Ströbel, Philipp

[["dc.bibliographiccitation.journal","Zeitschrift für Gastroenterologie"],["dc.contributor.author","Brunner, Marius"],["dc.contributor.author","Ammer-Herrmenau, Christoph"],["dc.contributor.author","Biggemann, Lorenz"],["dc.contributor.author","Ströbel, Philipp"],["dc.contributor.author","König, Alexander"],["dc.contributor.author","Ellenrieder, Volker"],["dc.contributor.author","Petzold, Golo"],["dc.date.accessioned","2022-10-04T10:22:18Z"],["dc.date.available","2022-10-04T10:22:18Z"],["dc.date.issued","2022"],["dc.description.abstract","Zusammenfassung\n Hintergrund Granulomatöse Erkrankungen wie Sarkoidose können die Diagnostik bei onkologischen Erkrankungen erschweren, da Metastasen bildmorphologisch häufig nicht von Granulomen zu unterscheiden sind. Die vorliegende Kasuistik beschreibt Diagnostik und Therapie eines Patienten mit fortgeschrittener Sarkoidose und einem hepatisch metastasierten Rektumkarzinom mit schlussendlichem Erreichen eines kurativen Stadiums.\n Fallbeschreibung Bei einem 71-jährigen Patienten wurde im Rahmen der Abklärung ungewollten Gewichtsverlustes sowie einer Anämie ein Adenokarzinom des Rektums diagnostiziert. Die weitere Umfelddiagnostik ergab bildmorphologisch den hochgradigen Verdacht auf multiple rechtshepatische, pulmonale und splenische Metastasen. Histologisch zeigten sich nach bronchoskopischer Biopsie der mediastinalen Lymphknoten jedoch nichtverkäsende Epitheloidzellgranulome als Manifestation einer bis dato nicht bekannten Sarkoidose. Aufgrund des stenosierenden Tumors erfolgte eine Rektumresektion mit Milzextirpation bei intraoperativ hochgradigem Verdacht auf Milzmetastasen. Histologisch zeigten sich in der Milz eine Beteiligung im Rahmen der Sarkoidose. Bei bildmorphologisch weiterhin suspekten rechtshepatischen Leberläsionen erfolgte postoperativ eine Stanzbiopsie einer Läsion, die histologisch sowohl eine Metastase des bekannten Rektumkarzinoms als auch eine Sarkoidose ergab. Es erfolgte eine pseudo(neo)adjuvante Therapie mit 5-Fluorouracil, Leukovorin und Oxaliplatin (FOLFOX) und Panitumumab (Anti-EGF-Antikörper). Bildmorphologisch zeigten sich posttherapeutisch 2 Leberläsionen regredient, mehrere weitere größenstabil. Es erfolgte eine erweiterte Hemihepatektomie rechts mit histologischem Nachweis von sowohl Metastasen als auch Sarkoidose-Herden. Der zu diesem Zeitpunkt tumorfreie Patient wurde in die engmaschige Nachsorge entlassen, die sich im weiteren Verlauf (13 Monate) bildmorphologisch ohne Rezidivhinweis zeigte.\n Diskussion Das gleichzeitige Auftreten von metastasierten Tumorerkrankungen und Sarkoidoseherden führt zu einem diagnostischen Dilemma, da die Manifestationen bildmorphologisch kaum unterschieden werden können. Dieser Fallbereich zeigt, dass eine umfassende histologische Aufarbeitung der unterschiedlichen betroffenen Organe mit konsekutiven Resektionen schlussendlich zu einer Tumorfreiheit des Patienten führen kann."],["dc.identifier.doi","10.1055/a-1880-1639"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/114638"],["dc.language.iso","de"],["dc.notes.intern","DOI-Import GROB-600"],["dc.relation.eissn","1439-7803"],["dc.relation.issn","0044-2771"],["dc.title","Metastase oder Sarkoidose – eine diagnostische Herausforderung beim metastasierten Rektumkarzinom"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["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","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.firstpage","1559"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","European Journal of Gastroenterology & Hepatology"],["dc.bibliographiccitation.lastpage","1565"],["dc.bibliographiccitation.volume","32"],["dc.contributor.author","Petzold, Golo"],["dc.contributor.author","Bremer, Sebastian C.B."],["dc.contributor.author","Knoop, Richard