Ströbel, Philipp

[["dc.bibliographiccitation.journal","Oncology Research and Treatment"],["dc.bibliographiccitation.volume","39"],["dc.contributor.author","Jo, Peter"],["dc.contributor.author","Kitz, Julia"],["dc.contributor.author","Conradi, Lena-Christin"],["dc.contributor.author","Azizian, A."],["dc.contributor.author","Bernhardt, M."],["dc.contributor.author","Wolff, Hendrik Andreas"],["dc.contributor.author","Schirmer, Markus Anton"],["dc.contributor.author","Koenig, A."],["dc.contributor.author","Grade, Marian"],["dc.contributor.author","Ghadimi, Michael B."],["dc.contributor.author","Stroebel, Philipp"],["dc.contributor.author","Schildhaus, Hans-Ulrich"],["dc.contributor.author","Gaedcke, Jochen"],["dc.date.accessioned","2018-11-07T10:20:53Z"],["dc.date.available","2018-11-07T10:20:53Z"],["dc.date.issued","2016"],["dc.format.extent","75"],["dc.identifier.isi","000371353700239"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/41971"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Karger"],["dc.publisher.place","Basel"],["dc.relation.issn","2296-5262"],["dc.relation.issn","2296-5270"],["dc.title","Heterogeneity of KRAS Mutation Status in Rectal Cancer"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1706"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Journal of Cancer"],["dc.bibliographiccitation.lastpage","1712"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Zschäbitz, Stefanie"],["dc.contributor.author","Erlmeier, Franziska"],["dc.contributor.author","Stöhr, Christine"],["dc.contributor.author","Herrmann, Edwin"],["dc.contributor.author","Polifka, Iris"],["dc.contributor.author","Agaimy, Abbas"],["dc.contributor.author","Trojan, Lutz"],["dc.contributor.author","Ströbel, Philipp"],["dc.contributor.author","Becker, Frank"],["dc.contributor.author","Wülfing, Christian"],["dc.contributor.author","Steffens, Sandra"],["dc.date.accessioned","2022-05-02T08:09:39Z"],["dc.date.available","2022-05-02T08:09:39Z"],["dc.date.issued","2022"],["dc.identifier.doi","10.7150/jca.63509"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/107432"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-561"],["dc.relation.issn","1837-9664"],["dc.title","Expression of Prostate-specific Membrane Antigen (PSMA) in Papillary Renal Cell Carcinoma - Overview and Report on a Large Multicenter Cohort"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","738"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Genes Chromosomes and Cancer"],["dc.bibliographiccitation.lastpage","749"],["dc.bibliographiccitation.volume","53"],["dc.contributor.author","Stroebel, Philipp"],["dc.contributor.author","Zettl, Andreas"],["dc.contributor.author","Shilo, Konstantin"],["dc.contributor.author","Chuang, Wen-Yu"],["dc.contributor.author","Nicholson, Andrew G."],["dc.contributor.author","Matsuno, Yoshihiro"],["dc.contributor.author","Gal, Anthony"],["dc.contributor.author","Laeng, Rolf Hubert"],["dc.contributor.author","Engel, Peter"],["dc.contributor.author","Capella, Carlo"],["dc.contributor.author","Marino, Mirella"],["dc.contributor.author","Chan, John Kwok-Cheung"],["dc.contributor.author","Rosenwald, Andreas"],["dc.contributor.author","Travis, William D."],["dc.contributor.author","Franks, Teri J."],["dc.contributor.author","Ellenberger, David"],["dc.contributor.author","Schaefer, Inga-Marie"],["dc.contributor.author","Marx, Alexander"],["dc.date.accessioned","2018-11-07T09:36:21Z"],["dc.date.available","2018-11-07T09:36:21Z"],["dc.date.issued","2014"],["dc.description.abstract","Thymic neuroendocrine tumors (TNET) are rare primary epithelial neoplasms of the thymus. This study aimed to determine clinically relevant parameters for their classification and for therapeutic decisions. We performed a comprehensive histological, clinical, and genetic study of 73 TNET cases (13 thymic typical carcinoids [TTC], 40 thymic atypical carcinoids [TAC], and 20 high-grade neuroendocrine carcinomas [HGNEC] of the thymus), contributed by multiple institutions. The mean number of chromosomal imbalances per tumor was 0.8 in TTC (31% aberrant cases) versus 1.1 in TAC (44% aberrant cases) versus 4.7 in