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Reuter-Jessen, Kirsten
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Reuter-Jessen, Kirsten
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Reuter-Jessen, Kirsten
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Reuter-Jessen, K.
Reuter, Kirsten
Reuter, K.
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2017Journal Article [["dc.bibliographiccitation.firstpage","270"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Oncology"],["dc.bibliographiccitation.lastpage","278"],["dc.bibliographiccitation.volume","93"],["dc.contributor.author","Overbeck, Tobias R."],["dc.contributor.author","Arnemann, Johanna"],["dc.contributor.author","Waldmann-Beushausen, Regina"],["dc.contributor.author","Schöndube, Friedrich A."],["dc.contributor.author","Reuter-Jessen, Kirsten"],["dc.contributor.author","Danner, Bernhard C."],["dc.contributor.author","Trümper, Lorenz"],["dc.date.accessioned","2019-01-29T11:57:51Z"],["dc.date.available","2019-01-29T11:57:51Z"],["dc.date.issued","2017"],["dc.description.abstract","ATP-binding cassette transport protein A3 (ABCA3) is expressed in non-small cell lung cancer (NSCLC). We hypothesize that high-level ABCA3 expression may have a negative prognostic impact in patients with NSCLC."],["dc.identifier.doi","10.1159/000477619"],["dc.identifier.pmid","28683465"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/57421"],["dc.language.iso","en"],["dc.notes.intern","DeepGreen Import"],["dc.notes.status","final"],["dc.publisher","S. Karger AG"],["dc.relation.eissn","1423-0232"],["dc.relation.issn","0030-2414"],["dc.rights","https://www.karger.com/Services/SiteLicenses"],["dc.title","ABCA3 Phenotype in Non-Small Cell Lung Cancer Indicates Poor Outcome"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]Details DOI PMID PMC2014Journal Article Research Paper [["dc.bibliographiccitation.firstpage","591"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","The Journal of Cell Biology"],["dc.bibliographiccitation.lastpage","606"],["dc.bibliographiccitation.volume","205"],["dc.contributor.author","Revelo, Natalia H."],["dc.contributor.author","Kamin, Dirk"],["dc.contributor.author","Truckenbrodt, Sven"],["dc.contributor.author","Wong, Aaron B."],["dc.contributor.author","Reuter-Jessen, Kirsten"],["dc.contributor.author","Reisinger, Ellen"],["dc.contributor.author","Moser, Tobias"],["dc.contributor.author","Rizzoli, S. O."],["dc.date.accessioned","2017-09-07T11:46:14Z"],["dc.date.available","2017-09-07T11:46:14Z"],["dc.date.issued","2014"],["dc.description.abstract","The molecular composition of the organelles involved in membrane recycling is difficult to establish as a result of the absence of suitable labeling tools. We introduce in this paper a novel probe, named membrane-binding fluorophore-cysteine-lysine-palmitoyl group (mCLING), which labels the plasma membrane and is taken up during endocytosis. It remains attached to membranes after fixation and permeabilization and can therefore be used in combination with immunostaining and super-resolution microscopy. We applied mCLING to mammalian-cultured cells, yeast, bacteria, primary cultured neurons, Drosophila melanogaster larval neuromuscular junctions, and mammalian tissue. mCLING enabled us to study the molecular composition of different trafficking organelles. We used it to address several questions related to synaptic vesicle recycling in the auditory inner hair cells from the organ of Corti and to investigate molecular differences between synaptic vesicles that recycle actively or spontaneously in cultured neurons. We conclude that mCLING enables the investigation of trafficking membranes in a broad range of preparations."],["dc.identifier.doi","10.1083/jcb.201402066"],["dc.identifier.gro","3142120"],["dc.identifier.isi","000336639000013"],["dc.identifier.pmid","24862576"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/10957"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/4766"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.eissn","1540-8140"],["dc.relation.issn","0021-9525"],["dc.rights","CC BY-NC-SA 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-sa/3.0"],["dc.title","A