Schütz, Ekkehard

[["dc.bibliographiccitation.artnumber","54"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Cancer Cell International"],["dc.bibliographiccitation.volume","22"],["dc.contributor.author","Packeiser, Eva-Maria"],["dc.contributor.author","Taher, Leila"],["dc.contributor.author","Kong, Weibo"],["dc.contributor.author","Ernst, Mathias"],["dc.contributor.author","Beck, Julia"],["dc.contributor.author","Hewicker-Trautwein, Marion"],["dc.contributor.author","Brenig, Bertram"],["dc.contributor.author","Schütz, Ekkehard"],["dc.contributor.author","Murua Escobar, Hugo"],["dc.contributor.author","Nolte, Ingo"],["dc.date.accessioned","2022-04-01T10:03:07Z"],["dc.date.accessioned","2022-08-18T12:37:01Z"],["dc.date.available","2022-04-01T10:03:07Z"],["dc.date.available","2022-08-18T12:37:01Z"],["dc.date.issued","2022-02-02"],["dc.date.updated","2022-07-29T12:17:32Z"],["dc.description.abstract","Abstract\r\n \r\n Background\r\n Canine prostate adenocarcinoma (PAC) and transitional cell carcinoma (TCC) are typically characterized by metastasis and chemoresistance. Cell lines are important model systems for developing new therapeutic strategies. However, as they adapt to culturing conditions and undergo clonal selection, they can diverge from the tissue from which they were originally derived. Therefore, a comprehensive characterization of cell lines and their original tissues is paramount.\r\n \r\n \r\n Methods\r\n This study compared the transcriptomes of nine canine cell lines derived from PAC, PAC metastasis and TCC to their respective original primary tumor or metastasis tissues. Special interests were laid on cell culture-related differences, epithelial to mesenchymal transition (EMT), the prostate and bladder cancer pathways, therapeutic targets in the PI3K-AKT signaling pathway and genes correlated with chemoresistance towards doxorubicin and carboplatin.\r\n \r\n \r\n Results\r\n Independent analyses for PAC, PAC metastasis and TCC revealed 1743, 3941 and 463 genes, respectively, differentially expressed in the cell lines relative to their original tissues (DEGs). While genes associated with tumor microenvironment were mostly downregulated in the cell lines, patient-specific EMT features were conserved. Furthermore, examination of the prostate and bladder cancer pathways revealed extensive concordance between cell lines and tissues. Interestingly, all cell lines preserved downstream PI3K-AKT signaling, but each featured a unique therapeutic target signature. Additionally, resistance towards doxorubicin was associated with G2/M cell cycle transition and cell membrane biosynthesis, while carboplatin resistance correlated with histone, m- and tRNA processing.\r\n \r\n \r\n Conclusion\r\n Comparative whole-transcriptome profiling of cell lines and their original tissues identifies models with conserved therapeutic target expression. Moreover, it is useful for selecting suitable negative controls, i.e., cell lines lacking therapeutic target expression, increasing the transfer efficiency from in vitro to primary neoplasias for new therapeutic protocols. In summary, the dataset presented here constitutes a rich resource for canine prostate and bladder cancer research."],["dc.identifier.citation","Cancer Cell International. 2022 Feb 02;22(1):54"],["dc.identifier.doi","10.1186/s12935-021-02422-9"],["dc.identifier.pii","2422"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/106087"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/112958"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-530"],["dc.publisher","BioMed Central"],["dc.relation.eissn","1475-2867"],["dc.rights.holder","The Author(s)"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject","Prostate cancer"],["dc.subject","Metastasis"],["dc.subject","Bladder cancer"],["dc.subject","TCC"],["dc.subject","Cell line"],["dc.subject","Dog"],["dc.subject","Gene expression"],["dc.subject","In