Reuter-Jessen, Kirsten

[["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"]]

[["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"]]

[["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"]]

[["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","JCO Precision Oncology"],["dc.bibliographiccitation.lastpage","7"],["dc.contributor.author","Hamacher, Rainer"],["dc.contributor.author","Kämpfe, Dietrich"],["dc.contributor.author","Reuter-Jessen, Kirsten"],["dc.contributor.author","Pöttgen, Christoph"],["dc.contributor.author","Podleska, Lars E."],["dc.contributor.author","Farzaliyev, Farhad"],["dc.contributor.author","Steinau, Hans-Ulrich"],["dc.contributor.author","Schuler, Martin"],["dc.contributor.author","Schildhaus, Hans-Ulrich"],["dc.contributor.author","Bauer, Sebastian"],["dc.date.accessioned","2020-12-10T18:41:38Z"],["dc.date.available","2020-12-10T18:41:38Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1200/PO.17.00107"],["dc.identifier.eissn","2473-4284"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77634"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Dramatic Response of a PD-L1–Positive Advanced Angiosarcoma of the Scalp to Pembrolizumab"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","e0239806"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","PLoS One"],["dc.bibliographiccitation.volume","15"],["dc.contributor.author","Jo, Peter"],["dc.contributor.author","Bernhardt, Markus"],["dc.contributor.author","Nietert, Manuel"],["dc.contributor.author","König, Alexander"],["dc.contributor.author","Azizian, Azadeh"],["dc.contributor.author","Schirmer, Markus A."],["dc.contributor.author","Grade, Marian"],["dc.contributor.author","Kitz, Julia"],["dc.contributor.author","Reuter-Jessen, Kirsten"],["dc.contributor.author","Ghadimi, Michael"],["dc.contributor.author","Ströbel, Philipp"],["dc.contributor.author","Schildhaus, Hans-Ulrich"],["dc.contributor.author","Gaedcke, Jochen"],["dc.contributor.editor","Deb, Sumitra"],["dc.date.accessioned","2021-04-14T08:31:16Z"],["dc.date.available","2021-04-14T08:31:16Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1371/journal.pone.0239806"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17654"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/83536"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.notes.intern","Merged from goescholar"],["dc.relation.eissn","1932-6203"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","KRAS mutation status concordance between the primary tumor and the corresponding metastasis in patients with rectal cancer"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]