Neeße, Albrecht

[["dc.bibliographiccitation.firstpage","161"],["dc.bibliographiccitation.journal","EBioMedicine"],["dc.bibliographiccitation.lastpage","168"],["dc.bibliographiccitation.volume","48"],["dc.contributor.author","Ramu, Iswarya"],["dc.contributor.author","Buchholz, Sören M."],["dc.contributor.author","Patzak, Melanie S."],["dc.contributor.author","Goetze, Robert G."],["dc.contributor.author","Singh, Shiv K."],["dc.contributor.author","Richards, Frances M."],["dc.contributor.author","Jodrell, Duncan I."],["dc.contributor.author","Sipos, Bence"],["dc.contributor.author","Ströbel, Philipp"],["dc.contributor.author","Ellenrieder, Volker"],["dc.contributor.author","Hessmann, Elisabeth"],["dc.contributor.author","Neesse, Albrecht"],["dc.date.accessioned","2020-12-10T14:23:31Z"],["dc.date.available","2020-12-10T14:23:31Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1016/j.ebiom.2019.09.024"],["dc.identifier.issn","2352-3964"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16852"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/71949"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY-NC-ND 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/4.0"],["dc.title","SPARC dependent collagen deposition and gemcitabine delivery in a genetically engineered mouse model of pancreas cancer"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1978"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Cancers"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Buchholz, Soeren M."],["dc.contributor.author","Goetze, Robert G."],["dc.contributor.author","Singh, Shiv K."],["dc.contributor.author","Ammer-Herrmenau, Christoph"],["dc.contributor.author","Richards, Frances M."],["dc.contributor.author","Jodrell, Duncan I."],["dc.contributor.author","Buchholz, Malte"],["dc.contributor.author","Michl, Patrick"],["dc.contributor.author","Ellenrieder, Volker"],["dc.contributor.author","Hessmann, Elisabeth"],["dc.contributor.author","Neesse, Albrecht"],["dc.date.accessioned","2021-04-14T08:25:07Z"],["dc.date.available","2021-04-14T08:25:07Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.3390/cancers12071978"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17498"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/81527"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.notes.intern","Merged from goescholar"],["dc.relation.eissn","2072-6694"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Depletion of Macrophages Improves Therapeutic Response to Gemcitabine in Murine Pancreas Cancer"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2561"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Gut"],["dc.bibliographiccitation.lastpage","2573"],["dc.bibliographiccitation.volume","71"],["dc.contributor.affiliation","Latif, Muhammad Umair; \r\n1\r\nDepartment of Gastroenterology, Gastrointestinal Oncology and Endocrinology, University Medical Center Göttingen, Gottingen, Niedersachsen, Germany"],["dc.contributor.affiliation","Schmidt, Geske Elisabeth; \r\n1\r\nDepartment of Gastroenterology, Gastrointestinal Oncology and Endocrinology, University Medical Center Göttingen, Gottingen, Niedersachsen, Germany"],["dc.contributor.affiliation","Mercan, Sercan; \r\n1\r\nDepartment of Gastroenterology, Gastrointestinal Oncology and Endocrinology, University Medical Center Göttingen, Gottingen, Niedersachsen, Germany"],["dc.contributor.affiliation","Rahman, Raza; \r\n2\r\nGastrointestinal Unit, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA"],["dc.contributor.affiliation","Gibhardt, Christine Silvia; \r\n3\r\nMolecular Physiology, Institute of Cardiovascular Physiology, University Medical Center Göttingen, Gottingen, Niedersachsen, Germany"],["dc.contributor.affiliation","Stejerean-Todoran, Ioana; \r\n3\r\nMolecular Physiology, Institute of Cardiovascular Physiology, University Medical Center Göttingen, Gottingen, Niedersachsen, Germany"],["dc.contributor.affiliation","Reutlinger, Kristina; \r\n1\r\nDepartment of Gastroenterology, Gastrointestinal Oncology and Endocrinology, University Medical Center Göttingen, Gottingen, Niedersachsen, Germany"],["dc.contributor.affiliation","Hessmann, Elisabeth; \r\n1\r\nDepartment of Gastroenterology, Gastrointestinal Oncology and Endocrinology, University Medical Center Göttingen, Gottingen, Niedersachsen, Germany"],["dc.contributor.affiliation","Singh, Shiv K; \r\n1\r\nDepartment of Gastroenterology, Gastrointestinal Oncology and Endocrinology, University Medical Center Göttingen, Gottingen, Niedersachsen, Germany"],["dc.contributor.affiliation","Moeed, Abdul; \r\n4\r\nInstitute for Microbiology and Hygiene, Medical Center-University of Freiburg, Freiburg, Baden-Württemberg, Germany"],["dc.contributor.affiliation","Rehman, Abdul; \r\n5\r\nInstitute of Pharmacology and Toxicology, University Medical Center Göttingen, Gottingen, Niedersachsen, Germany"],["dc.contributor.affiliation","Butt, Umer Javed; \r\n6\r\nClinical Neuroscience, Max-Planck-Institute for Experimental Medicine, Goettingen, Niedersachsen, Germany"],["dc.contributor.affiliation","Bohnenberger, Hanibal; \r\n7\r\nInstitute of Pathology, University Medical Center Göttingen, Gottingen, Germany"],["dc.contributor.affiliation","Stroebel, Philipp; \r\n7\r\nInstitute of Pathology, University Medical Center Göttingen, Gottingen, Germany"],["dc.contributor.affiliation","Bremer, Sebastian Christopher; \r\n1\r\nDepartment of Gastroenterology, Gastrointestinal Oncology and Endocrinology, University Medical Center Göttingen, Gottingen, Niedersachsen, Germany"],["dc.contributor.affiliation","Neesse, Albrecht; \r\n1\r\nDepartment of