F."],["dc.contributor.author","Amanzada, Ahmad"],["dc.contributor.author","Raddatz, Dirk"],["dc.contributor.author","Ellenrieder, Volker"],["dc.contributor.author","Ströbel, Philipp"],["dc.contributor.author","Kunsch, Steffen"],["dc.contributor.author","Neesse, Albrecht"],["dc.date.accessioned","2021-04-14T08:24:50Z"],["dc.date.available","2021-04-14T08:24:50Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1097/MEG.0000000000001675"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/81439"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.issn","0954-691X"],["dc.title","Noninvasive assessment of liver fibrosis in a real-world cohort of patients with known or suspected chronic liver disease using 2D-shear wave elastography"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2828"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Cancers"],["dc.bibliographiccitation.volume","14"],["dc.contributor.affiliation","Bremer, Sebastian C. B.; 1Clinic for Gastroenterology, Gastrointestinal Oncology and Endocrinology, University Medical Center Goettingen, Georg-August-University, 37075 Goettingen, Germany; alexander.koenig@med.uni-goettingen.de (A.O.K.); ahmad.amanzada@med.uni-goettingen.de (A.A.); volker.ellenrieder@med.uni-goettingen.de (V.E.)"],["dc.contributor.affiliation","Bittner, Gabi; 2Institute of Pathology, University Medical Center Goettingen, Georg-August-University, 37075 Goettingen, Germany; bittnergabi@outlook.de (G.B.); omar.elakad@med.uni-goettingen.de (O.E.); dinterhelen@gmail.com (H.D.); philipp.stroebel@med.uni-goettingen.de (P.S.); hanibal.bohnenberger@med.uni-goettingen.de (H.B.)"],["dc.contributor.affiliation","Elakad, Omar; 2Institute of Pathology, University Medical Center Goettingen, Georg-August-University, 37075 Goettingen, Germany; bittnergabi@outlook.de (G.B.); omar.elakad@med.uni-goettingen.de (O.E.); dinterhelen@gmail.com (H.D.); philipp.stroebel@med.uni-goettingen.de (P.S.); hanibal.bohnenberger@med.uni-goettingen.de (H.B.)"],["dc.contributor.affiliation","Dinter, Helen; 2Institute of Pathology, University Medical Center Goettingen, Georg-August-University, 37075 Goettingen, Germany; bittnergabi@outlook.de (G.B.); omar.elakad@med.uni-goettingen.de (O.E.); dinterhelen@gmail.com (H.D.); philipp.stroebel@med.uni-goettingen.de (P.S.); hanibal.bohnenberger@med.uni-goettingen.de (H.B.)"],["dc.contributor.affiliation","Gaedcke, Jochen; 3Clinic for General, Visceral and Pediatric Surgery, University Medical Center Goettingen, Georg-August-University, 37075 Goettingen, Germany; jochen.gaedcke@med.uni-goettingen.de"],["dc.contributor.affiliation","König, Alexander O.; 1Clinic for Gastroenterology, Gastrointestinal Oncology and Endocrinology, University Medical Center Goettingen, Georg-August-University, 37075 Goettingen, Germany; alexander.koenig@med.uni-goettingen.de (A.O.K.); ahmad.amanzada@med.uni-goettingen.de (A.A.); volker.ellenrieder@med.uni-goettingen.de (V.E.)"],["dc.contributor.affiliation","Amanzada, Ahmad; 1Clinic for Gastroenterology, Gastrointestinal Oncology and Endocrinology, University Medical Center Goettingen, Georg-August-University, 37075 Goettingen, Germany; alexander.koenig@med.uni-goettingen.de (A.O.K.); ahmad.amanzada@med.uni-goettingen.de (A.A.); volker.ellenrieder@med.uni-goettingen.de (V.E.)"],["dc.contributor.affiliation","Ellenrieder, Volker; 1Clinic for Gastroenterology, Gastrointestinal Oncology and Endocrinology, University Medical Center Goettingen, Georg-August-University, 37075 Goettingen, Germany; alexander.koenig@med.uni-goettingen.de (A.O.K.); ahmad.amanzada@med.uni-goettingen.de (A.A.); volker.ellenrieder@med.uni-goettingen.de (V.E.)"],["dc.contributor.affiliation","Freiherr von Hammerstein-Equord, Alexander; 4Clinic for Cardiac, Thoracic and Vascular Surgery, University Medical Center Goettingen, Georg-August-University, 37075 Goettingen, Germany; alexander.hammerstein@med.uni-goettingen.de"],["dc.contributor.affiliation","Ströbel, Philipp; 2Institute of Pathology, University Medical Center Goettingen, Georg-August-University, 37075 Goettingen, Germany; bittnergabi@outlook.de (G.B.); omar.elakad@med.uni-goettingen.de (O.E.); dinterhelen@gmail.com (H.D.); philipp.stroebel@med.uni-goettingen.de (P.S.); hanibal.bohnenberger@med.uni-goettingen.de (H.B.)"],["dc.contributor.affiliation","Bohnenberger, Hanibal; 2Institute of Pathology, University Medical Center Goettingen, Georg-August-University, 37075 Goettingen, Germany; bittnergabi@outlook.de (G.B.); omar.elakad@med.uni-goettingen.de (O.E.); dinterhelen@gmail.com (H.D.); philipp.stroebel@med.uni-goettingen.de (P.S.); hanibal.bohnenberger@med.uni-goettingen.de (H.B.)"],["dc.contributor.author","Bremer, Sebastian C. B."],["dc.contributor.author","Bittner, Gabi"],["dc.contributor.author","Elakad, Omar"],["dc.contributor.author","Dinter, Helen"],["dc.contributor.author","Gaedcke, Jochen"],["dc.contributor.author","König, Alexander O."],["dc.contributor.author","Amanzada, Ahmad"],["dc.contributor.author","Ellenrieder, Volker"],["dc.contributor.author","Freiherr von Hammerstein-Equord, Alexander"],["dc.contributor.author","Ströbel, Philipp"],["dc.contributor.author","Bohnenberger, Hanibal"],["dc.date.accessioned","2022-07-01T07:35:31Z"],["dc.date.available","2022-07-01T07:35:31Z"],["dc.date.issued","2022"],["dc.date.updated","2022-07-08T10:03:36Z"],["dc.description.abstract","Tumor grading is a robust prognostic predictor in patients with neuroendocrine neoplasms (NEN) and guides therapy, especially in tumors with high proliferation. NEN can be separated into well-differentiated and poorly differentiated types. The more aggressive NEN have been further separated into neuroendocrine tumors (NET G3) with a better prognosis and neuroendocrine carcinomas (NEC) with a worse prognosis. Despite this distinction’s tremendous clinical and therapeutic relevance, optimal diagnostic biomarkers are still lacking. In this study, we analyzed the protein expression and prognostic impact of Enhancer of Zeste Homolog 2 (EZH2) by immunohistochemistry in 219 tissue samples of gastroenteropancreatic (GEP-NEN) and pulmonary NEN (P-NEN). EZH2 was almost exclusively expressed in NEN with a proliferation rate above 20% (G3), while all low-grade tumors were nearly negative. Among high-grade NEN, 65% showed high and 35% low expression of EZH2. In this group, the high expression of EZH2 was significantly associated with poor overall survival and NEC histology. Interestingly, EZH2 seems to act independently of Polycomb Repressive Complex 2 (PRC2) in NEN. In conclusion, we propose EZH2 as a robust biomarker for distinguishing between NET G3 and NEC among gastroenteropancreatic and pulmonary NEN."],["dc.description.sponsorship","Deutsche Krebshilfe"],["dc.description.sponsorship","University Medical Center Göttingen"],["dc.description.sponsorship","Else-Kröner-Fresenius-Stiftung"],["dc.description.sponsorship","Open-Access-Publikationsfonds 2022"],["dc.identifier.doi","10.3390/cancers14122828"],["dc.identifier.pii","cancers14122828"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/112190"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/112412"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-581"],["dc.relation.eissn","2072-6694"],["dc.rights","CC BY 4.0"],["dc.title","Enhancer of Zeste Homolog 2 (EZH2) Is a Marker of High-Grade Neuroendocrine Neoplasia in Gastroenteropancreatic and Pulmonary Tract and Predicts Poor Prognosis"],["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","e0188876"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","PLoS One"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Koenig, Alexander"],["dc.contributor.author","Krug, Sebastian"],["dc.contributor.author","Mueller, Daniela"],["dc.contributor.author","Barth, Peter J."],["dc.contributor.author","Koenig, Ute"],["dc.contributor.author","Scharf, Michael"],["dc.contributor.author","Ellenrieder, Volker"],["dc.contributor.author","Michl, Patrick"],["dc.contributor.author","Moll, Roland"],["dc.contributor.author","Homayunfar, Kia"],["dc.contributor.author","Kann, Peter Herbert"],["dc.contributor.author","Stroebel, Philipp"],["dc.contributor.author","Gress, Thomas