new probe for super-resolution imaging of membranes elucidates trafficking pathways"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS1996Journal Article [["dc.bibliographiccitation.firstpage","C162"],["dc.bibliographiccitation.issue","a1"],["dc.bibliographiccitation.journal","Acta Crystallographica Section A Foundations of Crystallography"],["dc.bibliographiccitation.lastpage","C163"],["dc.bibliographiccitation.volume","52"],["dc.contributor.author","Romier, C."],["dc.contributor.author","Reuter, K."],["dc.contributor.author","Suck, D."],["dc.contributor.author","Ficner, Ralf"],["dc.date.accessioned","2022-03-01T11:47:05Z"],["dc.date.available","2022-03-01T11:47:05Z"],["dc.date.issued","1996"],["dc.identifier.doi","10.1107/S0108767396092744"],["dc.identifier.pii","S0108767396092744"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/103906"],["dc.notes.intern","DOI-Import GROB-531"],["dc.relation.issn","0108-7673"],["dc.rights.uri","http://journals.iucr.org/services/copyrightpolicy.html"],["dc.title","RNA modification by base exchange: structure of tRNA-guanine transglycosylase"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]Details DOI1996Journal Article [["dc.bibliographiccitation.firstpage","2850"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","The EMBO Journal"],["dc.bibliographiccitation.lastpage","2857"],["dc.bibliographiccitation.volume","15"],["dc.contributor.author","Romier, C."],["dc.contributor.author","Reuter, K."],["dc.contributor.author","Suck, D."],["dc.contributor.author","Ficner, Ralf"],["dc.date.accessioned","2022-03-01T11:46:04Z"],["dc.date.available","2022-03-01T11:46:04Z"],["dc.date.issued","1996"],["dc.identifier.doi","10.1002/j.1460-2075.1996.tb00646.x"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/103550"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-531"],["dc.relation.issn","0261-4189"],["dc.title","Crystal structure of tRNA-guanine transglycosylase: RNA modification by base exchange."],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]Details DOI2017Journal Article [["dc.bibliographiccitation.firstpage","704"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Histopathology"],["dc.bibliographiccitation.lastpage","710"],["dc.bibliographiccitation.volume","70"],["dc.contributor.author","Buerger, Tobias"],["dc.contributor.author","Schaefer, Inga-Marie"],["dc.contributor.author","Kueffer, Stefan"],["dc.contributor.author","Bohnenberger, Hanibal"],["dc.contributor.author","Reuter-Jessen, Kirsten"],["dc.contributor.author","Chan, John Kwok-Cheung"],["dc.contributor.author","Emmert, Alexander"],["dc.contributor.author","Hinterthaner, Marc"],["dc.contributor.author","Marx, Alexander"],["dc.contributor.author","Stroebel, Philipp"],["dc.date.accessioned","2018-11-07T10:25:44Z"],["dc.date.available","2018-11-07T10:25:44Z"],["dc.date.issued","2017"],["dc.description.abstract","AimsThe vast majority of type A thymomas are diagnosed in tumour stages 1 or 2, and metastatic cases are exceedingly rare. The histological and genetic features of such metastatic type A thymomas have not been described in detail. Methods and resultsFive metastatic type A thymomas in tumour stage Masaoka IVb that had been reviewed by a panel of expert pathologists were analysed using comparative genomic hybridization (CGH). Cases 1, 2 and 3 showed the prototypical morphology of type A thymomas with mainly solid growth patterns. These cases displayed only very subtle nuclear irregularities and slight nuclear crowding, but no other atypical features. Mitoses were absent. Cases 3 and 4, in contrast, had a distinctly atypical morphology. CGH revealed partially recurrent alterations in four cases (with and without atypical morphology), including gains on chromosome 1q (one case), 17q (two cases), chromosome 19 (three cases) and 22q (one case) and losses on chromosome 17p (two cases) and 22q (one case). ConclusionRare metastatic type A thymomas, both with typical and atypical' histological features, show partially recurrent genomic alterations that differ from the much more frequent localized and indolent tumours. The fact that these alterations were recurring