Gastroenterology, Gastrointestinal Oncology and Endocrinology, University Medical Center Göttingen, Gottingen, Niedersachsen, Germany"],["dc.contributor.affiliation","Bogeski, Ivan; \r\n3\r\nMolecular Physiology, Institute of Cardiovascular Physiology, University Medical Center Göttingen, Gottingen, Niedersachsen, Germany"],["dc.contributor.affiliation","Ellenrieder, Volker; \r\n1\r\nDepartment of Gastroenterology, Gastrointestinal Oncology and Endocrinology, University Medical Center Göttingen, Gottingen, Niedersachsen, Germany"],["dc.contributor.author","Latif, Muhammad Umair"],["dc.contributor.author","Schmidt, Geske Elisabeth"],["dc.contributor.author","Mercan, Sercan"],["dc.contributor.author","Rahman, Raza"],["dc.contributor.author","Gibhardt, Christine Silvia"],["dc.contributor.author","Stejerean-Todoran, Ioana"],["dc.contributor.author","Reutlinger, Kristina"],["dc.contributor.author","Hessmann, Elisabeth"],["dc.contributor.author","Singh, Shiv K."],["dc.contributor.author","Moeed, Abdul"],["dc.contributor.author","Rehman, Abdul"],["dc.contributor.author","Butt, Umer Javed"],["dc.contributor.author","Bohnenberger, Hanibal"],["dc.contributor.author","Stroebel, Philipp"],["dc.contributor.author","Bremer, Sebastian Christopher"],["dc.contributor.author","Neesse, Albrecht"],["dc.contributor.author","Bogeski, Ivan"],["dc.contributor.author","Ellenrieder, Volker"],["dc.date.accessioned","2022-12-07T08:25:00Z"],["dc.date.available","2022-12-07T08:25:00Z"],["dc.date.issued","2022-04-01"],["dc.date.updated","2022-12-07T00:46:04Z"],["dc.description.abstract","ObjectivesNon-alcoholic fatty liver disease (NAFLD) can persist in the stage of simple hepatic steatosis or progress to steatohepatitis (NASH) with an increased risk for cirrhosis and cancer. We examined the mechanisms controlling the progression to severe NASH in order to develop future treatment strategies for this disease.DesignNFATc1 activation and regulation was examined in livers from patients with NAFLD, cultured and primary hepatocytes and in transgenic mice with differential hepatocyte-specific expression of the transcription factor (Alb-cre, NFATc1c.a\r\n. and NFATc1Δ/Δ\r\n). Animals were fed with high-fat western diet (WD) alone or in combination with tauroursodeoxycholic acid (TUDCA), a candidate drug for NAFLD treatment. NFATc1-dependent ER stress-responses, NLRP3 inflammasome activation and disease progression were assessed both in vitro and in vivo.ResultsNFATc1 expression was weak in healthy livers but strongly induced in advanced NAFLD stages, where it correlates with liver enzyme values as well as hepatic inflammation and fibrosis. Moreover, high-fat WD increased NFATc1 expression, nuclear localisation and activation to promote NAFLD progression, whereas hepatocyte-specific depletion of the transcription factor can prevent mice from disease acceleration. Mechanistically, NFATc1 drives liver cell damage and inflammation through ER stress sensing and activation of the PERK-CHOP unfolded protein response (UPR). Finally, NFATc1-induced disease progression towards NASH can be blocked by TUDCA administration.ConclusionNFATc1 stimulates NAFLD progression through chronic ER stress sensing and subsequent activation of terminal UPR signalling in hepatocytes. Interfering with ER stress-responses, for example, by TUDCA, protects fatty livers from progression towards manifest NASH."],["dc.description.sponsorship","the Volkswagen-Stiftung"],["dc.description.sponsorship","http://dx.doi.org/10.13039/501100001659Deutsche Forschungsgemeinschaft"],["dc.description.sponsorship","German Cancer Aid"],["dc.identifier","35365570"],["dc.identifier.doi","10.1136/gutjnl-2021-325013"],["dc.identifier.pmid","35365570"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/118455"],["dc.identifier.url","https://sfb1190.med.uni-goettingen.de/production/literature/publications/173"],["dc.language.iso","en"],["dc.publisher","BMJ Publishing Group Ltd and British Society of Gastroenterology"],["dc.relation","SFB 1190: Transportmaschinen und Kontaktstellen zellulärer Kompartimente"],["dc.relation","SFB 1190 | P17: Die Rolle mitochondrialer Kontaktstellen im Rahmen tumorrelevanter Calcium- und Redox-Signalwege"],["dc.relation.eissn","1468-3288"],["dc.relation.issn","0017-5749"],["dc.relation.workinggroup","RG Bogeski"],["dc.rights","CC BY-NC 4.0"],["dc.rights.uri","http://creativecommons.org/licenses/by-nc/4.0/"],["dc.title","NFATc1 signaling drives chronic ER stress responses to promote NAFLD progression"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","ueg2.12262"],["dc.bibliographiccitation.journal","United European Gastroenterology Journal"],["dc.contributor.author","Ammer‐Herrmenau, Christoph"],["dc.contributor.author","Wolf, Laurin"],["dc.contributor.author","Nasrin, Syeda S."],["dc.contributor.author","Ramu, Iswarya"],["dc.contributor.author","Roggiolani, Roberta"],["dc.contributor.author","Goetze, Robert G."],["dc.contributor.author","Buchholz, Soeren M."],["dc.contributor.author","Sendler, Mathias"],["dc.contributor.author","Ellenrieder, Volker"],["dc.contributor.author","Neesse, Albrecht"],["dc.date.accessioned","2022-07-01T07:35:08Z"],["dc.date.available","2022-07-01T07:35:08Z"],["dc.date.issued","2022"],["dc.description.abstract","Background:Acute pancreatitis(AP) is a frequent cause for hospitalization.How-ever, moleculardeterminantsthat modulateseverity of experimentalpancreatitisareonlypartiallyunderstood.Objective:To investigatethe role of secreted protein acidic and rich in cysteine(SPARC)duringcerulein‐inducedAPinmice.Methods:APwasinducedbyrepeatedceruleininjectionsinSPARCknock‐outmice(SPARC−/−)andcontrollittermates(SPARC+/+).Secretedproteinacidicandrichincysteine