M."],["dc.contributor.author","Rinke, Anja"],["dc.contributor.editor","Ahmad, Aamir"],["dc.date.accessioned","2020-12-10T18:42:05Z"],["dc.date.available","2020-12-10T18:42:05Z"],["dc.date.issued","2017"],["dc.identifier.doi","10.1371/journal.pone.0188876"],["dc.identifier.eissn","1932-6203"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15672"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77798"],["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","Clinicopathological hallmarks and biomarkers of colorectal neuroendocrine neoplasms"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","227"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Digestion"],["dc.bibliographiccitation.lastpage","235"],["dc.bibliographiccitation.volume","102"],["dc.contributor.affiliation","Bremer, Sebastian C.B.; \r\n aClinic for Gastroenterology and Gastrointestinal Oncology, University Medical Center Goettingen, Georg-August-University, Goettingen, Germany"],["dc.contributor.affiliation","Conradi, Lena-Christin; \r\n bClinic for General, Visceral and Pediatric Surgery, University Medical Center Goettingen, Georg-August-University, Goettingen, Germany"],["dc.contributor.affiliation","Mechie, Nicolae-Catalin; \r\n aClinic for Gastroenterology and Gastrointestinal Oncology, University Medical Center Goettingen, Georg-August-University, Goettingen, Germany"],["dc.contributor.affiliation","Amanzada, Ahmad; \r\n aClinic for Gastroenterology and Gastrointestinal Oncology, University Medical Center Goettingen, Georg-August-University, Goettingen, Germany"],["dc.contributor.affiliation","Mavropoulou, Eirini; \r\n aClinic for Gastroenterology and Gastrointestinal Oncology, University Medical Center Goettingen, Georg-August-University, Goettingen, Germany"],["dc.contributor.affiliation","Kitz, Julia; \r\n cInstitute of Pathology, University Medical Center Goettingen, Georg-August-University, Goettingen, Germany"],["dc.contributor.affiliation","Ghadimi, Michael; \r\n bClinic for General, Visceral and Pediatric Surgery, University Medical Center Goettingen, Georg-August-University, Goettingen, Germany"],["dc.contributor.affiliation","Ellenrieder, Volker; \r\n aClinic for Gastroenterology and Gastrointestinal Oncology, University Medical Center Goettingen, Georg-August-University, Goettingen, Germany"],["dc.contributor.affiliation","Ströbel, Philipp; \r\n cInstitute of Pathology, University Medical Center Goettingen, Georg-August-University, Goettingen, Germany"],["dc.contributor.affiliation","Hessmann, Elisabeth; \r\n aClinic for Gastroenterology and Gastrointestinal Oncology, University Medical Center Goettingen, Georg-August-University, Goettingen, Germany"],["dc.contributor.affiliation","Gaedcke, Jochen; \r\n bClinic for General, Visceral and Pediatric Surgery, University Medical Center Goettingen, Georg-August-University, Goettingen, Germany"],["dc.contributor.affiliation","Bohnenberger, Hanibal; \r\n cInstitute of Pathology, University Medical Center Goettingen, Georg-August-University, Goettingen, Germany"],["dc.contributor.author","Bremer, Sebastian C. B."],["dc.contributor.author","Mechie, Nicolae-Catalin"],["dc.contributor.author","Mavropoulou, Eirini"],["dc.contributor.author","Ellenrieder, Volker"],["dc.contributor.author","Hessmann, Elisabeth"],["dc.contributor.author","Conradi, Lena-Christin"],["dc.contributor.author","Amanzada, Ahmad"],["dc.contributor.author","Kitz, Julia"],["dc.contributor.author","Ghadimi, Michael"],["dc.contributor.author","Ströbel, Philipp"],["dc.contributor.author","Gaedcke, Jochen"],["dc.contributor.author","Bohnenberger, Hanibal"],["dc.date.accessioned","2021-04-26T11:54:07Z"],["dc.date.available","2021-04-26T11:54:07Z"],["dc.date.issued","2021"],["dc.date.updated","2022-03-21T21:17:53Z"],["dc.description.abstract","Colorectal cancer (CRC) is the leading gastrointestinal malignancy. The development from premalignant intraepithelial lesions leading to invasive cancer is paradigmatic for the stepwise