points to a link between clinical behaviour and molecular features. Our findings may have implications for the management and treatment of such tumours."],["dc.identifier.doi","10.1111/his.13138"],["dc.identifier.isi","000397588600003"],["dc.identifier.pmid","27926794"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42916"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Wiley"],["dc.relation.issn","1365-2559"],["dc.relation.issn","0309-0167"],["dc.title","Metastatic type A thymoma: morphological and genetic correlation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS1997Journal Article [["dc.bibliographiccitation.firstpage","125"],["dc.bibliographiccitation.issue","2-3"],["dc.bibliographiccitation.journal","Medical Microbiology and Immunology"],["dc.bibliographiccitation.lastpage","134"],["dc.bibliographiccitation.volume","186"],["dc.contributor.author","Bereswill, S."],["dc.contributor.author","Faßbinder, F."],["dc.contributor.author","Völzing, C."],["dc.contributor.author","Haas, R."],["dc.contributor.author","Reuter, K."],["dc.contributor.author","Ficner, Ralf"],["dc.contributor.author","Kist, M."],["dc.date.accessioned","2022-03-01T11:44:35Z"],["dc.date.available","2022-03-01T11:44:35Z"],["dc.date.issued","1997"],["dc.identifier.doi","10.1007/s004300050054"],["dc.identifier.pii","71860125.430"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/103060"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-531"],["dc.relation.eissn","1432-1831"],["dc.relation.issn","0300-8584"],["dc.rights.uri","http://www.springer.com/tdm"],["dc.title","Cloning and functional characterization of the genes encoding 3-dehydroquinate synthase (aroB) and tRNA-guanine transglycosylase (tgt) from Helicobacter pylori"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]Details DOI2020Journal Article [["dc.bibliographiccitation.firstpage","603"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Translational Lung Cancer Research"],["dc.bibliographiccitation.lastpage","616"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Overbeck, Tobias Raphael"],["dc.contributor.author","Cron, Dana Alina"],["dc.contributor.author","Schmitz, Katja"],["dc.contributor.author","Rittmeyer, Achim"],["dc.contributor.author","Körber, Wolfgang"],["dc.contributor.author","Hugo, Sara"],["dc.contributor.author","Schnalke, Juliane"],["dc.contributor.author","Lukat, Laura"],["dc.contributor.author","Hugo, Tabea"],["dc.contributor.author","Hinterthaner, Marc"],["dc.contributor.author","Reuter-Jessen, Kirsten"],["dc.contributor.author","Rosenthal, Tessa"],["dc.contributor.author","Moecks, Joachim"],["dc.contributor.author","Bleckmann, Annalen"],["dc.contributor.author","Schildhaus, Hans-Ulrich"],["dc.date.accessioned","2021-04-14T08:25:11Z"],["dc.date.available","2021-04-14T08:25:11Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.21037/tlcr-19-339"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/81546"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","2226-4477"],["dc.relation.issn","2218-6751"],["dc.title","Top-level MET gene copy number gain defines a subtype of poorly differentiated pulmonary adenocarcinomas with poor prognosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]Details DOI2020Journal Article [["dc.bibliographiccitation.firstpage","3574"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","Cancer Medicine"],["dc.bibliographiccitation.lastpage","3583"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Elakad, Omar"],["dc.contributor.author","Lois, Anna‐Maria"],["dc.contributor.author","Schmitz, Katja"],["dc.contributor.author","Yao, Sha"],["dc.contributor.author","Hugo, Sara"],["dc.contributor.author","Lukat, Laura"],["dc.contributor.author","Hinterthaner, Marc"],["dc.contributor.author","Danner, Bernhard C."],["dc.contributor.author","Reuter‐Jessen, Kirsten"],["dc.contributor.author","Schildhaus, Hans‐Ulrich"],["dc.contributor.author","Ströbel, Philipp"],["dc.contributor.author","Bohnenberger, Hanibal"],["dc.contributor.author","von Hammerstein‐Equord, Alexander"],["dc.date.accessioned","2021-04-14T08:26:56Z"],["dc.date.available","2021-04-14T08:26:56Z"],["dc.date.issued","2020"],["dc.description.abstract","Abstract