expressionand severity of AP were determinedby histopathologicalscoring, immunohistochemistry,and biochemicalassays. For functionalanalysis,primary murine acinar cell cultures with subsequentamylase release assays wereemployed.Proteomeprofiler assay and ELISA were conductedfrom pancreatictissuelysates,andco‐immunofluorescencewasperformed.Results:Upon cerulein induction,SPARC expressionwas robustly induced inpancreaticstellate cells (PSCs) but not in acinar cells. Genetic SPARC ablationresultedinattenuatedseverityofAPwithsignificantlyreducedlevelsofpancreaticnecrosis, apoptosis,immune cell infiltration,and reduced fibrosis upon chronicstimulation.However,the release of amylase upon cerulein stimulationin primaryacinar cell culture from SPARC+/+and SPARC−/−was indistinguishable.Notably,immunecellderivedC‐C MotifChemokineLigand2(CCL2)washighlyelevatedinSPARC+/+pancreatictissue potentiallylinking PSC derived SPARC with CCL2 in-ductioninAP.Conclusion:SPARCmediatestheseverityofAP.ThepotentiallinkbetweenSPARCandtheCCL2axiscouldopennewavenuesfortailoredtherapeuticinterventionsinAPpatientsandwarrantsfurtherinvestigations."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2022"],["dc.identifier.doi","10.1002/ueg2.12262"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/112096"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-581"],["dc.relation.eissn","2050-6414"],["dc.relation.issn","2050-6406"],["dc.rights","CC BY-NC-ND 4.0"],["dc.title","Activity of acute pancreatitis is modified by secreted protein acidic and rich in cysteine ablation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e0163651"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Rasch, Sebastian"],["dc.contributor.author","Phillip, Veit"],["dc.contributor.author","Reichel, Stephanie"],["dc.contributor.author","Rau, Bettina M."],["dc.contributor.author","Zapf, Christian"],["dc.contributor.author","Rosendahl, Jonas"],["dc.contributor.author","Halms, Ulrich"],["dc.contributor.author","Zachaeus, Markus"],["dc.contributor.author","Mueller, Martin"],["dc.contributor.author","Kleger, Alexander"],["dc.contributor.author","Neesse, Albrecht"],["dc.contributor.author","Hampe, Jochen"],["dc.contributor.author","Ellrichmann, Mark"],["dc.contributor.author","Rueckert, Felix"],["dc.contributor.author","Strauss, Peter"],["dc.contributor.author","Arlt, Alexander"],["dc.contributor.author","Ellenrieder, Volker"],["dc.contributor.author","Gress, Thomas M."],["dc.contributor.author","Hartwig, Werner"],["dc.contributor.author","Klar, Ernst"],["dc.contributor.author","Moessner, Joachim"],["dc.contributor.author","Post, Stephen G."],["dc.contributor.author","Schmid, Roland M."],["dc.contributor.author","Seufferlein, Thomas"],["dc.contributor.author","Siech, Marco"],["dc.contributor.author","Werner, Jens"],["dc.contributor.author","Will, Uwe"],["dc.contributor.author","Alguel, Hana"],["dc.date.accessioned","2018-11-07T10:08:18Z"],["dc.date.available","2018-11-07T10:08:18Z"],["dc.date.issued","2016"],["dc.description.abstract","Background Necrotising pancreatitis, and particularly infected necrosis, are still associated with high morbidity and mortality. Since 2011, a step-up approach with lower morbidity rates compared to initial open necrosectomy has been established. However, mortality and complication rates of this complex treatment are hardly studied thereafter. Methods The German Pancreatitis Study Group performed a multicenter, retrospective study including 220 patients with necrotising pancreatitis requiring intervention, treated at 10 hospitals in Germany between January 2008 and June 2014. Data were analysed for the primary endpoints \"severe complications\" and \"mortality\" as well as secondary endpoints including \"length of hospital stay\", \"follow up\", and predisposing or prognostic factors. Results Of all patients 13.6% were treated primarily with surgery and 86.4% underwent a step-up approach. More men (71.8%) required intervention for necrotising pancreatitis. The most frequent etiology was biliary (41.4%) followed by alcohol (29.1%). Compared to open necrosectomy, the step-up approach was associated with a lower number of severe complications (primary composite endpoint including sepsis, persistent multiorgan dysfunction syndrome (MODS) and erosion bleeding: 44.7% vs. 73.3%), lower mortality (10.5% vs. 33.3%) and lower rates of diabetes mellitus type 3c (4.7% vs. 33.3%). Low hematocrit and low blood urea nitrogen at admission as well as a history of acute pancreatitis were prognostic for less complications in necrotising pancreatitis. A combination of drainage with endoscopic necrosectomy resulted in the lowest rate of severe complications. Conclusion A step-up approach starting with minimal invasive drainage techniques and endoscopic necrosectomy results in a significant reduction of morbidity and mortality in necrotising pancreatitis compared to a primarily surgical intervention."],["dc.identifier.doi","10.1371/journal.pone.0163651"],["dc.identifier.isi","000384167300063"],["dc.identifier.pmid","27668746"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13762"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/39449"],["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 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Open Surgical versus Minimal Invasive Necrosectomy of the Pancreas-A Retrospective Multicenter Analysis of the German Pancreatitis Study