Schütz, Ekkehard

[["dc.bibliographiccitation.artnumber","e0154602"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Schuetz, Ekkehard"],["dc.contributor.author","Wehrhahn, Christin"],["dc.contributor.author","Wanjek, Marius"],["dc.contributor.author","Bortfeld, Ralf"],["dc.contributor.author","Wemheuer, Wilhelm E."],["dc.contributor.author","Beck, Julia"],["dc.contributor.author","Brenig, Bertram"],["dc.date.accessioned","2018-11-07T10:15:21Z"],["dc.date.available","2018-11-07T10:15:21Z"],["dc.date.issued","2016"],["dc.description.abstract","Background With the availability of massive SNP data for several economically important cattle breeds, haplotype tests have been performed to identify unknown recessive disorders. A number of so-called lethal haplotypes, have been uncovered in Holstein Friesian cattle and, for at least seven of these, the causative mutations have been identified in candidate genes. However, several lethal haplotypes still remain elusive. Here we report the molecular genetic causes of lethal haplotype 5 (HH5) and cholesterol deficiency (CDH). A targeted enrichment for the known genomic regions, followed by massive parallel sequencing was used to interrogate for causative mutations in a case/control approach. Methods Targeted enrichment for the known genomic regions, followed by massive parallel sequencing was used in a case/control approach. PCRs for the causing mutations were developed and compared to routine imputing in 2,100 (HH5) and 3,100 (CDH) cattle. Results HH5 is caused by a deletion of 138kbp, spanning position 93,233kb to 93,371kb on chromosome 9 (BTA9), harboring only dimethyl-adenosine transferase 1 (TFB1M). The deletion breakpoints are flanked by bovine long interspersed nuclear elements Bov-B (upstream) and L1ME3 (downstream), suggesting a homologous recombination/deletion event. TFB1M di-methylates adenine residues in the hairpin loop at the 3'-end of mitochondrial 12S rRNA, being essential for synthesis and function of the small ribosomal subunit of mitochondria. Homozygous TFB1M(-/-) mice reportedly exhibit embryonal lethality with developmental defects. A 2.8% allelic frequency was determined for the German HF population. CDH results from a 1.3kbp insertion of an endogenous retrovirus (ERV2-1-LTR_BT) into exon 5 of the APOB gene at BTA11: 77,959kb. The insertion is flanked by 6bp target site duplications as described for insertions mediated by retroviral integrases. A premature stop codon in the open reading frame of APOB is generated, resulting in a truncation of the protein to a length of only < 140 amino acids. Such early truncations have been shown to cause an inability of chylomicron excretion from intestinal cells, resulting in malabsorption of cholesterol. The allelic frequency of this mutation in the German HF population was 6.7%, which is substantially higher than reported so far. Compared to PCR assays inferring the genetic variants directly, the routine imputing used so far showed a diagnostic sensitivity of as low as 91% (HH5) and 88% (CDH), with a high specificity for both (>= 99.7%). Conclusion With the availability of direct genetic tests it will now be possible to more effectively reduce the carrier frequency and ultimately eliminate the disorders from the HF populations. Beside this, the fact that repetitive genomic elements (RE) are involved in both diseases, underline the evolutionary importance of RE, which can be detrimental as here, but also advantageous over generations."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2016"],["dc.identifier.doi","10.1371/journal.pone.0154602"],["dc.identifier.isi","000375212600046"],["dc.identifier.pmid","27128314"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13249"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40795"],["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","The Holstein Friesian Lethal Haplotype 5 (HH5) Results from a Complete Deletion of TBF1M and Cholesterol Deficiency (CDH) from an ERV-(LTR) Insertion into the Coding Region of APOB"],["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","549"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Cancer Cell"],["dc.bibliographiccitation.lastpage","+"],["dc.bibliographiccitation.volume","31"],["dc.contributor.author","Mohr, Sebastian"],["dc.contributor.author","Döbele, Carmen"],["dc.contributor.author","Comoglio, Federico"],["dc.contributor.author","Berg, Tobias"],["dc.contributor.author","Beck, Julia"],["dc.contributor.author","Bohnenberger, Hanibal"],["dc.contributor.author","Alexe, Gabriela"],["dc.contributor.author","Corso, Jasmin"],["dc.contributor.author","Ströbel, Philipp"],["dc.contributor.author","Wachter, Astrid"],["dc.contributor.author","Beißbarth, Tim"],["dc.contributor.author","Schnuetgen, Frank"],["dc.contributor.author","Cremer, Anjali"],["dc.contributor.author","Haetscher, Nadine"],["dc.contributor.author","Goellner, Stefanie"],["dc.contributor.author","Rouhi, Arefeh"],["dc.contributor.author","Palmqvist, Lars"],["dc.contributor.author","Rieger, Michael