vitro model"],["dc.subject","Targeted therapy"],["dc.title","RNA-seq of nine canine prostate cancer cell lines reveals diverse therapeutic target signatures"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","11481"],["dc.bibliographiccitation.issue","21"],["dc.bibliographiccitation.journal","International Journal of Molecular Sciences"],["dc.bibliographiccitation.volume","22"],["dc.contributor.affiliation","Thiemeyer, Heike; 1Small Animal Clinic, University of Veterinary Medicine Hannover, Foundation, 30559 Hannover, Germany; heike.thiemeyer@icloud.com (H.T.); jan.torben.schille@tiho-hannover.de (J.T.S.); eva-maria.packeiser@tiho-hannover.de (E.-M.P.); lisa.harder@tiho-hannover.de (L.K.H.); ingo.nolte@tiho-hannover.de (I.N.)"],["dc.contributor.affiliation","Taher, Leila; 3Institute of Biomedical Informatics, Graz University of Technology, 8010 Graz, Austria; leila.taher@tugraz.at"],["dc.contributor.affiliation","Schille, Jan Torben; 1Small Animal Clinic, University of Veterinary Medicine Hannover, Foundation, 30559 Hannover, Germany; heike.thiemeyer@icloud.com (H.T.); jan.torben.schille@tiho-hannover.de (J.T.S.); eva-maria.packeiser@tiho-hannover.de (E.-M.P.); lisa.harder@tiho-hannover.de (L.K.H.); ingo.nolte@tiho-hannover.de (I.N.)"],["dc.contributor.affiliation","Packeiser, Eva-Maria; 1Small Animal Clinic, University of Veterinary Medicine Hannover, Foundation, 30559 Hannover, Germany; heike.thiemeyer@icloud.com (H.T.); jan.torben.schille@tiho-hannover.de (J.T.S.); eva-maria.packeiser@tiho-hannover.de (E.-M.P.); lisa.harder@tiho-hannover.de (L.K.H.); ingo.nolte@tiho-hannover.de (I.N.)"],["dc.contributor.affiliation","Harder, Lisa K.; 1Small Animal Clinic, University of Veterinary Medicine Hannover, Foundation, 30559 Hannover, Germany; heike.thiemeyer@icloud.com (H.T.); jan.torben.schille@tiho-hannover.de (J.T.S.); eva-maria.packeiser@tiho-hannover.de (E.-M.P.); lisa.harder@tiho-hannover.de (L.K.H.); ingo.nolte@tiho-hannover.de (I.N.)"],["dc.contributor.affiliation","Hewicker-Trautwein, Marion; 4Institute of Pathology, University of Veterinary Medicine Hannover, Foundation, 30559 Hannover, Germany; marion.hewicker-trautwein@tiho-hannover.de"],["dc.contributor.affiliation","Brenig, Bertram; 5Institute of Veterinary Medicine, University of Göttingen, 37077 Göttingen, Germany; bbrenig@gwdg.de"],["dc.contributor.affiliation","Schütz, Ekkehard; 6Chronix Biomedical GmbH, 37079 Göttingen, Germany; esc@chronixbiomedical.de (E.S.); jbeck@chronixbiomedical.de (J.B.)"],["dc.contributor.affiliation","Beck, Julia; 6Chronix Biomedical GmbH, 37079 Göttingen, Germany; esc@chronixbiomedical.de (E.S.); jbeck@chronixbiomedical.de (J.B.)"],["dc.contributor.affiliation","Nolte, Ingo; 1Small Animal Clinic, University of Veterinary Medicine Hannover, Foundation, 30559 Hannover, Germany; heike.thiemeyer@icloud.com (H.T.); jan.torben.schille@tiho-hannover.de (J.T.S.); eva-maria.packeiser@tiho-hannover.de (E.-M.P.); lisa.harder@tiho-hannover.de (L.K.H.); ingo.nolte@tiho-hannover.de (I.N.)"],["dc.contributor.affiliation","Murua Escobar, Hugo; 1Small Animal Clinic, University of Veterinary Medicine Hannover, Foundation, 30559 Hannover, Germany; heike.thiemeyer@icloud.com (H.T.); jan.torben.schille@tiho-hannover.de (J.T.S.); eva-maria.packeiser@tiho-hannover.de (E.-M.P.); lisa.harder@tiho-hannover.de (L.K.H.); ingo.nolte@tiho-hannover.de (I.N.)"],["dc.contributor.author","Thiemeyer, Heike"],["dc.contributor.author","Taher, Leila"],["dc.contributor.author","Schille, Jan Torben"],["dc.contributor.author","Packeiser, Eva-Maria"],["dc.contributor.author","Harder, Lisa K."],["dc.contributor.author","Hewicker-Trautwein, Marion"],["dc.contributor.author","Brenig, Bertram"],["dc.contributor.author","Schütz, Ekkehard"],["dc.contributor.author","Beck, Julia"],["dc.contributor.author","Nolte, Ingo"],["dc.contributor.author","Murua