Group"],["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.issue","14"],["dc.bibliographiccitation.journal","Cancers"],["dc.bibliographiccitation.volume","14"],["dc.contributor.affiliation","Versemann, Lennart; 1Department of Gastroenterology, Gastrointestinal Oncology and Endocrinology, University Medical Center Goettingen, 37075 Goettingen, Germany; lennart.versemann@t-online.de (L.V.); shilpapatil528@gmail.com (S.P.); benjamin.steuber@med.uni-goettingen.de (B.S.); zhe.zhang@med.uni-goettingen.de (Z.Z.); wkopp@med.uni-goettingen.de (W.K.); albrecht.neesse@med.uni-goettingen.de (A.N.); shiv.singh@med.uni-goettingen.de (S.K.S.); volker.ellenrieder@med.uni-goettingen.de (V.E.)"],["dc.contributor.affiliation","Patil, Shilpa; 1Department of Gastroenterology, Gastrointestinal Oncology and Endocrinology, University Medical Center Goettingen, 37075 Goettingen, Germany; lennart.versemann@t-online.de (L.V.); shilpapatil528@gmail.com (S.P.); benjamin.steuber@med.uni-goettingen.de (B.S.); zhe.zhang@med.uni-goettingen.de (Z.Z.); wkopp@med.uni-goettingen.de (W.K.); albrecht.neesse@med.uni-goettingen.de (A.N.); shiv.singh@med.uni-goettingen.de (S.K.S.); volker.ellenrieder@med.uni-goettingen.de (V.E.)"],["dc.contributor.affiliation","Steuber, Benjamin; 1Department of Gastroenterology, Gastrointestinal Oncology and Endocrinology, University Medical Center Goettingen, 37075 Goettingen, Germany; lennart.versemann@t-online.de (L.V.); shilpapatil528@gmail.com (S.P.); benjamin.steuber@med.uni-goettingen.de (B.S.); zhe.zhang@med.uni-goettingen.de (Z.Z.); wkopp@med.uni-goettingen.de (W.K.); albrecht.neesse@med.uni-goettingen.de (A.N.); shiv.singh@med.uni-goettingen.de (S.K.S.); volker.ellenrieder@med.uni-goettingen.de (V.E.)"],["dc.contributor.affiliation","Zhang, Zhe; 1Department of Gastroenterology, Gastrointestinal Oncology and Endocrinology, University Medical Center Goettingen, 37075 Goettingen, Germany; lennart.versemann@t-online.de (L.V.); shilpapatil528@gmail.com (S.P.); benjamin.steuber@med.uni-goettingen.de (B.S.); zhe.zhang@med.uni-goettingen.de (Z.Z.); wkopp@med.uni-goettingen.de (W.K.); albrecht.neesse@med.uni-goettingen.de (A.N.); shiv.singh@med.uni-goettingen.de (S.K.S.); volker.ellenrieder@med.uni-goettingen.de (V.E.)"],["dc.contributor.affiliation","Kopp, Waltraut; 1Department of Gastroenterology, Gastrointestinal Oncology and Endocrinology, University Medical Center Goettingen, 37075 Goettingen, Germany; lennart.versemann@t-online.de (L.V.); shilpapatil528@gmail.com (S.P.); benjamin.steuber@med.uni-goettingen.de (B.S.); zhe.zhang@med.uni-goettingen.de (Z.Z.); wkopp@med.uni-goettingen.de (W.K.); albrecht.neesse@med.uni-goettingen.de (A.N.); shiv.singh@med.uni-goettingen.de (S.K.S.); volker.ellenrieder@med.uni-goettingen.de (V.E.)"],["dc.contributor.affiliation","Krawczyk, Hannah Elisa; 2Clinical Research Unit 5002, KFO5002, University Medical Center Göttingen, 37075 Göttingen, Germany; elisa.krawczyk@outlook.de (H.E.K.); silke.kaulfuss@med.uni-goettingen.de (S.K.); bernd.wollnik@med.uni-goettingen.de (B.W.); philipp.stroebel@med.uni-goettingen.de (P.S.)"],["dc.contributor.affiliation","Kaulfuß, Silke; 2Clinical Research Unit 5002, KFO5002, University Medical Center Göttingen, 37075 Göttingen, Germany; elisa.krawczyk@outlook.de (H.E.K.); silke.kaulfuss@med.uni-goettingen.de (S.K.); bernd.wollnik@med.uni-goettingen.de (B.W.); philipp.stroebel@med.uni-goettingen.de (P.S.)"],["dc.contributor.affiliation","Wollnik, Bernd; 2Clinical Research Unit 5002, KFO5002, University Medical Center Göttingen, 37075 Göttingen, Germany; elisa.krawczyk@outlook.de (H.E.K.); silke.kaulfuss@med.uni-goettingen.de (S.K.); bernd.wollnik@med.uni-goettingen.de (B.W.); philipp.stroebel@med.uni-goettingen.de (P.S.)"],["dc.contributor.affiliation","Ströbel, Philipp; 2Clinical Research Unit 5002, KFO5002, University Medical Center Göttingen, 37075 Göttingen, Germany; elisa.krawczyk@outlook.de (H.E.K.); silke.kaulfuss@med.uni-goettingen.de (S.K.); bernd.wollnik@med.uni-goettingen.de (B.W.); philipp.stroebel@med.uni-goettingen.de (P.S.)"],["dc.contributor.affiliation","Neesse, Albrecht; 1Department of Gastroenterology, Gastrointestinal Oncology and Endocrinology, University Medical Center Goettingen, 37075 Goettingen, Germany; lennart.versemann@t-online.de (L.V.); shilpapatil528@gmail.com (S.P.); benjamin.steuber@med.uni-goettingen.de (B.S.); zhe.zhang@med.uni-goettingen.de (Z.Z.); wkopp@med.uni-goettingen.de (W.K.); albrecht.neesse@med.uni-goettingen.de (A.N.); shiv.singh@med.uni-goettingen.de (S.K.S.); volker.ellenrieder@med.uni-goettingen.de (V.E.)"],["dc.contributor.affiliation","Singh, Shiv K.; 1Department of Gastroenterology, Gastrointestinal Oncology and Endocrinology, University Medical Center Goettingen, 37075 Goettingen, Germany; lennart.versemann@t-online.de (L.V.); shilpapatil528@gmail.com (S.P.); benjamin.steuber@med.uni-goettingen.de (B.S.); zhe.zhang@med.uni-goettingen.de (Z.Z.); wkopp@med.uni-goettingen.de (W.K.); albrecht.neesse@med.uni-goettingen.de (A.N.); shiv.singh@med.uni-goettingen.de (S.K.S.); volker.ellenrieder@med.uni-goettingen.de (V.E.)"],["dc.contributor.affiliation","Ellenrieder, Volker; 1Department of Gastroenterology, Gastrointestinal Oncology and Endocrinology, University Medical Center Goettingen, 37075 Goettingen, Germany; lennart.versemann@t-online.de (L.V.); shilpapatil528@gmail.com (S.P.); benjamin.steuber@med.uni-goettingen.de (B.S.); zhe.zhang@med.uni-goettingen.de (Z.Z.); wkopp@med.uni-goettingen.de (W.K.); albrecht.neesse@med.uni-goettingen.de (A.N.); shiv.singh@med.uni-goettingen.de (S.K.S.); volker.ellenrieder@med.uni-goettingen.de (V.E.)"],["dc.contributor.affiliation","Hessmann, Elisabeth; 1Department of