Bohnenberger, Hanibal

[["dc.bibliographiccitation.firstpage","549"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Cancer Cell"],["dc.bibliographiccitation.lastpage","+"],["dc.bibliographiccitation.volume","31"],["dc.contributor.author","Mohr, Sebastian"],["dc.contributor.author","Döbele, Carmen"],["dc.contributor.author","Comoglio, Federico"],["dc.contributor.author","Berg, Tobias"],["dc.contributor.author","Beck, Julia"],["dc.contributor.author","Bohnenberger, Hanibal"],["dc.contributor.author","Alexe, Gabriela"],["dc.contributor.author","Corso, Jasmin"],["dc.contributor.author","Ströbel, Philipp"],["dc.contributor.author","Wachter, Astrid"],["dc.contributor.author","Beißbarth, Tim"],["dc.contributor.author","Schnuetgen, Frank"],["dc.contributor.author","Cremer, Anjali"],["dc.contributor.author","Haetscher, Nadine"],["dc.contributor.author","Goellner, Stefanie"],["dc.contributor.author","Rouhi, Arefeh"],["dc.contributor.author","Palmqvist, Lars"],["dc.contributor.author","Rieger, Michael A."],["dc.contributor.author","Schroeder, Timm"],["dc.contributor.author","Boenig, Halvard"],["dc.contributor.author","Meuller-Tidow, Carsten"],["dc.contributor.author","Kuchenbauer, Florian"],["dc.contributor.author","Schuetz, Ekkehard"],["dc.contributor.author","Green, Anthony R."],["dc.contributor.author","Urlaub, Henning"],["dc.contributor.author","Stegmaier, Kimberly"],["dc.contributor.author","Humphries, R. Keith"],["dc.contributor.author","Serve, Hubert"],["dc.contributor.author","Oellerich, Thomas"],["dc.date.accessioned","2018-11-07T10:25:02Z"],["dc.date.available","2018-11-07T10:25:02Z"],["dc.date.issued","2017"],["dc.description.abstract","The transcription factor Meis1 drives myeloid leukemogenesis in the context of Hox gene overexpression but is currently considered undruggable. We therefore investigated whether myeloid progenitor cells transformed by Hoxa9 and Meis1 become addicted to targetable signaling pathways. A comprehensive (phospho) proteomic analysis revealed that Meis1 increased Syk protein expression and activity. Syk upregulation occurs through a Meis1-dependent feedback loop. By dissecting this loop, we show that Syk is a direct target of miR-146a, whose expression is indirectly regulated by Meis1 through the transcription factor PU. 1. In the context of Hoxa9 overexpression, Syk signaling induces Meis1, recapitulating several leukemogenic features of Hoxa9/Meis1-driven leukemia. Finally, Syk inhibition disrupts the identified regulatory loop, prolonging survival of mice with Hoxa9/Meis1-driven leukemia."],["dc.identifier.doi","10.1016/j.ccell.2017.03.001"],["dc.identifier.isi","000398670600010"],["dc.identifier.pmid","28399410"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14438"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42772"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Cell Press"],["dc.relation.issn","1878-3686"],["dc.relation.issn","1535-6108"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Hoxa9 and Meis1 Cooperatively Induce Addiction to Syk Signaling by Suppressing miR-146a in Acute Myeloid Leukemia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e16712"],["dc.bibliographiccitation.issue","31"],["dc.bibliographiccitation.journal","Medicine"],["dc.bibliographiccitation.volume","98"],["dc.contributor.author","Buentzel, Judith"],["dc.contributor.author","Yao, Sha"],["dc.contributor.author","Elakad, Omar"],["dc.contributor.author","Lois, Anna-Maria"],["dc.contributor.author","Brünies, Jana"],["dc.contributor.author","König, Julia"],["dc.contributor.author","Hinterthaner, Marc"],["dc.contributor.author","Danner, Bernhard C."],["dc.contributor.author","Ströbel, Philipp"],["dc.contributor.author","Emmert, Alexander"],["dc.contributor.author","Bohnenberger, Hanibal"],["dc.date.accessioned","2019-08-09T06:40:34Z"],["dc.date.available","2019-08-09T06:40:34Z"],["dc.date.issued","2019"],["dc.description.abstract","Molecular characterization of lung cancer specimens after radical surgery offers additional prognostic information and may help to guide adjuvant therapeutic procedures. The transcriptional regulators alpha thalassemia/mental retardation X-linked (ATRX) and death domain-associated protein (DAXX) have recently been described in different cancer entities as a useful prognostic biomarker. This study was initiated to explore their protein expression patterns and prognostic value in patients with operable lung cancer disease.The protein abundance (in the following text also named protein expression) of ATRX and DAXX were analyzed by immunohistochemistry in 194 samples of squamous cell lung carcinoma (SQCLC), 111 samples of pulmonary adenocarcinoma (AC) and 40 samples of small cell lung