HGNEC (75% aberrant cases). Gains of 8q24 (MYC gene locus) were the most frequent alteration and one of the overlapping features between carcinoids and HGNEC. The 5-year survival rates for TTC, TAC, and HGNEC were 100, 60, and 30%. The 10-year survival rates for TTC and TAC were 50 and 30% (P=0.002). Predictive mitotic cut-off values for TTC versus TAC were 2.5 per 10 high-power fields (HPF; indicating a higher death rate, P=0.062) and 15 per 10 HPF (indicating higher risk of recurrence, P=0.036) for separating HGNEC from TAC. We conclude that the current histopathologic classifications of TNET reflect tumor biology and provide important information for therapeutic management. (C) 2014 Wiley Periodicals, Inc."],["dc.identifier.doi","10.1002/gcc.22183"],["dc.identifier.isi","000339670200003"],["dc.identifier.pmid","24764238"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/32598"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","1098-2264"],["dc.relation.issn","1045-2257"],["dc.title","Tumor Genetics and Survival of Thymic Neuroendocrine Neoplasms: A Multi-Institutional Clinicopathologic Study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["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","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.firstpage","S142"],["dc.bibliographiccitation.journal","Radiotherapy and Oncology"],["dc.bibliographiccitation.volume","127"],["dc.contributor.author","Fokas, E."],["dc.contributor.author","Fietkau, R."],["dc.contributor.author","Hartmann, A."],["dc.contributor.author","Hohenberger, W."],["dc.contributor.author","Grützmann, R."],["dc.contributor.author","Ghadimi, M."],["dc.contributor.author","Liersch, T."],["dc.contributor.author","Ströbel, P."],["dc.contributor.author","Grabenbauer, G."],["dc.contributor.author","Wittekind, C."],["dc.contributor.author","Sauer, R."],["dc.contributor.author","Kaufmann, M."],["dc.contributor.author","Hothorn, T."],["dc.contributor.author","Rödel, C."],["dc.date.accessioned","2020-12-10T15:21:57Z"],["dc.date.available","2020-12-10T15:21:57Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1016/S0167-8140(18)30588-7"],["dc.identifier.issn","0167-8140"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/73225"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","OC-0278: NAR score as surrogate for disease-free survival in the CAO/ARO/AIO-04 phase 3 rectal cancer trial"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e75485"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Beck, Julia"],["dc.contributor.author","Hennecke, Silvia"],["dc.contributor.author","Bornemann-Kolatzki, Kirsten"],["dc.contributor.author","Urnovitz, Howard B."],["dc.contributor.author","Neumann, Stephan"],["dc.contributor.author","Stroebel, Philipp"],["dc.contributor.author","Kaup, Franz-Josef"],["dc.contributor.author","Brenig, Bertram"],["dc.contributor.author","Schuetz, Ekkehard"],["dc.date.accessioned","2018-11-07T09:19:45Z"],["dc.date.available","2018-11-07T09:19:45Z"],["dc.date.issued","2013"],["dc.description.abstract","Mammary tumors are the most frequent cancers in female dogs exhibiting a variety of histopathological differences. There is lack of knowledge about the genomes of these common dog tumors. Five tumors of three different histological subtypes were evaluated. Massive parallel sequencing (MPS) was performed in comparison to the respective somatic genome of each animal. Copy number and structural aberrations were validated using droplet digital PCR (ddPCR). Using mate-pair sequencing chromosomal aneuploidies were found in two tumors, frequent smaller deletions were found in one, inter-chromosomal fusions in one other, whereas one tumor was almost normal. These aberrations affect several known cancer associated genes such as cMYC, and KIT. One common deletion of the proximal end of CFA27, harboring the tumor suppressor gene PFDN5 was detected in four tumors. Using ddPCR, this deletion was validated and detected in 50% of tumors (N = 20). Breakpoint specific dPCRs were established for four tumors and tumor specific cell-free DNA (cfDNA) was detected in the plasma. In one animal tumor-specific