Gastroenterology, Gastrointestinal Oncology and Endocrinology, University Medical Center Goettingen, 37075 Goettingen, Germany; lennart.versemann@t-online.de (L.V.); shilpapatil528@gmail.com (S.P.); benjamin.steuber@med.uni-goettingen.de (B.S.); zhe.zhang@med.uni-goettingen.de (Z.Z.); wkopp@med.uni-goettingen.de (W.K.); albrecht.neesse@med.uni-goettingen.de (A.N.); shiv.singh@med.uni-goettingen.de (S.K.S.); volker.ellenrieder@med.uni-goettingen.de (V.E.)"],["dc.contributor.author","Versemann, Lennart"],["dc.contributor.author","Patil, Shilpa"],["dc.contributor.author","Steuber, Benjamin"],["dc.contributor.author","Zhang, Zhe"],["dc.contributor.author","Kopp, Waltraut"],["dc.contributor.author","Krawczyk, Hannah Elisa"],["dc.contributor.author","Kaulfuß, Silke"],["dc.contributor.author","Wollnik, Bernd"],["dc.contributor.author","Ströbel, Philipp"],["dc.contributor.author","Neesse, Albrecht"],["dc.contributor.author","Singh, Shiv K."],["dc.contributor.author","Ellenrieder, Volker"],["dc.contributor.author","Hessmann, Elisabeth"],["dc.date.accessioned","2022-08-04T08:34:43Z"],["dc.date.available","2022-08-04T08:34:43Z"],["dc.date.issued","2022-07-15"],["dc.date.updated","2022-08-03T11:58:42Z"],["dc.description.abstract","Epigenetic alterations contribute to the aggressiveness and therapy resistance of Pancreatic Ductal Adenocarcinoma (PDAC). However, epigenetic regulators, including Enhancer of Zeste Homolog 2 (EZH2), reveal a strong context-dependent activity. Our study aimed to examine the context-defining molecular prerequisites of oncogenic EZH2 activity in PDAC to assess the therapeutic efficacy of targeting EZH2. Our preclinical study using diverse PDAC models demonstrates that the TP53 status determines oncogenic EZH2 activity. Only in TP53-wildtype (wt) PDAC subtypes was EZH2 blockade associated with a favorable PDAC prognosis mainly through cell-death response. We revealed that EZH2 depletion increases p53wt stability by the de-repression of CDKN2A. Therefore, our study provides preclinical evidence that an intact CDKN2A-p53wt axis is indispensable for a beneficial outcome of EZH2 depletion and highlights the significance of molecular stratification to improve epigenetic targeting in PDAC. \r\n \r\n \r\n Abstract\r\n Pancreatic Ductal Adenocarcinoma (PDAC) represents a lethal malignancy with a consistently poor outcome. Besides mutations in PDAC driver genes, the aggressive tumor biology of the disease and its remarkable therapy resistance are predominantly installed by potentially reversible epigenetic dysregulation. However, epigenetic regulators act in a context-dependent manner with opposing implication on tumor progression, thus critically determining the therapeutic efficacy of epigenetic targeting. Herein, we aimed at exploring the molecular prerequisites and underlying mechanisms of oncogenic Enhancer of Zeste Homolog 2 (EZH2) activity in PDAC progression. Preclinical studies in EZH2 proficient and deficient transgenic and orthotopic in vivo PDAC models and transcriptome analysis identified the TP53 status as a pivotal context-defining molecular cue determining oncogenic EZH2 activity in PDAC. Importantly, the induction of pro-apoptotic gene signatures and processes as well as a favorable PDAC prognosis upon EZH2 depletion were restricted to p53 wildtype (wt) PDAC subtypes. Mechanistically, we illustrate that EZH2 blockade de-represses CDKN2A transcription for the subsequent posttranslational stabilization of p53wt expression and function. Together, our findings suggest an intact CDKN2A-p53wt axis as a prerequisite for the anti-tumorigenic consequences of EZH2 depletion and emphasize the significance of molecular stratification for the successful implementation of epigenetic targeting in PDAC."],["dc.description.sponsorship","Wilhelm-Sander Stiftung"],["dc.description.sponsorship","German Cancer Aid"],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft"],["dc.description.sponsorship","Ministry for Science and Culture in Lower Saxony/Volkswagenstiftung"],["dc.description.sponsorship","China Scholarship Council"],["dc.identifier.doi","10.3390/cancers14143451"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/112631"],["dc.language.iso","en"],["dc.relation.eissn","2072-6694"],["dc.rights","CC BY 4.0"],["dc.title","TP53-Status-Dependent Oncogenic EZH2 Activity in Pancreatic Cancer"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","304"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","BMC Gastroenterology"],["dc.bibliographiccitation.volume","21"],["dc.contributor.author","Ammer-Herrmenau, C."],["dc.contributor.author","Asendorf, T."],["dc.contributor.author","Beyer, G."],["dc.contributor.author","Buchholz, S. M."],["dc.contributor.author","Cameron, S."],["dc.contributor.author","Damm, M."],["dc.contributor.author","Frost, F."],["dc.contributor.author","Henker, R."],["dc.contributor.author","Jaster, R."],["dc.contributor.author","Phillip, V."],["dc.contributor.author","Placzek, M."],["dc.contributor.author","Ratei, C."],["dc.contributor.author","Sirtl, S."],["dc.contributor.author","van den Berg, T."],["dc.contributor.author","Weingarten, M. J."],["dc.contributor.author","Woitalla, J."],["dc.contributor.author","Mayerle, J."],["dc.contributor.author","Ellenrieder, V."],["dc.contributor.author","Neesse, A."],["dc.date.accessioned","2021-11-25T11:03:17Z"],["dc.date.accessioned","2022-08-18T12:35:27Z"],["dc.date.available","2021-11-25T11:03:17Z"],["dc.date.available","2022-08-18T12:35:27Z"],["dc.date.issued","2021-07-31"],["dc.date.updated","2022-07-29T12:07:19Z"],["dc.description.abstract","Abstract\r\n \r\n