A."],["dc.contributor.author","Schroeder, Timm"],["dc.contributor.author","Boenig, Halvard"],["dc.contributor.author","Meuller-Tidow, Carsten"],["dc.contributor.author","Kuchenbauer, Florian"],["dc.contributor.author","Schuetz, Ekkehard"],["dc.contributor.author","Green, Anthony R."],["dc.contributor.author","Urlaub, Henning"],["dc.contributor.author","Stegmaier, Kimberly"],["dc.contributor.author","Humphries, R. Keith"],["dc.contributor.author","Serve, Hubert"],["dc.contributor.author","Oellerich, Thomas"],["dc.date.accessioned","2018-11-07T10:25:02Z"],["dc.date.available","2018-11-07T10:25:02Z"],["dc.date.issued","2017"],["dc.description.abstract","The transcription factor Meis1 drives myeloid leukemogenesis in the context of Hox gene overexpression but is currently considered undruggable. We therefore investigated whether myeloid progenitor cells transformed by Hoxa9 and Meis1 become addicted to targetable signaling pathways. A comprehensive (phospho) proteomic analysis revealed that Meis1 increased Syk protein expression and activity. Syk upregulation occurs through a Meis1-dependent feedback loop. By dissecting this loop, we show that Syk is a direct target of miR-146a, whose expression is indirectly regulated by Meis1 through the transcription factor PU. 1. In the context of Hoxa9 overexpression, Syk signaling induces Meis1, recapitulating several leukemogenic features of Hoxa9/Meis1-driven leukemia. Finally, Syk inhibition disrupts the identified regulatory loop, prolonging survival of mice with Hoxa9/Meis1-driven leukemia."],["dc.identifier.doi","10.1016/j.ccell.2017.03.001"],["dc.identifier.isi","000398670600010"],["dc.identifier.pmid","28399410"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14438"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42772"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Cell Press"],["dc.relation.issn","1878-3686"],["dc.relation.issn","1535-6108"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Hoxa9 and Meis1 Cooperatively Induce Addiction to Syk Signaling by Suppressing miR-146a in Acute Myeloid Leukemia"],["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","550"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Nucleic Acids Research"],["dc.bibliographiccitation.lastpage","556"],["dc.bibliographiccitation.volume","37"],["dc.contributor.author","Gordon, Paul M. K."],["dc.contributor.author","Schuetz, Ekkehard"],["dc.contributor.author","Beck, Julia"],["dc.contributor.author","Urnovitz, Howard B."],["dc.contributor.author","Graham, Catherine"],["dc.contributor.author","Clark, Renee"],["dc.contributor.author","Dudas, Sandor"],["dc.contributor.author","Czub, Stefanie"],["dc.contributor.author","Sensen, Maria"],["dc.contributor.author","Brenig, Bertram"],["dc.contributor.author","Groschup, Martin H."],["dc.contributor.author","Church, Robert B."],["dc.contributor.author","Sensen, Christoph W."],["dc.date.accessioned","2018-11-07T08:33:15Z"],["dc.date.available","2018-11-07T08:33:15Z"],["dc.date.issued","2009"],["dc.description.abstract","To gain insight into the disease progression of transmissible spongiform encephalopathies (TSE), we searched for disease-specific patterns in circulating nucleic acids (CNA) in elk and cattle. In a 25-month time-course experiment, CNAs were isolated from blood samples of 24 elk (Cervus elaphus) orally challenged with chronic wasting disease (CWD) infectious material. In a separate experiment, blood-sample CNAs from 29 experimental cattle (Bos taurus) 40 months post-inoculation with clinical bovine spongiform encephalopathy (BSE) were analyzed according to the same protocol. Next-generation sequencing provided broad elucidation of sample CNAs: we detected infection-specific sequences as early as 11 months in elk (i.e. at least 3 months before the appearance of the first clinical signs) and we established CNA patterns related to BSE in cattle at least 4 months prior to clinical signs. In elk, a progression of CNA sequence patterns was found to precede and correlate with macro-observable disease progression, including delayed CWD progression in elk with PrP genotype LM. Some of the patterns identified contain transcription-factor-binding