cancer (SCLC). The protein levels of ATRX and DAXX were correlated with clinicopathological characteristics and patient outcome.ATRX showed strong protein expression in 16.2% of AC, 11.9% of SQCLC, and 42.5% of SCLC. DAXX was highly expressed in 54.9% of AC, 76.2% of SQCLC, and 82.5% of SCLC. Immunostaining of both ATRX and DAXX were seen in 14.4% of AC, 11.3% of SQCLC, and 42.5% of SCLC. High protein expression of ATRX was a favorable prognostic marker for patients with AC (hazard ratio 0.38, P = .02). Sub-group analyses showed a significant correlation between ATRX and the clinical stage of SQCLC and SCLC. Histological grading and ATRX were also significantly associated in cases of SQCLC.The presence of ATRX and DAXX are correlated with lung cancer histology. Strong ATRX protein expression is associated with a significantly longer overall survival in patients with AC."],["dc.description.sponsorship","Open-Access-Publikationafonds 2019"],["dc.identifier.doi","10.1097/MD.0000000000016712"],["dc.identifier.pmid","31374064"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16343"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/62353"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.eissn","1536-5964"],["dc.relation.issn","0025-7974"],["dc.rights","CC BY-NC-ND 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/4.0"],["dc.title","Expression and prognostic impact of alpha thalassemia/mental retardation X-linked and death domain-associated protein in human lung cancer"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1220"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","European Journal of Immunology"],["dc.bibliographiccitation.lastpage","1233"],["dc.bibliographiccitation.volume","50"],["dc.contributor.author","Kaiser, Tina K."],["dc.contributor.author","Li, Hu"],["dc.contributor.author","Roßmann, Laura"],["dc.contributor.author","Reichardt, Sybille D."],["dc.contributor.author","Bohnenberger, Hanibal"],["dc.contributor.author","Feldmann, Claus"],["dc.contributor.author","Reichardt, Holger M."],["dc.date.accessioned","2021-04-14T08:27:15Z"],["dc.date.available","2021-04-14T08:27:15Z"],["dc.date.issued","2020"],["dc.description.abstract","Abstract Glucocorticoids (GCs) are widely used to treat acute graft‐versus‐host disease (aGvHD) due to their immunosuppressive activity, but they also reduce the beneficial graft‐versus‐leukemia (GvL) effect of the allogeneic T cells contained in the graft. Here, we tested whether aGvHD therapy could be improved by delivering GCs with the help of inorganic–organic hybrid nanoparticles (IOH‐NPs) that preferentially target myeloid cells. IOH‐NPs containing the GC betamethasone (BMP‐NPs) efficiently reduced morbidity, mortality, and tissue damage in a totally MHC mismatched mouse model of aGvHD. Therapeutic activity was lost in mice lacking the GC receptor (GR) in myeloid cells, confirming the cell type specificity of our approach. BMP‐NPs had no relevant systemic activity but suppressed cytokine and chemokine gene expression locally in the small intestine, which presumably explains their mode of action. Most importantly, BMP‐NPs delayed the development of an adoptively transferred B cell lymphoma better than the free drug, although the overall incidence was unaffected. Our findings thus suggest that employing IOH‐NPs could diminish the risk of relapse associated with GC therapy of aGvHD patients while still allowing to efficiently ameliorate the disease."],["dc.description.abstract","Clinical symptoms and histological hallmarks of acute graft‐versus‐host disease in mice are ameliorated by glucocorticoids when specifically delivered to macrophages with the help of nanoparticles. In addition, this therapeutic intervention improves the graft‐versus‐leukemia effect compared to the free drug, and thus presumably reduces the risk of relapse. image"],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft http://dx.doi.org/10.13039/501100001659"],["dc.identifier.doi","10.1002/eji.201948464"],["dc.identifier.eissn","1521-4141"],["dc.identifier.issn","0014-2980"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/82221"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","1521-4141"],["dc.relation.issn","0014-2980"],["dc.rights","This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited."],["dc.title","Glucocorticoids delivered by inorganic–organic hybrid nanoparticles mitigate acute graft‐versus‐host disease and sustain graft‐versus‐leukemia activity"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2523"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Translational Lung Cancer