Background\r\n Acute pancreatitis (AP) is an inflammatory disorder that causes a considerable economic health burden. While the overall mortality is low, around 20% of patients have a complicated course of disease resulting in increased morbidity and mortality. There is an emerging body of evidence that the microbiome exerts a crucial impact on the pathophysiology and course of AP. For several decades multiple clinical and laboratory parameters have been evaluated, and complex scoring systems were developed to predict the clinical course of AP upon admission. However, the majority of scoring systems are determined after several days and achieve a sensitivity around 70% for early prediction of severe AP. Thus, continued efforts are required to investigate reliable biomarkers for the early prediction of severity in order to guide early clinical management of AP patients.\r\n\r\n \r\n \r\n Methods\r\n We designed a multi-center, prospective clinical-translational study to test whether the orointestinal microbiome may serve as novel early predictor of the course, severity and outcome of patients with AP. We will recruit 400 AP patients and obtain buccal and rectal swabs within 72 h of admission to the hospital. Following DNA extraction, microbiome analysis will be performed using 3rd generation sequencing Oxford Nanopore Technologies (ONT) for 16S rRNA and metagenomic sequencing. Alpha- and beta-diversity will be determined and correlated to the revised Atlanta classification and additional clinical outcome parameters such as the length of hospital stay, number and type of complications, number of interventions and 30-day mortality.\r\n \r\n \r\n Discussion\r\n If AP patients show a distinct orointestinal microbiome dependent on the severity and course of the disease, microbiome sequencing could rapidly be implemented in the early clinical management of AP patients in the future.\r\n Trial registration: ClinicalTrials.gov Identifier: NCT04777812"],["dc.description.sponsorship","Open-Access-Publikationsfonds 2021"],["dc.identifier.citation","BMC Gastroenterology. 2021 Jul 31;21(1):304"],["dc.identifier.doi","10.1186/s12876-021-01885-4"],["dc.identifier.pii","1885"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/93521"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/112940"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-448"],["dc.publisher","BioMed Central"],["dc.relation.eissn","1471-230X"],["dc.rights","CC BY 4.0"],["dc.rights.holder","The Author(s)"],["dc.subject","Acute pancreatitis"],["dc.subject","Biomarker"],["dc.subject","Orointestinale microbiome"],["dc.subject","Metagenomic sequencing"],["dc.subject","Multicentric"],["dc.subject","Oxford nanopore technologies"],["dc.subject","ONT"],["dc.subject","P-MAPS"],["dc.subject","Prospective"],["dc.subject","Severity"],["dc.subject","NCT04777812"],["dc.title","Study protocol P-MAPS: microbiome as predictor of severity in acute pancreatitis—a prospective multicentre translational study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","58"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Cells"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Hasselluhn, Marie C."],["dc.contributor.author","Klein, Lukas"],["dc.contributor.author","Patzak, Melanie S."],["dc.contributor.author","Buchholz, Sören M."],["dc.contributor.author","Ströbel, Philipp"],["dc.contributor.author","Ellenrieder, Volker"],["dc.contributor.author","Maisonneuve, Patrick"],["dc.contributor.author","Neesse, Albrecht"],["dc.date.accessioned","2021-04-14T08:27:45Z"],["dc.date.available","2021-04-14T08:27:45Z"],["dc.date.issued","2019-12-24"],["dc.description.sponsorship","Deutsche Krebshilfe"],["dc.identifier.doi","10.3390/cells9010058"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/82390"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.publisher","MDPI"],["dc.relation.eissn","2073-4409"],["dc.rights","https://creativecommons.org/licenses/by/4.0/"],["dc.title","Stromal Features of the Primary Tumor Are Not Prognostic in Genetically Engineered Mice of Pancreatic Cancer"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","3463"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Cells"],["dc.bibliographiccitation.volume","10"],["dc.contributor.affiliation","Patil, Shilpa; 1Department of Gastroenterology, Gastrointestinal Oncology and Endocrinology, University Medical Center Goettingen, 37075 Goettingen, Germany; shilpapatil528@gmail.com (S.P.); kristina.reutlinger@med.uni-goettingen.de (K.R.); wkopp@med.uni-goettingen.de (W.K.); lennart.versemann@t-online.de (L.V.); jspitali@med.uni-goettingen.de (J.S.); shiv.singh@med.uni-goettingen.de (S.K.S.); volker.ellenrieder@med.uni-goettingen.de (V.E.); albrecht.neesse@med.uni-goettingen.de (A.N.)"],["dc.contributor.affiliation","Forster, Teresa; 2Department of Gastroenterology, Endocrinology, Metabolism and Clinical Infectiology, Philipps University Marburg, 35043 Marburg, Germany; terry.forster@web.de"],["dc.contributor.affiliation","Reutlinger, Kristina; 1Department of Gastroenterology, Gastrointestinal Oncology and Endocrinology, University Medical Center Goettingen, 37075 Goettingen, Germany; shilpapatil528@gmail.com (S.P.); kristina.reutlinger@med.uni-goettingen.de (K.R.); wkopp@med.uni-goettingen.de (W.K.); lennart.versemann@t-online.de (L.V.); jspitali@med.uni-goettingen.de (J.S.); shiv.singh@med.uni-goettingen.de (S.K.S.); volker.ellenrieder@med.uni-goettingen.de (V.E.); albrecht.neesse@med.uni-goettingen.de (A.N.)"],["dc.contributor.affiliation","Kopp, Waltraut; 1Department of Gastroenterology, Gastrointestinal Oncology and