sites linked to endogenous retroviral integration. These patterns suggest that retroviruses may be connected to the manifestation of TSEs. Our results may become useful for the early diagnosis of TSE in live elk and cattle."],["dc.identifier.doi","10.1093/nar/gkn963"],["dc.identifier.isi","000262963400031"],["dc.identifier.pmid","19059996"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?goescholar/4005"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/17531"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","0305-1048"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Disease-specific motifs can be identified in circulating nucleic acids from live elk and cattle infected with transmissible spongiform encephalopathies"],["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.artnumber","e75485"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Beck, Julia"],["dc.contributor.author","Hennecke, Silvia"],["dc.contributor.author","Bornemann-Kolatzki, Kirsten"],["dc.contributor.author","Urnovitz, Howard B."],["dc.contributor.author","Neumann, Stephan"],["dc.contributor.author","Stroebel, Philipp"],["dc.contributor.author","Kaup, Franz-Josef"],["dc.contributor.author","Brenig, Bertram"],["dc.contributor.author","Schuetz, Ekkehard"],["dc.date.accessioned","2018-11-07T09:19:45Z"],["dc.date.available","2018-11-07T09:19:45Z"],["dc.date.issued","2013"],["dc.description.abstract","Mammary tumors are the most frequent cancers in female dogs exhibiting a variety of histopathological differences. There is lack of knowledge about the genomes of these common dog tumors. Five tumors of three different histological subtypes were evaluated. Massive parallel sequencing (MPS) was performed in comparison to the respective somatic genome of each animal. Copy number and structural aberrations were validated using droplet digital PCR (ddPCR). Using mate-pair sequencing chromosomal aneuploidies were found in two tumors, frequent smaller deletions were found in one, inter-chromosomal fusions in one other, whereas one tumor was almost normal. These aberrations affect several known cancer associated genes such as cMYC, and KIT. One common deletion of the proximal end of CFA27, harboring the tumor suppressor gene PFDN5 was detected in four tumors. Using ddPCR, this deletion was validated and detected in 50% of tumors (N = 20). Breakpoint specific dPCRs were established for four tumors and tumor specific cell-free DNA (cfDNA) was detected in the plasma. In one animal tumor-specific cfDNA was found >1 year after surgery, attributable to a lung metastasis. Paired-end sequencing proved that copy-number imbalances of the tumor are reflected by the cfDNA. This report on chromosomal instability of canine mammary cancers reveals similarities to human breast cancers as well as special canine alterations. This animal model provides a framework for using MPS for screening for individual cancer biomarkers with cost effective confirmation and monitoring using ddPCR. The possibility exists that ddPCR can be expanded to screening for common cancer related variants."],["dc.identifier.doi","10.1371/journal.pone.0075485"],["dc.identifier.isi","000325423500069"],["dc.identifier.pmid","24098698"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/9419"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/28716"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Public Library Science"],["dc.relation.issn","1932-6203"],["dc.rights","CC BY 2.5"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.5"],["dc.title","Genome Aberrations in Canine Mammary Carcinomas and Their Detection in Cell-Free Plasma DNA"],["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","35379"],["dc.bibliographiccitation.issue","23"],["dc.bibliographiccitation.journal","Oncotarget"],["dc.bibliographiccitation.lastpage","35389"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Liu, Wen"],["dc.contributor.author","Beck, Julia"],["dc.contributor.author","Schmidt, Laura C."],["dc.contributor.author","Roolf, Catrin"],["dc.contributor.author","Pews-Davtyan, Anahit"],["dc.contributor.author","Ruetgen, Barbara C."],["dc.contributor.author","Hammer, Sabine"],["dc.contributor.author","Willenbrock, Saskia"],["dc.contributor.author","Sekora, Anett"],["dc.contributor.author","Rolfs, Arndt"],["dc.contributor.author","Beller, Matthias"],["dc.contributor.author","Brenig, Bertram"],["dc.contributor.author","Nolte, Ingo"],["dc.contributor.author","Junghanss, Christian"],["dc.contributor.author","Schuetz, Ekkehard"],["dc.contributor.author","Escobar, Hugo