carcinogenesis of epithelial cancers, but the knowledge of the underlying mechanism of carcinogenesis and progression of CRC is still incomplete. The understanding of epigenetic mechanisms of carcinogenesis has led to new therapeutic approaches during the last years. Enhancer of zeste homolog 2 (EZH2) is one central epigenetic silencer of the polycomb repressor complex 2 (PRC2) that is already in clinical use as a novel drug target and is associated with poorer prognosis in several cancer entities."],["dc.identifier","31694013"],["dc.identifier.doi","10.1159/000504093"],["dc.identifier.pmid","31694013"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/84358"],["dc.language.iso","en"],["dc.publisher","S. Karger AG"],["dc.relation.eissn","1421-9867"],["dc.relation.issn","0012-2823"],["dc.relation.issn","1421-9867"],["dc.rights.uri","https://www.karger.com/Services/SiteLicenses"],["dc.title","Enhancer of Zeste Homolog 2 in Colorectal Cancer Development and Progression"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Zeitschrift für Gastroenterologie"],["dc.contributor.author","Petzold, Golo"],["dc.contributor.author","Ströbel, Philipp"],["dc.contributor.author","Seif Amir Hosseini, Ali"],["dc.contributor.author","Ellenrieder, Volker"],["dc.contributor.author","Neesse, Albrecht"],["dc.date.accessioned","2021-12-01T09:21:00Z"],["dc.date.available","2021-12-01T09:21:00Z"],["dc.date.issued","2021"],["dc.description.abstract","Abstract Cystic liver lesions (CLL) are common and, in the majority of cases, benign. However, the range of differential diagnoses of CLL is wide. A combination of medical history, blood test results, and imaging can help find the correct diagnosis. We report the case of a 38-year-old immunocompromised female patient with a history of thymectomy and postoperative radiation 3 years prior due to thymoma. Subsequently, the patient was referred to our department for clarification of a cystic liver lesion. During short-term follow-up, the lesion increased in size, and due to the contrast agent behavior in the ultrasound and MRI examination, the suspicion of a biliary cystadenocarcinoma was considered. Furthermore, imaging showed several subcentimetric liver lesions of unknown dignity. Finally, pericystectomy and atypical partial liver resection was performed. Histology revealed a cystic metastasis of the malignant B3 thymoma and a cavernous hemangioma. Liver metastases of a thymoma are rare, and this is the first case of a cystic liver metastasis of a thymoma. The presented case illustrates that in the management of CLLs beside imaging techniques, the medical history with previous conditions should be considered, especially in past malignancies."],["dc.description.abstract","Abstract Cystic liver lesions (CLL) are common and, in the majority of cases, benign. However, the range of differential diagnoses of CLL is wide. A combination of medical history, blood test results, and imaging can help find the correct diagnosis. We report the case of a 38-year-old immunocompromised female patient with a history of thymectomy and postoperative radiation 3 years prior due to thymoma. Subsequently, the patient was referred to our department for clarification of a cystic liver lesion. During short-term follow-up, the lesion increased in size, and due to the contrast agent behavior in the ultrasound and MRI examination, the suspicion of a biliary cystadenocarcinoma was considered. Furthermore, imaging showed several subcentimetric liver lesions of unknown dignity. Finally, pericystectomy and atypical partial liver resection was performed. Histology revealed a cystic metastasis of the malignant B3 thymoma and a cavernous hemangioma. Liver metastases of a thymoma are rare, and this is the first case of a cystic liver metastasis of a thymoma. The presented case illustrates that in the management of CLLs beside imaging techniques, the medical history with previous conditions should be considered, especially in past