Endocrinology, University Medical Center Goettingen, 37075 Goettingen, Germany; shilpapatil528@gmail.com (S.P.); kristina.reutlinger@med.uni-goettingen.de (K.R.); wkopp@med.uni-goettingen.de (W.K.); lennart.versemann@t-online.de (L.V.); jspitali@med.uni-goettingen.de (J.S.); shiv.singh@med.uni-goettingen.de (S.K.S.); volker.ellenrieder@med.uni-goettingen.de (V.E.); albrecht.neesse@med.uni-goettingen.de (A.N.)"],["dc.contributor.affiliation","Versemann, Lennart; 1Department of Gastroenterology, Gastrointestinal Oncology and Endocrinology, University Medical Center Goettingen, 37075 Goettingen, Germany; shilpapatil528@gmail.com (S.P.); kristina.reutlinger@med.uni-goettingen.de (K.R.); wkopp@med.uni-goettingen.de (W.K.); lennart.versemann@t-online.de (L.V.); jspitali@med.uni-goettingen.de (J.S.); shiv.singh@med.uni-goettingen.de (S.K.S.); volker.ellenrieder@med.uni-goettingen.de (V.E.); albrecht.neesse@med.uni-goettingen.de (A.N.)"],["dc.contributor.affiliation","Spitalieri, Jessica; 1Department of Gastroenterology, Gastrointestinal Oncology and Endocrinology, University Medical Center Goettingen, 37075 Goettingen, Germany; shilpapatil528@gmail.com (S.P.); kristina.reutlinger@med.uni-goettingen.de (K.R.); wkopp@med.uni-goettingen.de (W.K.); lennart.versemann@t-online.de (L.V.); jspitali@med.uni-goettingen.de (J.S.); shiv.singh@med.uni-goettingen.de (S.K.S.); volker.ellenrieder@med.uni-goettingen.de (V.E.); albrecht.neesse@med.uni-goettingen.de (A.N.)"],["dc.contributor.affiliation","Gaedcke, Jochen; 3Clinical Research Unit KFO5002, University Medical Center Goettingen, 37075 Goettingen, Germany; jochen.gaedcke@med.uni-goettingen.de (J.G.); philipp.stroebel@med.uni-goettingen.de (P.S.)"],["dc.contributor.affiliation","Ströbel, Philipp; 3Clinical Research Unit KFO5002, University Medical Center Goettingen, 37075 Goettingen, Germany; jochen.gaedcke@med.uni-goettingen.de (J.G.); philipp.stroebel@med.uni-goettingen.de (P.S.)"],["dc.contributor.affiliation","Singh, Shiv K.; 1Department of Gastroenterology, Gastrointestinal Oncology and Endocrinology, University Medical Center Goettingen, 37075 Goettingen, Germany; shilpapatil528@gmail.com (S.P.); kristina.reutlinger@med.uni-goettingen.de (K.R.); wkopp@med.uni-goettingen.de (W.K.); lennart.versemann@t-online.de (L.V.); jspitali@med.uni-goettingen.de (J.S.); shiv.singh@med.uni-goettingen.de (S.K.S.); volker.ellenrieder@med.uni-goettingen.de (V.E.); albrecht.neesse@med.uni-goettingen.de (A.N.)"],["dc.contributor.affiliation","Ellenrieder, Volker; 1Department of Gastroenterology, Gastrointestinal Oncology and Endocrinology, University Medical Center Goettingen, 37075 Goettingen, Germany; shilpapatil528@gmail.com (S.P.); kristina.reutlinger@med.uni-goettingen.de (K.R.); wkopp@med.uni-goettingen.de (W.K.); lennart.versemann@t-online.de (L.V.); jspitali@med.uni-goettingen.de (J.S.); shiv.singh@med.uni-goettingen.de (S.K.S.); volker.ellenrieder@med.uni-goettingen.de (V.E.); albrecht.neesse@med.uni-goettingen.de (A.N.)"],["dc.contributor.affiliation","Neesse, Albrecht; 1Department of Gastroenterology, Gastrointestinal Oncology and Endocrinology, University Medical Center Goettingen, 37075 Goettingen, Germany; shilpapatil528@gmail.com (S.P.); kristina.reutlinger@med.uni-goettingen.de (K.R.); wkopp@med.uni-goettingen.de (W.K.); lennart.versemann@t-online.de (L.V.); jspitali@med.uni-goettingen.de (J.S.); shiv.singh@med.uni-goettingen.de (S.K.S.); volker.ellenrieder@med.uni-goettingen.de (V.E.); albrecht.neesse@med.uni-goettingen.de (A.N.)"],["dc.contributor.affiliation","Hessmann, Elisabeth; 1Department of Gastroenterology, Gastrointestinal Oncology and Endocrinology, University Medical Center Goettingen, 37075 Goettingen, Germany; shilpapatil528@gmail.com (S.P.); kristina.reutlinger@med.uni-goettingen.de (K.R.); wkopp@med.uni-goettingen.de (W.K.); lennart.versemann@t-online.de (L.V.); jspitali@med.uni-goettingen.de (J.S.); shiv.singh@med.uni-goettingen.de (S.K.S.); volker.ellenrieder@med.uni-goettingen.de (V.E.); albrecht.neesse@med.uni-goettingen.de (A.N.)"],["dc.contributor.author","Patil, Shilpa"],["dc.contributor.author","Forster, Teresa"],["dc.contributor.author","Reutlinger, Kristina"],["dc.contributor.author","Kopp, Waltraut"],["dc.contributor.author","Versemann, Lennart"],["dc.contributor.author","Spitalieri, Jessica"],["dc.contributor.author","Gaedcke, Jochen"],["dc.contributor.author","Ströbel, Philipp"],["dc.contributor.author","Singh, Shiv K."],["dc.contributor.author","Ellenrieder, Volker"],["dc.contributor.author","Hessmann, Elisabeth"],["dc.contributor.author","Neesse, Albrecht"],["dc.contributor.editor","Cavestro, Giulia Martina"],["dc.date.accessioned","2022-01-11T14:08:09Z"],["dc.date.available","2022-01-11T14:08:09Z"],["dc.date.issued","2021"],["dc.date.updated","2022-02-09T13:20:00Z"],["dc.description.abstract","Background: The Nuclear Factor of Activated T-cells 1 (NFATc1) transcription factor and the methyltransferase Enhancer of Zeste Homolog 2 (EZH2) significantly contribute to the aggressive phenotype of pancreatic ductal adenocarcinoma (PDAC). Herein, we aimed at dissecting the mechanistic background of their interplay in PDAC progression. Methods: NFATc1 and EZH2 mRNA and protein expression and complex formation were determined in transgenic PDAC models and human PDAC specimens. NFATc1 binding on the Ezh2 gene and the consequences of perturbed NFATc1 expression on Ezh2 transcription were explored by Chromatin Immunoprecipitation (ChIP) and upon transgenic or siRNA-mediated interference with NFATc1 expression, respectively. Integrative analyses of RNA- and ChIP-seq data was performed