Escobar, Hugo"],["dc.date.accessioned","2021-12-01T09:22:50Z"],["dc.date.available","2021-12-01T09:22:50Z"],["dc.date.issued","2021"],["dc.date.updated","2022-09-03T23:17:38Z"],["dc.description.abstract","Prostate cancer (PCa) in dogs is a highly malignant disease akin to its human counterpart. In contrast to the situation in humans, multi-gene approaches facilitating risk stratification of canine PCa are barely established. The aims of this study were the characterization of the transcriptional landscape of canine PCa and the identification of diagnostic, prognostic and/or therapeutic biomarkers through a multi-step screening approach. RNA-Sequencing of ten malignant tissues and fine-needle aspirations (FNA), and 14 nonmalignant tissues and FNAs was performed to find differentially expressed genes (DEGs) and deregulated pathways. The 4098 observed DEGs were involved in 49 pathways. These 49 pathways could be grouped into five superpathways summarizing the hallmarks of canine PCa: (i) inflammatory response and cytokines; (ii) regulation of the immune system and cell death; (iii) cell surface and PI3K signaling; (iv) cell cycle; and (v) phagosome and autophagy. Among the highly deregulated, moderately to strongly expressed DEGs that were members of one or more superpathways, 169 DEGs were listed in relevant databases and/or the literature and included members of the PCa pathway, oncogenes, prostate-specific genes, and druggable genes. These genes are novel and promising candidate diagnostic, prognostic and/or therapeutic canine PCa biomarkers."],["dc.description.abstract","Prostate cancer (PCa) in dogs is a highly malignant disease akin to its human counterpart. In contrast to the situation in humans, multi-gene approaches facilitating risk stratification of canine PCa are barely established. The aims of this study were the characterization of the transcriptional landscape of canine PCa and the identification of diagnostic, prognostic and/or therapeutic biomarkers through a multi-step screening approach. RNA-Sequencing of ten malignant tissues and fine-needle aspirations (FNA), and 14 nonmalignant tissues and FNAs was performed to find differentially expressed genes (DEGs) and deregulated pathways. The 4098 observed DEGs were involved in 49 pathways. These 49 pathways could be grouped into five superpathways summarizing the hallmarks of canine PCa: (i) inflammatory response and cytokines; (ii) regulation of the immune system and cell death; (iii) cell surface and PI3K signaling; (iv) cell cycle; and (v) phagosome and autophagy. Among the highly deregulated, moderately to strongly expressed DEGs that were members of one or more superpathways, 169 DEGs were listed in relevant databases and/or the literature and included members of the PCa pathway, oncogenes, prostate-specific genes, and druggable genes. These genes are novel and promising candidate diagnostic, prognostic and/or therapeutic canine PCa biomarkers."],["dc.identifier.doi","10.3390/ijms222111481"],["dc.identifier.pii","ijms222111481"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/94494"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-478"],["dc.relation.eissn","1422-0067"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0/"],["dc.title","An RNA-Seq-Based Framework for Characterizing Canine Prostate Cancer and Prioritizing Clinically Relevant Biomarker Candidate Genes"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Scientific Reports"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Granados-Soler, José Luis"],["dc.contributor.author","Bornemann-Kolatzki, Kirsten"],["dc.contributor.author","Beck, Julia"],["dc.contributor.author","Brenig, Bertram"],["dc.contributor.author","Schütz, Ekkehard"],["dc.contributor.author","Betz, Daniela"],["dc.contributor.author","Junginger, Johannes"],["dc.contributor.author","Hewicker-Trautwein, Marion"],["dc.contributor.author","Murua