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.firstpage","S1448"],["dc.bibliographiccitation.issue","S15"],["dc.bibliographiccitation.journal","Journal of Thoracic Disease"],["dc.bibliographiccitation.lastpage","S1457"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Bohnenberger, Hanibal"],["dc.contributor.author","Dinter, Helen"],["dc.contributor.author","König, Alexander"],["dc.contributor.author","Ströbel, Philipp"],["dc.date.accessioned","2020-12-10T18:42:54Z"],["dc.date.available","2020-12-10T18:42:54Z"],["dc.date.issued","2017"],["dc.identifier.doi","10.21037/jtd.2017.02.02"],["dc.identifier.eissn","2077-6624"],["dc.identifier.issn","2072-1439"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/78124"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Neuroendocrine tumors of the thymus and mediastinum"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["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.issue","19"],["dc.bibliographiccitation.journal","Cancer Research"],["dc.bibliographiccitation.volume","74"],["dc.contributor.author","Bohnenberger, Hanibal"],["dc.contributor.author","Stroebel, Philipp"],["dc.contributor.author","Henric-Petri, Hannah"],["dc.contributor.author","Lenz, Christof"],["dc.contributor.author","Emmert, Alexander"],["dc.contributor.author","Bremmer, Felix"],["dc.contributor.author","Strecker, Jasmin"],["dc.contributor.author","Holland, Rainer"],["dc.contributor.author","Hinterthaner, Marc"],["dc.contributor.author","Corso, Jasmin"],["dc.contributor.author","Wagner, Sebastian"],["dc.contributor.author","Kueffer, Stefan"],["dc.contributor.author","Sebastian, Martin"],["dc.contributor.author","Bergmann, Lothar"],["dc.contributor.author","Danner, Bernd"],["dc.contributor.author","Schoendube, Friedrich Albert"],["dc.contributor.author","Serve, Hubert"],["dc.contributor.author","Urlaub, Henning"],["dc.contributor.author","Oellerich, Thomas"],["dc.date.accessioned","2018-11-07T09:33:49Z"],["dc.date.available","2018-11-07T09:33:49Z"],["dc.date.issued","2014"],["dc.identifier.doi","10.1158/1538-7445.AM2014-2487"],["dc.identifier.isi","000349906903219"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/32050"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Assoc Cancer Research"],["dc.publisher.place","Philadelphia"],["dc.relation.conference","105th Annual Meeting of the American-Association-for-Cancer-Research (AACR)"],["dc.relation.eventlocation","San Diego, CA"],["dc.relation.issn","1538-7445"],["dc.relation.issn","0008-5472"],["dc.title","Comprehensive quantitative proteomic profiling of lung cancers reveals novel biomarkers and potential drug targets"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["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","704"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Histopathology"],["dc.bibliographiccitation.lastpage","710"],["dc.bibliographiccitation.volume","70"],["dc.contributor.author","Buerger, Tobias"],["dc.contributor.author","Schaefer, Inga-Marie"],["dc.contributor.author","Kueffer, Stefan"],["dc.contributor.author","Bohnenberger, Hanibal"],["dc.contributor.author","Reuter-Jessen, Kirsten"],["dc.contributor.author","Chan, John Kwok-Cheung"],["dc.contributor.author","Emmert, Alexander"],["dc.contributor.author","Hinterthaner, Marc"],["dc.contributor.author","Marx, Alexander"],["dc.contributor.author","Stroebel, Philipp"],["dc.date.accessioned","2018-11-07T10:25:44Z"],["dc.date.available","2018-11-07T10:25:44Z"],["dc.date.issued","2017"],["dc.description.abstract","AimsThe vast majority of type A thymomas are diagnosed in tumour stages 1 or 2, and metastatic cases are exceedingly rare. The histological and genetic features of such metastatic type A thymomas have not been described in detail. Methods and resultsFive metastatic type A thymomas in tumour stage Masaoka IVb that had been reviewed by a panel of expert pathologists were analysed using comparative genomic hybridization (CGH). Cases 1, 2 and 3 showed the prototypical morphology of type A thymomas with mainly solid growth patterns. These cases displayed only very subtle nuclear irregularities and slight nuclear crowding, but no other atypical features. Mitoses were absent. Cases 3 and 4, in contrast, had a distinctly atypical morphology. CGH revealed partially recurrent alterations in four cases (with and without atypical morphology), including gains on chromosome 1q (one case), 17q (two cases), chromosome 19 (three cases) and 22q (one case) and losses on chromosome 17p (two cases) and 22q (one case). ConclusionRare metastatic type A thymomas, both with typical and atypical' histological features, show partially recurrent genomic alterations that differ from the much more frequent localized and indolent tumours. The fact that these alterations were recurring points to a link between clinical behaviour and molecular features. Our findings may have implications for the management and treatment of such tumours."],["dc.identifier.doi","10.1111/his.13138"],["dc.identifier.isi","000397588600003"],["dc.identifier.pmid","27926794"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42916"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Wiley"],["dc.relation.issn","1365-2559"],["dc.relation.issn","0309-0167"],["dc.title","Metastatic type A thymoma: morphological and genetic correlation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["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","323"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Virchows Archiv"],["dc.bibliographiccitation.lastpage","327"],["dc.bibliographiccitation.volume","476"],["dc.contributor.author","Porubsky, Stefan"],["dc.contributor.author","Jessup, Peter"],["dc.contributor.author","Kee, Damien"],["dc.contributor.author","Sharma, Rajiv"],["dc.contributor.author","Ochi, Ayame"],["dc.contributor.author","Xu, Huiling"],["dc.contributor.author","Froelich, Jens J."],["dc.contributor.author","Nott, Louise"],["dc.contributor.author","Scott, Clare"],["dc.contributor.author","Awad, Raef"],["dc.contributor.author","Moldovan, Cristina"],["dc.contributor.author","Hardikar, Ashutosh A."],["dc.contributor.author","Bohnenberger, Hanibal"],["dc.contributor.author","Küffer, Stefan"],["dc.contributor.author","Ströbel, Philipp"],["dc.contributor.author","Marx, Alexander"],["dc.date.accessioned","2020-12-10T14:10:36Z"],["dc.date.available","2020-12-10T14:10:36Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1007/s00428-019-02644-3"],["dc.identifier.eissn","1432-2307"],["dc.identifier.issn","0945-6317"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/70816"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Potentially actionable FGFR2 high-level amplification in thymic sebaceous carcinoma"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]