to explore NFATc1-/EZH2-dependent gene signatures. Results: NFATc1 targets the Ezh2 gene for transcriptional activation and biochemically interacts with the methyltransferase in murine and human PDAC. Surprisingly, our genome-wide binding and expression analyses do not link the protein complex to joint gene regulation. In contrast, our findings provide evidence for chromatin-independent functions of the NFATc1:EZH2 complex and reveal posttranslational EZH2 phosphorylation at serine 21 as a prerequisite for robust complex formation. Conclusion: Our findings disclose a previously unknown NFATc1-EZH2 axis operational in the pancreas and provide mechanistic insights into the conditions fostering NFATc1:EZH2 complex formation in PDAC."],["dc.description.abstract","Background: The Nuclear Factor of Activated T-cells 1 (NFATc1) transcription factor and the methyltransferase Enhancer of Zeste Homolog 2 (EZH2) significantly contribute to the aggressive phenotype of pancreatic ductal adenocarcinoma (PDAC). Herein, we aimed at dissecting the mechanistic background of their interplay in PDAC progression. Methods: NFATc1 and EZH2 mRNA and protein expression and complex formation were determined in transgenic PDAC models and human PDAC specimens. NFATc1 binding on the Ezh2 gene and the consequences of perturbed NFATc1 expression on Ezh2 transcription were explored by Chromatin Immunoprecipitation (ChIP) and upon transgenic or siRNA-mediated interference with NFATc1 expression, respectively. Integrative analyses of RNA- and ChIP-seq data was performed to explore NFATc1-/EZH2-dependent gene signatures. Results: NFATc1 targets the Ezh2 gene for transcriptional activation and biochemically interacts with the methyltransferase in murine and human PDAC. Surprisingly, our genome-wide binding and expression analyses do not link the protein complex to joint gene regulation. In contrast, our findings provide evidence for chromatin-independent functions of the NFATc1:EZH2 complex and reveal posttranslational EZH2 phosphorylation at serine 21 as a prerequisite for robust complex formation. Conclusion: Our findings disclose a previously unknown NFATc1-EZH2 axis operational in the pancreas and provide mechanistic insights into the conditions fostering NFATc1:EZH2 complex formation in PDAC."],["dc.identifier.doi","10.3390/cells10123463"],["dc.identifier.eissn","2073-4409"],["dc.identifier.pii","cells10123463"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/97947"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-507"],["dc.publisher","MDPI"],["dc.relation.eissn","2073-4409"],["dc.rights","Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/)."],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0/"],["dc.title","Chromatin-Independent Interplay of NFATc1 and EZH2 in Pancreatic Cancer"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","123"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","BMC Gastroenterology"],["dc.bibliographiccitation.volume","18"],["dc.contributor.author","Tsaknakis, Birgit"],["dc.contributor.author","Masri, Rawan"],["dc.contributor.author","Amanzada, Ahmad"],["dc.contributor.author","Petzold, Golo"],["dc.contributor.author","Ellenrieder, Volker"],["dc.contributor.author","Neesse, Albrecht"],["dc.contributor.author","Kunsch, Steffen"],["dc.date.accessioned","2019-07-09T11:45:36Z"],["dc.date.available","2019-07-09T11:45:36Z"],["dc.date.issued","2018"],["dc.description.abstract","BACKGROUND: The mortality due to hemorrhage of esophageal varices (EV) is still high. The predominant cause for EV is liver cirrhosis, which has a high prevalence in Western Europe. Therefore, non-invasive screening markers for the presence of EV are of interest. Here, we aim to investigate whether non-inflammatory gall bladder wall thickening (GBWT) may serve as predictor for the presence of EV in comparison and combination with other non-invasive clinical and laboratory parameters. METHODS: One hundred ninety four patients were retrospectively enrolled in the study. Abdominal ultrasound, upper endoscopy and blood tests were evaluated. GBWT, spleen size and the presence of ascites were evaluated by ultrasound. Platelet count and Child-Pugh-score were also recorded. The study population was categorized in two groups: 122 patients without esophageal varices (non EV) compared to 72 patients with EV were analyzed by uni-and multivariate analysis. RESULTS: In the EV group 46% showed a non-inflammatory GBWT of ≥4 mm, compared to 12% in the non-EV group (p < 0.01). GBWT was significantly higher in EV patients compared to the non-EV group (mean: 4.4 mm vs. 2.8 mm, p < 0.0001), and multivariate analysis confirmed GBWT as independent predictor for EV (p < 0.04). The platelets/GBWT ratio (cut-off > 46.2) had a sensitivity and specificity of 78 and 86%, PPV 76% and NPV of 87%, and ROC analysis calculated the AUC of 0.864 (CI 0.809-0.919). CONCLUSIONS: GBWT occurs significantly more often in patients with EV. However, because of the low sensitivity, combination with other non-invasive parameters such as platelet count is recommended."],["dc.identifier.doi","10.1186/s12876-018-0852-5"],["dc.identifier.pmid","30071840"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15253"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59263"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.publisher","BioMed Central"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Gall bladder wall thickening as non-invasive screening parameter for esophageal varices – a comparative endoscopic – sonographic study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]