Background Targeting fibroblast growth factor receptor 1 (FGFR1) is a potential treatment for squamous cell lung cancer (SQCLC). So far, treatment decision in clinical studies is based on gene amplification. However, only a minority of patients have shown durable response. Furthermore, former studies have revealed contrasting results regarding the impact of FGFR1 amplification and expression on patient's prognosis. Aims Here, we analyzed prevalence and correlation of FGFR1 gene amplification and protein expression in human lung cancer and their impact on overall survival. Materials \\u0026 Methods FGFR1 gene amplification and protein expression were analyzed by fluorescence in situ hybridization and immunohistochemistry (IHC) in 208 SQCLC and 45 small cell lung cancers (SCLC). Furthermore, FGFR1 protein expression was analyzed in 121 pulmonary adenocarcinomas (ACs). Amplification and expression were correlated to each other, clinicopathological characteristics, and overall survival. Results FGFR1 was amplified in 23% of SQCLC and 8% of SCLC. Amplification was correlated to males (P = .027) but not to overall survival. Specificity of immunostaining was verified by cellular CRISPR/Cas9 FGFR1 knockout. FGFR1 was strongly expressed in 9% of SQCLC, 35% of AC, and 4% of SCLC. Expression was correlated to females (P = .0187) and to the absence of lymph node metastasis in SQCLC (P = .018) with no significant correlation to overall survival. Interestingly, no significant correlation between amplification and expression was detected. Discussion FGFR1 gene amplification does not seem to correlate to protein expression. Conclusion We believe that patient selection for FGFR1 inhibitors in clinical studies should be reconsidered. Neither FGFR1 amplification nor expression influences patient's prognosis."],["dc.description.abstract","Fibroblast growh factor receptor 1 (FGFR1) is considered a potential molecular target in squamous cell lung cancer. However, prevalence of gene amplification as well as correlation to protein overexpression have to be established. Our work has evaluated prevalence and correlation of FGFR1 gene amplification and protein expression in 421 lung cancer patient samples. image"],["dc.description.sponsorship","Deutsche Krebshilfe Foundation"],["dc.description.sponsorship","Else‐Kroener‐Fresenius Foundation"],["dc.description.sponsorship","University Medical Center Goettingen"],["dc.description.sponsorship","Chinese Scholarship Council"],["dc.identifier.doi","10.1002/cam4.2994"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17450"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/82118"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.notes.intern","Merged from goescholar"],["dc.relation.eissn","2045-7634"],["dc.relation.issn","2045-7634"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Fibroblast growth factor receptor 1 gene amplification and protein expression in human lung cancer"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]Details DOI2022Journal Article [["dc.bibliographiccitation.firstpage","95"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Der Onkologe"],["dc.bibliographiccitation.lastpage","99"],["dc.bibliographiccitation.volume","28"],["dc.contributor.author","Reuter-Jessen, Kirsten"],["dc.contributor.author","Ströbel, Philipp"],["dc.date.accessioned","2022-02-01T10:31:55Z"],["dc.date.available","2022-02-01T10:31:55Z"],["dc.date.issued","2022"],["dc.identifier.doi","10.1007/s00761-021-01070-y"],["dc.identifier.pii","1070"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/98978"],["dc.language.iso","de"],["dc.notes.intern","DOI-Import GROB-517"],["dc.relation.eissn","1433-0415"],["dc.relation.issn","0947-8965"],["dc.rights.uri","https://www.springer.com/tdm"],["dc.title","Molekulare Diagnostik in der Pathologie: etablierte Marker und Innovationen"],["dc.title.translated","Molecular diagnostics in pathology: established markers and innovations"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]Details DOI2017Journal Article [["dc.bibliographiccitation.firstpage","1507"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Gastroenterology"],["dc.bibliographiccitation.lastpage","+"],["dc.bibliographiccitation.volume","152"],["dc.contributor.author","Chen, Nai-Ming"],["dc.contributor.author","Neeße, Albrecht"],["dc.contributor.author","Dyck, Moritz Lino"],["dc.contributor.author","Steuber, Benjamin"],["dc.contributor.author","König, Alexander Otto"],["dc.contributor.author","Lubeseder-Martellato, Clara"],["dc.contributor.author","Winter, Thore"],["dc.contributor.author","Forster, Teresa"],["dc.contributor.author","Bohnenberger, Hanibal"],["dc.contributor.author","Kitz, Julia"],["dc.contributor.author","Reuter-Jessen, Kirsten"],["dc.contributor.author","Griesmann, Heidi"],["dc.contributor.author","Gaedcke, Jochen"],["dc.contributor.author","Grade, Marian"],["dc.contributor.author","Zhang, J."],["dc.contributor.author","Tsai, Wan-Chi"],["dc.contributor.author","Siveke, Jens T."],["dc.contributor.author","Schildhaus, Hans-Ulrich"],["dc.contributor.author","Ströbel, Philipp"],["dc.contributor.author","Johnsen, Steven Arthur"],["dc.contributor.author","Ellenrieder, Volker"],["dc.contributor.author","Heßmann, Elisabeth"],["dc.date.accessioned","2018-11-07T10:24:16Z"],["dc.date.available","2018-11-07T10:24:16Z"],["dc.date.issued","2017"],["dc.description.abstract","BACKGROUND & AIMS: The ability of exocrine pancreatic cells to change the cellular phenotype is required for tissue regeneration upon injury, but also contributes to their malignant transformation and tumor progression. We investigated context-dependent signaling and transcription mechanisms that determine pancreatic cell fate decisions toward regeneration and malignancy. In particular, we studied the function and regulation of the inflammatory transcription factor nuclear factor of activated T cells 1 (NFATC1) in pancreatic cell plasticity and tissue adaptation. METHODS: We analyzed cell plasticity during pancreatic regeneration and transformation in mice with pancreas-specific expression of a constitutively active form of NFATC1, or depletion of enhancer of zeste 2 homologue 2 (EZH2), in the context of wild-type or constitutively activate Kras, respectively. Acute and chronic pancreatitis were induced by intraperitoneal injection of caerulein. EZH2-dependent regulation of NFATC1 expression was studied in mouse in human pancreatic tissue and cells by immunohistochemistry, immunoblotting, and quantitative reverse transcription polymerase chain reaction. We used genetic and pharmacologic approaches of EZH2 and NFATC1 inhibition to study the consequences of pathway disruption on pancreatic morphology and function. Epigenetic modifications on the NFATC1 gene were investigated by chromatin immunoprecipitation assays. RESULTS: NFATC1 was rapidly and transiently induced in early adaptation to acinar cell injury in human samples and in mice, where it promoted acinar cell trans-differentiation and blocked proliferation of metaplastic pancreatic cells. However, in late stages of regeneration, Nfatc1 was epigenetically silenced by EZH2-dependent histone methylation, to enable acinar cell redifferentiation and prevent organ atrophy and exocrine insufficiency. In contrast, oncogenic activation of KRAS signaling in pancreatic ductal adenocarcinoma cells reversed the EZH2-dependent effects on the NFATC1 gene and was required for EZH2-mediated transcriptional activation of NFATC1. CONCLUSIONS: In studies of human and mouse pancreatic cells and tissue, we identified context-specific epigenetic regulation of NFATc1 activity as an important mechanism of pancreatic cell plasticity. Inhibitors of EZH2 might therefore interfere with oncogenic activity of NFATC1 and be used in treatment of pancreatic ductal adenocarcinoma."],["dc.identifier.doi","10.1053/j.gastro.2017.01.043"],["dc.identifier.isi","000401811300041"],["dc.identifier.pmid","28188746"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42625"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","W B Saunders Co-elsevier Inc"],["dc.relation.issn","1528-0012"],["dc.relation.issn","0016-5085"],["dc.title","Context-Dependent Epigenetic Regulation of Nuclear Factor of Activated T Cells 1 in Pancreatic Plasticity"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS