["dc.date.issued","2013"],["dc.description.abstract","Background Resistance of the highly aggressive glioblastoma multiforme (GBM) to drug therapy is a major clinical problem resulting in a poor patient’s prognosis. Beside promoter methylation of the O 6 -methylguanine-DNA-methyltransferase (MGMT) gene the efflux transporters ABCB1 and ABCG2 have been suggested as pivotal factors contributing to drug resistance, but the methylation of ABCB1 and ABCG2 has not been assessed before in GBM. Methods Therefore, we evaluated the proportion and prognostic significance of promoter methylation of MGMT, ABCB1 and ABCG2 in 64 GBM patient samples using pyrosequencing technology. Further, the single nucleotide polymorphisms MGMT C-56 T (rs16906252), ABCB1 C3435T (rs1045642) and ABCG2 C421A (rs2231142) were determined using the restriction fragment length polymorphism method (RFLP). To study a correlation between promoter methylation and gene expression, we analyzed MGMT, ABCB1 and ABCG2 expression in 20 glioblastoma and 7 non-neoplastic brain samples. Results Despite a significantly increased MGMT and ABCB1 promoter methylation in GBM tissue, multivariate regression analysis revealed no significant association between overall survival of glioblastoma patients and MGMT or ABCB1 promoter methylation. However, a significant negative correlation between promoter methylation and expression could be identified for MGMT but not for ABCB1 and ABCG2. Furthermore, MGMT promoter methylation was significantly associated with the genotypes of the MGMT C-56 T polymorphism showing a higher methylation level in the T allele bearing GBM. Conclusions In summary, the data of this study confirm the previous published relation of MGMT promoter methylation and gene expression, but argue for no pivotal role of MGMT, ABCB1 and ABCG2 promoter methylation in GBM patients’ survival."],["dc.identifier.doi","10.1186/1471-2407-13-617"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/10052"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58024"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY 2.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.0"],["dc.title","Epigenetic modulation of the drug resistance genes MGMT, ABCB1 and ABCG2 in glioblastoma multiforme"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["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"]]