Research"],["dc.bibliographiccitation.lastpage","2538"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Yao, Sha"],["dc.contributor.author","Peng, Luogen"],["dc.contributor.author","Elakad, Omar"],["dc.contributor.author","Küffer, Stefan"],["dc.contributor.author","Hinterthaner, Marc"],["dc.contributor.author","Danner, Bernhard C."],["dc.contributor.author","Hammerstein-Equord, Alexander von"],["dc.contributor.author","Ströbel, Philipp"],["dc.contributor.author","Bohnenberger, Hanibal"],["dc.date.accessioned","2021-08-12T07:45:40Z"],["dc.date.available","2021-08-12T07:45:40Z"],["dc.date.issued","2021"],["dc.description.sponsorship","Open-Access-Publikationsfonds 2021"],["dc.identifier.doi","10.21037/tlcr-20-1039"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/88522"],["dc.notes.intern","DOI Import GROB-448"],["dc.relation.eissn","2226-4477"],["dc.relation.issn","2218-6751"],["dc.relation.orgunit","Institut für Pathologie"],["dc.rights","CC BY-NC-ND 4.0"],["dc.title","One carbon metabolism in human lung cancer"],["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","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","e28814"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Medicine"],["dc.bibliographiccitation.volume","101"],["dc.contributor.author","Tirilomi, Anna"],["dc.contributor.author","Elakad, Omar"],["dc.contributor.author","Yao, Sha"],["dc.contributor.author","Li, Yuchan"],["dc.contributor.author","Hinterthaner, Marc"],["dc.contributor.author","Danner, Bernhard C."],["dc.contributor.author","Ströbel, Philipp"],["dc.contributor.author","Tirilomis, Theodor"],["dc.contributor.author","Bohnenberger, Hanibal"],["dc.contributor.author","von Hammerstein-Equord, Alexander"],["dc.date.accessioned","2022-02-23T13:44:43Z"],["dc.date.available","2022-02-23T13:44:43Z"],["dc.date.issued","2022-02-11"],["dc.description.abstract","Lung cancer remains the worldwide leading cause of cancer-related death. Currently, prognostic biomarkers for the detection and stratification of lung cancer are being investigated for clinical use. The surface protein cluster of differentiation 49b (CD49b) plays an important role in promoting cell proliferation and invasion in different tumor entities and blocking CD49b improved the tumor immune response. Overexpression of CD49b has been associated with unfavorable survival rates in several malignant tumor entities, such as prostate cancer, gastric cancer and colon cancer. Therefore, we aimed to analyze the protein expression of CD49b in patients with different types of lung cancer and additionally to identify the influence of CD49b on clinicopathological characteristics and overall survival.Expression levels of CD49b were retrospective analyzed by immunohistochemistry in 92 cases of pulmonary adenocarcinoma (AC), 85 cases of squamous cell lung carcinoma (SQCLC) and 32 cases of small cell lung cancer (SCLC) and correlated with clinicopathological characteristics and patients' overall survival.A strong expression of CD49b was most seen in SQCLC (78%), followed by AC (48%) and SCLC (9%). All patients combined, strong expression of CD49b correlated significantly with poorer overall survival. However, an increased expression of CD49b correlated significantly with a poorer survival rate only in SQCLC. In AC and SCLC, no significant correlation could be demonstrated in this regard.In our study, CD49b expression was associated with poor overall survival in patients with SQCLC. Accordingly, CD49b could serve as a new prognostic biomarker and, moreover, be a potential new drug target in SQCLC."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2022"],["dc.identifier.doi","10.1097/MD.0000000000028814"],["dc.identifier.pmid","35147120"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/100370"],["dc.language.iso","en"],["dc.relation.eissn","1536-5964"],["dc.relation.issn","0025-7974"],["dc.relation.issn","1536-5964"],["dc.rights","CC BY 4.0"],["dc.title","Expression and prognostic impact of CD49b in human lung cancer"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["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","1505"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Cellular and Molecular Gastroenterology and Hepatology"],["dc.bibliographiccitation.lastpage","1518"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Muzzi, Chiara"],["dc.contributor.author","Watanabe, Norika"],["dc.contributor.author","Twomey, Eric"],["dc.contributor.author","Meers, Garrit K."],["dc.contributor.author","Reichardt, Holger M."],["dc.contributor.author","Bohnenberger, Hanibal"],["dc.contributor.author","Reichardt, Sybille