Murua"],["dc.date.accessioned","2018-11-07T10:12:52Z"],["dc.date.available","2018-11-07T10:12:52Z"],["dc.date.issued","2016"],["dc.description.abstract","Protein kinase inhibitors are widely used in chemotherapeutic cancer regimens. Maleimide derivatives such as SB-216763 act as GSK-3 inhibitor targeting cell proliferation, cell death and cell cycle progression. Herein, the two arylindolylmaleimide derivatives PDA-66 and PDA-377 were evaluated as potential chemotherapeutic agents on canine B-cell lymphoma cell lines. Canine lymphoma represents a naturally occurring model closely resembling the human high-grade non-Hodgkin's lymphoma (NHL). PDA-66 showed more pronounced effects on both cell lines. Application of 2.5 mu M PDA-66 resulted in a significant induction of apoptosis (approx. 11 %), decrease of the metabolic activity (approx. 95 %), anti-proliferative effect (approx. 85 %) and cell death within 48h. Agent induced mode of action was characterized by whole transcriptome sequencing, 12 h and 24 h post-agent exposure. Key PDA-66-modulated pathways identified were cell cycle, DNA replication and p53 signaling. Expression analyses indicated that the drug acting mechanism is mediated through DNA replication and cycle arrest involving the spindle assembly checkpoint. In conclusion, both PDA derivatives displayed strong anti-proliferation activity in canine B-cell lymphoma cells. The cell and molecular PDA-induced effect characterization and the molecular characterization of the agent acting mechanism provides the basis for further evaluation of a potential drug for canine lymphoma serving as model for human NHL."],["dc.description.sponsorship","Chinese Scholarship Council (CSC)"],["dc.identifier.doi","10.18632/oncotarget.9297"],["dc.identifier.isi","000377752100139"],["dc.identifier.pmid","27177088"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14133"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40322"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Impact Journals Llc"],["dc.relation.issn","1949-2553"],["dc.rights.access","openAccess"],["dc.title","Characterization of the novel indolylmaleimides' PDA-66 and PDA-377 effect on canine lymphoma 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.artnumber","e0129208"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Brenig, Bertram"],["dc.contributor.author","Schuetz, Ekkehard"],["dc.contributor.author","Hardt, Michael"],["dc.contributor.author","Scheuermann, Petra"],["dc.contributor.author","Freick, Markus"],["dc.date.accessioned","2018-11-07T09:55:52Z"],["dc.date.available","2018-11-07T09:55:52Z"],["dc.date.issued","2015"],["dc.description.abstract","Aristaless-like homeobox 4 (ALX4) gene is an important transcription regulator in skull and limb development. In humans and mice ALX4 mutations or loss of function result in a number of skeletal and organ malformations, including polydactyly, tibial hemimelia, omphalocele, biparietal foramina, impaired mammary epithelial morphogenesis, alopecia, coronal craniosynostosis, hypertelorism, depressed nasal bridge and ridge, bifid nasal tip, hypogonadism, and body agenesis. Here we show that a complex skeletal malformation of the hind limb in Galloway cattle together with other developmental anomalies is a recessive autosomal disorder most likely caused by a duplication of 20 bp in exon 2 of the bovine ALX4 gene. A second duplication of 34 bp in exon 4 of the same gene has no known effect, although both duplications result in a frameshift and premature stop codon leading to a truncated protein. Genotyping of 1,688 Black/Red/Belted/Riggit Galloway (GA) and 289 White Galloway (WGA) cattle showed that the duplication in exon 2 has allele frequencies of 1% in GA and 6% in WGA and the duplication in exon 4 has frequencies of 23% in GA and 38% in WGA. Both duplications were not detected in 876 randomly selected German Holstein Friesian and 86 cattle of 21 other breeds. Hence, we have identified a candidate causative mutation for tibial hemimelia syndrome in Galloway cattle and selection against this mutation can be used to eliminate the mutant allele from the breed."