malignancies."],["dc.identifier.doi","10.1055/a-1659-4419"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/94320"],["dc.language.iso","de"],["dc.notes.intern","DOI-Import GROB-478"],["dc.relation.eissn","1439-7803"],["dc.relation.issn","0044-2771"],["dc.title","Liver metastasis mimicking a liver cyst of a thymoma in a 38-year-old immunocompromised patient"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["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.firstpage","491"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Molecular Cancer Therapeutics"],["dc.bibliographiccitation.lastpage","502"],["dc.bibliographiccitation.volume","15"],["dc.contributor.author","Zhang, L."],["dc.contributor.author","Baumgart, Sandra"],["dc.contributor.author","Chen, Nai-Ming"],["dc.contributor.author","Zhang, J."],["dc.contributor.author","Billadeau, Daniel D."],["dc.contributor.author","Gaisina, Irina N."],["dc.contributor.author","Kozikowski, Alan P."],["dc.contributor.author","Singh, Shiv K."],["dc.contributor.author","Fink, Daniel"],["dc.contributor.author","Ströbel, Philipp"],["dc.contributor.author","Klindt, Caroline"],["dc.contributor.author","Bamlet, William R."],["dc.contributor.author","König, Alexander O."],["dc.contributor.author","Heßmann, Elisabeth"],["dc.contributor.author","Gress, Thomas M."],["dc.contributor.author","Ellenrieder, Volker"],["dc.contributor.author","Neeße, Albrecht"],["dc.date.accessioned","2020-12-10T18:37:46Z"],["dc.date.available","2020-12-10T18:37:46Z"],["dc.date.issued","2016"],["dc.description.abstract","We aimed to investigate the mechanistic, functional, and therapeutic role of glycogen synthase kinase 3 beta (GSK-3 beta) in the regulation and activation of the proinflammatory oncogenic transcription factor nuclear factor of activated T cells (NFATc2) in pancreatic cancer. IHC, qPCR, immunoblotting, immunofluorescence microscopy, and proliferation assays were used to analyze mouse and human tissues and cell lines. Protein-protein interactions and promoter regulation were analyzed by coimmunoprecipitation, DNA pulldown, reporter, and ChIP assays. Preclinical assays were performed using a variety of pancreatic cancer cells lines, xenografts, and a genetically engineered mouse model (GEMM). GSK-3 beta-dependent SP2 phosphorylationmediates NFATc2 protein stability in the nucleus of pancreatic cancer cells stimulating pancreatic cancer growth. In addition to protein stabilization, GSK-3 beta also maintains NFATc2 activation through a distinct mechanism involving stabilization of NFATc2-STAT3 complexes independent of SP2 phosphorylation. For NFATc2-STAT3 complex formation, GSK-3 beta-mediated phosphorylation of STAT3 at Y705 is required to stimulate euchromatin formation of NFAT target promoters, such as cyclin-dependent kinase-6, which promotes tumor growth. Finally, preclinical experiments suggest that targeting the NFATc2-STAT3-GSK-3b module inhibits proliferation and tumor growth and interferes with inflammation-induced pancreatic cancer progression in Kras(G12D) mice. In conclusion, we describe a novel mechanism by which GSK3 beta fine-tunes NFATc2 and STAT3 transcriptional networks to integrate upstream signaling events that govern pancreatic cancer progression and growth. Furthermore, the therapeutic potential of GSK-3 beta is demonstrated for the first time in a relevant Kras and inflammation-induced GEMM for pancreatic cancer. (C) 2016 AACR."],["dc.identifier.doi","10.1158/1535-7163.MCT-15-0309"],["dc.identifier.eissn","1538-8514"],["dc.identifier.isi","000373595600015"],["dc.identifier.issn","1535-7163"],["dc.identifier.pmid","26823495"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77088"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Assoc Cancer Research"],["dc.relation.issn","1538-8514"],["dc.relation.issn","1535-7163"],["dc.title","GSK-3 beta Governs Inflammation-Induced NFATc2 Signaling Hubs to Promote Pancreatic Cancer Progression"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]