D."],["dc.date.accessioned","2021-06-01T09:41:22Z"],["dc.date.available","2021-06-01T09:41:22Z"],["dc.date.issued","2021"],["dc.identifier.doi","10.1016/j.jcmgh.2020.12.006"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17779"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/84897"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","2352-345X"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","The Glucocorticoid Receptor in Intestinal Epithelial Cells Alleviates Colitis and Associated Colorectal Cancer in Mice"],["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.firstpage","33"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","The Journal of Pathology: Clinical Research"],["dc.bibliographiccitation.lastpage","47"],["dc.bibliographiccitation.volume","8"],["dc.contributor.affiliation","Fichtner, Alexander; 1\r\nInstitute of Pathology\r\nUniversity Medical Centre Göttingen\r\nGöttingen Germany"],["dc.contributor.affiliation","Joost, Jasmin; 1\r\nInstitute of Pathology\r\nUniversity Medical Centre Göttingen\r\nGöttingen Germany"],["dc.contributor.affiliation","Brockmeyer, Philipp; 2\r\nDepartment of Oral and Maxillofacial Surgery\r\nUniversity Medical Centre Göttingen\r\nGöttingen Germany"],["dc.contributor.affiliation","Kauffmann, Philipp; 2\r\nDepartment of Oral and Maxillofacial Surgery\r\nUniversity Medical Centre Göttingen\r\nGöttingen Germany"],["dc.contributor.affiliation","Schliephake, Henning; 2\r\nDepartment of Oral and Maxillofacial Surgery\r\nUniversity Medical Centre Göttingen\r\nGöttingen Germany"],["dc.contributor.affiliation","Hammerstein‐Equord, Alexander; 3\r\nDepartment of Thoracic and Cardiovascular Surgery\r\nUniversity Medical Centre Göttingen\r\nGöttingen Germany"],["dc.contributor.affiliation","Kueffer, Stefan; 1\r\nInstitute of Pathology\r\nUniversity Medical Centre Göttingen\r\nGöttingen Germany"],["dc.contributor.affiliation","Urlaub, Henning; 4\r\nBioanalytical Mass Spectrometry Group\r\nMax Planck Institute for Biophysical Chemistry\r\nGöttingen Germany"],["dc.contributor.affiliation","Oellerich, Thomas; 6\r\nDepartment of Medicine II, Haematology/Oncology\r\nGoethe University\r\nFrankfurt Germany"],["dc.contributor.affiliation","Ströbel, Philipp; 1\r\nInstitute of Pathology\r\nUniversity Medical Centre Göttingen\r\nGöttingen Germany"],["dc.contributor.affiliation","Bohnenberger, Hanibal; 1\r\nInstitute of Pathology\r\nUniversity Medical Centre Göttingen\r\nGöttingen Germany"],["dc.contributor.affiliation","Bremmer, Felix; 1\r\nInstitute of Pathology\r\nUniversity Medical Centre Göttingen\r\nGöttingen Germany"],["dc.contributor.author","Richter, Annika"],["dc.contributor.author","Fichtner, Alexander"],["dc.contributor.author","Joost, Jasmin"],["dc.contributor.author","Brockmeyer, Philipp"],["dc.contributor.author","Kauffmann, Philipp"],["dc.contributor.author","Schliephake, Henning"],["dc.contributor.author","Hammerstein‐Equord, Alexander"],["dc.contributor.author","Kueffer, Stefan"],["dc.contributor.author","Urlaub, Henning"],["dc.contributor.author","Oellerich, Thomas"],["dc.contributor.author","Bremmer, Felix"],["dc.contributor.author","Ströbel, Philipp"],["dc.contributor.author","Bohnenberger, Hanibal"],["dc.date.accessioned","2021-12-01T09:23:20Z"],["dc.date.available","2021-12-01T09:23:20Z"],["dc.date.issued","2021"],["dc.date.updated","2022-03-20T23:05:20Z"],["dc.description.abstract","Abstract The differentiation between a pulmonary metastasis and a newly developed squamous cell carcinoma of the lung in patients with prior head and neck squamous cell carcinoma (HNSCC) is difficult due to a lack of biomarkers but is crucially important for the prognosis and therapy of the affected patient. By using high‐resolution mass spectrometry in combination with stable isotope labelling by amino acids in cell culture, we identified 379 proteins that are differentially expressed in squamous cell carcinomas of the lung and the head and neck. Of those, CAV1, CAV2, LGALS1, LGALS7, CK19, and UGDH were tested by immunohistochemistry on 194 tissue samples (98 lung and 96 HNSCCs). The combination of CAV1 and LGALS7 was able to distinguish the origin of the squamous cell carcinoma with high accuracy (area under the curve 0.876). This biomarker panel was tested on a cohort of 12 clinically classified lung tumours of unknown origin after HNSCC. Nine of those tumours were immunohistochemically classifiable."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2021"],["dc.identifier.doi","10.1002/cjp2.244"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/94624"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-478"],["dc.relation.eissn","2056-4538"],["dc.rights","CC BY-NC-ND 4.0"],["dc.title","Quantitative proteomics identifies biomarkers to distinguish pulmonary from head and neck squamous cell carcinomas by immunohistochemistry"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]