cfDNA was found >1 year after surgery, attributable to a lung metastasis. Paired-end sequencing proved that copy-number imbalances of the tumor are reflected by the cfDNA. This report on chromosomal instability of canine mammary cancers reveals similarities to human breast cancers as well as special canine alterations. This animal model provides a framework for using MPS for screening for individual cancer biomarkers with cost effective confirmation and monitoring using ddPCR. The possibility exists that ddPCR can be expanded to screening for common cancer related variants."],["dc.identifier.doi","10.1371/journal.pone.0075485"],["dc.identifier.isi","000325423500069"],["dc.identifier.pmid","24098698"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/9419"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/28716"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Public Library Science"],["dc.relation.issn","1932-6203"],["dc.rights","CC BY 2.5"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.5"],["dc.title","Genome Aberrations in Canine Mammary Carcinomas and Their Detection in Cell-Free Plasma DNA"],["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","894"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","ANNALS OF CLINICAL AND TRANSLATIONAL NEUROLOGY"],["dc.bibliographiccitation.lastpage","905"],["dc.bibliographiccitation.volume","2"],["dc.contributor.author","Belharazem, Djeda"],["dc.contributor.author","Schalke, Berthold"],["dc.contributor.author","Gold, Ralf"],["dc.contributor.author","Nix, Wilfred"],["dc.contributor.author","Vitacolonna, Mario"],["dc.contributor.author","Hohenberger, Peter"],["dc.contributor.author","Roessner, Eric"],["dc.contributor.author","Schulze, Torsten J."],["dc.contributor.author","Saruhan-Direskeneli, Gueher"],["dc.contributor.author","Yilmaz, Vuslat"],["dc.contributor.author","Ott, German"],["dc.contributor.author","Stroebel, Philipp"],["dc.contributor.author","Marx, Alexander"],["dc.date.accessioned","2018-11-07T09:51:57Z"],["dc.date.available","2018-11-07T09:51:57Z"],["dc.date.issued","2015"],["dc.description.abstract","Objective: The capacity of thymomas to generate mature CD4+ effector T cells from immature precursors inside the tumor and export them to the blood is associated with thymoma-associated myasthenia gravis (TAMG). Why TAMG (+) thymomas generate and export more mature CD4+ T cells than MG(-) thymomas is unknown. Methods: Unfixed thymoma tissue, thymocytes derived thereof, peripheral blood mononuclear cells (PBMCs), T-cell subsets and B cells were analysed using qRT-PCR and western blotting. Survival of PBMCs was measured by MTT assay. FAS-mediated apoptosis in PBMCs was quantified by flow cytometry. NF-kappa B in PBMCs was inhibited by the NF-kappa B-Inhibitor, EF24 prior to FAS-Ligand (FASLG) treatment for apoptosis induction. Results: Expression levels of the apoptosis inhibitor cellular FLICE-like inhibitory protein (c-FLIP) in blood T cells and intratumorous thymocytes were higher in TAMG(+) than in MG(-) thymomas and non-neoplastic thymic remnants. Thymocytes and PBMCs of TAMG patients showed nuclear NF-kappa B accumulation and apoptosis resistance to FASLG stimulation that was sensitive to NF-kappa B blockade. Thymoma removal reduced cFLIP expression in PBMCs. Interpretation: We conclude that thymomas induce cFLIP overexpression in thymocytes and their progeny, blood T cells. We suggest that the stronger cFLIP overexpression in TAMG(+) compared to MG(-) thymomas allows for the more efficient generation of mature CD4+ T cells in TAMG(+) thymomas. cFLIP overexpression in thymocytes and exported CD4+ T cells of patients with TAMG might contribute to the pathogenesis of TAMG by impairing central and peripheral T-cell tolerance."],["dc.identifier.doi","10.1002/acn3.210"],["dc.identifier.isi","000367238200003"],["dc.identifier.pmid","26401511"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/36014"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","2328-9503"],["dc.title","cFLIP overexpression in T cells in thymoma-associated myasthenia gravis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]