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2015"],["dc.identifier.doi","10.1371/journal.pone.0129208"],["dc.identifier.isi","000356329900052"],["dc.identifier.pmid","26076463"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/11957"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/36844"],["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","A 20 bp Duplication in Exon 2 of the Aristaless-Like Homeobox 4 Gene (ALX4) Is the Candidate Causative Mutation for Tibial Hemimelia Syndrome in Galloway Cattle"],["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.artnumber","1031894"],["dc.bibliographiccitation.journal","Frontiers in Genetics"],["dc.bibliographiccitation.volume","13"],["dc.contributor.affiliation","Oellerich, Michael; \r\n1\r\nDepartment of Clinical Pharmacology, University Medical Center Göttingen, Göttingen, Germany"],["dc.contributor.affiliation","Budde, Klemens; \r\n2\r\nDepartment of Nephrology and Intensive Care, Charité—Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany"],["dc.contributor.affiliation","Osmanodja, Bilgin; \r\n2\r\nDepartment of Nephrology and Intensive Care, Charité—Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany"],["dc.contributor.affiliation","Bornemann-Kolatzki, Kirsten; \r\n3\r\nChronix Biomedical GmbH, Göttingen, Germany"],["dc.contributor.affiliation","Beck, Julia; \r\n3\r\nChronix Biomedical GmbH, Göttingen, Germany"],["dc.contributor.affiliation","Schütz, Ekkehard; \r\n3\r\nChronix Biomedical GmbH, Göttingen, Germany"],["dc.contributor.affiliation","Walson, Philip D.; \r\n1\r\nDepartment of Clinical Pharmacology, University Medical Center Göttingen, Göttingen, Germany"],["dc.contributor.author","Oellerich, Michael"],["dc.contributor.author","Budde, Klemens"],["dc.contributor.author","Osmanodja, Bilgin"],["dc.contributor.author","Bornemann-Kolatzki, Kirsten"],["dc.contributor.author","Beck, Julia"],["dc.contributor.author","Schütz, Ekkehard"],["dc.contributor.author","Walson, Philip D."],["dc.date.accessioned","2022-12-01T08:31:30Z"],["dc.date.available","2022-12-01T08:31:30Z"],["dc.date.issued","2022"],["dc.date.updated","2022-11-11T13:12:26Z"],["dc.description.abstract","There is a need to improve personalized immunosuppression in organ transplantation to reduce premature graft loss. Biomarkers are needed to better detect rejection, asymptomatic graft injury, and under-immunosuppression. Assessment of minimal necessary exposure to guide tapering and prevent immune activation is also important. There is robust clinical evidence from a large number of published studies supporting the role of dd-cfDNA for monitoring graft integrity and detection or exclusion of rejection. Dd-cfDNA indicates graft cell death without being rejection specific. It can be determined in plasma through droplet digital PCR using preselected SNPs or next generation sequencing. Changes in recipient cfDNA (e.g., by infection) can affect the results of dd-cfDNA fractional determination. This limitation can be overcome using absolute dd-cfDNA quantification. The combination of fractional and absolute determination including total cfDNA is recommended for meaningful interpretation of the results. The value proposition for the patient includes earlier transplant injury detection and intervention, less full blown rejection risk, an alternative to invasive biopsies, and personalized immunosuppression with potential for improved long-term outcome. Transplant physicians benefit from better immunosuppressive guidance and having an alternative when biopsies are refused or contraindicated. Further advantages are improved biopsy interpretation, less trial and error changes in immunosuppression, and less time dealing with complications. The laboratory medicine specialist can provide more effective services. Hospital management and insurance companies could benefit from more cost-effective surveillance of transplant recipients. Potential cost savings would result from fewer biopsies as a result of the tests’ high negative predictive value, fewer re-transplantations, and less organ failure with return to dialysis. A pathway to implementation and metrics is suggested to measure the effectiveness of dd-cfDNA testing."],["dc.identifier.doi","10.3389/fgene.2022.1031894"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/118187"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-621"],["dc.relation.eissn","1664-8021"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0/"],["dc.title","Donor-derived cell-free DNA as a diagnostic tool in transplantation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Scientific Reports"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Taher, Leila"],["dc.contributor.author","Beck, Julia"],["dc.contributor.author","Liu, Wen"],["dc.contributor.author","Roolf, Catrin"],["dc.contributor.author","Soller, Jan T."],["dc.contributor.author","Rütgen, Barbara C."],["dc.contributor.author","Hammer, Sabine E."],["dc.contributor.author","Chodisetti, Murali"],["dc.contributor.author","Sender, Sina"],["dc.contributor.author","Sterenczak, Katharina