Escobar, Hugo"],["dc.contributor.author","Nolte, Ingo"],["dc.date.accessioned","2021-04-14T08:27:35Z"],["dc.date.available","2021-04-14T08:27:35Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1038/s41598-020-57942-7"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/82340"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","2045-2322"],["dc.title","Analysis of Copy-Number Variations and Feline Mammary Carcinoma Survival"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e0131280"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Hennecke, Silvia"],["dc.contributor.author","Beck, Julia"],["dc.contributor.author","Bornemann-Kolatzki, Kirsten"],["dc.contributor.author","Neumann, Stephan"],["dc.contributor.author","Escobar, Hugo Murua"],["dc.contributor.author","Nolte, Ingo"],["dc.contributor.author","Hammer, Susanne Conradine"],["dc.contributor.author","Hewicker-Trautwein, Marion"],["dc.contributor.author","Junginger, Johannes"],["dc.contributor.author","Kaup, Franz-Josef"],["dc.contributor.author","Brenig, Bertram"],["dc.contributor.author","Schuetz, Ekkehard"],["dc.date.accessioned","2018-11-07T09:55:07Z"],["dc.date.available","2018-11-07T09:55:07Z"],["dc.date.issued","2015"],["dc.description.abstract","Background A somatic deletion at the proximal end of canine chromosome 27 (CFA27) was recently reported in 50% of malignant mammary tumors. This region harbours the tumor suppressor gene prefoldin subunit 5 (PFDN5) and the deletion correlated with a higher Ki-67 score. PFDN5 has been described to repress c-MYC and is, therefore, a candidate tumor-suppressor and cancer-driver gene in canine mammary cancer. Aim of this study was to confirm the recurrent deletion in a larger number of tumors. Methods Droplet digital PCR for PFDN5 was performed in DNA from 102 malignant, 40 benign mammary tumors/dysplasias, 11 non-neoplastic mammary tissues and each corresponding genomic DNA from leukocytes. The copy number of PFDN5 was normalized to a reference amplicon on canine chromosome 32 (CFA32). Z-scores were calculated, based on Gaussian distributed normalized PFDN5 copy numbers of the leukocyte DNA. Z-scores <= -3.0 in tissue were considered as being indicative of the PFDN5 deletion and called as such. The Ki-67 proliferation index was assessed in a subset of 79 tissue samples by immunohistochemistry. Results The deletion was confirmed in 24% of all malignant tumors, detected in only 7.5% of the benign tumors and was not present in any normal mammary tissue sample. The subgroup of solid carcinomas (n = 9) showed the highest frequency of the deletion (67%) and those malignomas without microscopical high fraction of benign tissue (n = 71) had a 32% frequency (p < 0.01 vs. benign samples). The Ki-67 score was found to be significantly higher (p<0.05) in the PFDN5-deleted group compared to malignant tumors without the deletion. Conclusions A somatic deletion of the PFDN5 gene is recurrently present in canine mammary cancer, supporting a potential role in carcinogenesis. The association of this deletion with higher Ki-67 indicates an increased proliferation rate and thus a link to tumor aggressiveness can be hypothesized. The confirmation of earlier results warrants further studies on PFDN5 as cancer-driver gene."],["dc.description.sponsorship","Open-Access Publikationsfonds 2015"],["dc.identifier.doi","10.1371/journal.pone.0131280"],["dc.identifier.isi","000358153000106"],["dc.identifier.pmid","26132936"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12021"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/36681"],["dc.notes","Silvia Hennecke (University of Göttingen) is the submitting author of this article."],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Public Library Science"],["dc.relation.issn","1932-6203"],["dc.rights.access","openAccess"],["dc.title","Prevalence of the Prefoldin Subunit 5 Gene Deletion in Canine Mammary Tumors"],["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"]]