A."],["dc.contributor.author","Fuellen, Georg"],["dc.contributor.author","Junghanss, Christian"],["dc.contributor.author","Brenig, Bertram"],["dc.contributor.author","Nolte, Ingo"],["dc.contributor.author","Schütz, Ekkehard"],["dc.contributor.author","Murua Escobar, Hugo"],["dc.date.accessioned","2020-12-10T18:10:09Z"],["dc.date.available","2020-12-10T18:10:09Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1038/s41598-018-23207-7"],["dc.identifier.eissn","2045-2322"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15424"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/73867"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0/"],["dc.title","Comparative High-Resolution Transcriptome Sequencing of Lymphoma Cell Lines and de novo Lymphomas Reveals Cell-Line-Specific Pathway Dysregulation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","18"],["dc.bibliographiccitation.journal","BMC Genetics"],["dc.bibliographiccitation.volume","17"],["dc.contributor.author","Brenig, Bertram"],["dc.contributor.author","Schuetz, Ekkehard"],["dc.date.accessioned","2018-11-07T10:19:27Z"],["dc.date.available","2018-11-07T10:19:27Z"],["dc.date.issued","2016"],["dc.description.abstract","Background: Methods for parentage control in cattle have changed since their initial implementation in the late 1950's from blood group typing to more current single nucleotide polymorphism determination. In the early 1990's, 12 microsatellites were selected by the International Society for Animal Genetics based on their informativeness and robustness in a variety of different cattle breeds. Since then this panel is used as standard in cattle herd book breeding and its application is accompanied by recurrent international comparison tests ensuring permanent validity for the most common commercial dairy and beef cattle breeds for example Holstein Friesian, Simmental, Angus, and Hereford. Although, nearly every parentage can be resolved using these microsatellites, cases with very close relatives became an emerging resolution problem during recent years. This is mainly due to an increase of monomorphism and a trend to the fixation of alleles, although no direct selection against their variability was applied. Thus other effects must be presumed resulting in a loss of polymorphism information content, heterozygosity, and exclusion probabilities. Results: To determine changes of allele frequencies and exclusion probabilities, we analyzed the development of these parameters for the 12 microsatellites from 2004 to 2014. One hundred sixty eight thousand recorded Holstein Friesian cattle genotypes were evaluated. During this period certain alleles of nine microsatellites increased significantly (t-values >5). When calculating the exclusion probabilities for 11 microsatellites, reduction was determined for the three situations, i.e. one parent is wrongly identified (p = 0.01), both parents are wrongly identified (p = 0.005), and the genotype of one parent is missing (p = 0.048). With the addition of BM1818 to the marker set in 2009, this development was corrected leading to significant increases in exclusion probabilities. Although, the exclusion probabilities for the three family situations using the 12 microsatellites are >99 %, the clarification of 142 relationships in 40,000 situations where one parent is missing will still be impossible. Twenty-five sires were identified that are responsible for the most significant microsatellite allele increases in the population. The corresponding alleles are mainly associated with milk protein and fat yield, body weight at birth and weaning, as well as somatic cell score, milk fat percentage, and longissimus muscle area. Conclusions: Our data show that most of the microsatellites used for parentage control in cattle show directional changes in allele frequencies consistent with the history of artificial selection in the German Holstein population."],["dc.description.sponsorship","Erxleben Research & Innovation Council [ERIC-BR1959-2014-01]"],["dc.identifier.doi","10.1186/s12863-016-0327-z"],["dc.identifier.isi","000367905500001"],["dc.identifier.pmid","26747197"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12664"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/41661"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Biomed Central Ltd"],["dc.relation.issn","1471-2156"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Recent development of allele frequencies and exclusion probabilities of microsatellites used for parentage control in the German Holstein Friesian cattle population"],["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.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"]]