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Schneider, Günter
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Schneider, Günter
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Schneider, Günter
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Schneider, G.
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2021Journal Article [["dc.bibliographiccitation.artnumber","S004520682100883X"],["dc.bibliographiccitation.firstpage","105505"],["dc.bibliographiccitation.journal","Bioorganic Chemistry"],["dc.contributor.author","Lier, Svenja"],["dc.contributor.author","Sellmer, Andreas"],["dc.contributor.author","Orben, Felix"],["dc.contributor.author","Heinzlmeir, Stephanie"],["dc.contributor.author","Krauß, Lukas"],["dc.contributor.author","Schneeweis, Christian"],["dc.contributor.author","Hassan, Zonera"],["dc.contributor.author","Schneider, Carolin"],["dc.contributor.author","Schäfer, Arlette"],["dc.contributor.author","Pongratz, Herwig"],["dc.contributor.author","Schneider, Günter"],["dc.date.accessioned","2021-12-01T09:23:03Z"],["dc.date.available","2021-12-01T09:23:03Z"],["dc.date.issued","2021"],["dc.identifier.doi","10.1016/j.bioorg.2021.105505"],["dc.identifier.pii","S004520682100883X"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/94548"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-478"],["dc.relation.issn","0045-2068"],["dc.rights.uri","https://www.elsevier.com/tdm/userlicense/1.0/"],["dc.title","A novel Cereblon E3 ligase modulator with antitumor activity in gastrointestinal cancer"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]Details DOI2022Journal Article [["dc.bibliographiccitation.journal","Cell Biology and Toxicology"],["dc.contributor.author","Kiweler, Nicole"],["dc.contributor.author","Schwarz, Helena"],["dc.contributor.author","Nguyen, Alexandra"],["dc.contributor.author","Matschos, Stephanie"],["dc.contributor.author","Mullins, Christina"],["dc.contributor.author","Piée-Staffa, Andrea"],["dc.contributor.author","Brachetti, Christina"],["dc.contributor.author","Roos, Wynand P."],["dc.contributor.author","Schneider, Günter"],["dc.contributor.author","Linnebacher, Michael"],["dc.contributor.author","Krämer, Oliver H."],["dc.date.accessioned","2022-06-01T09:39:57Z"],["dc.date.available","2022-06-01T09:39:57Z"],["dc.date.issued","2022"],["dc.description.abstract","Abstract The epigenetic modifier histone deacetylase-2 (HDAC2) is frequently dysregulated in colon cancer cells. Microsatellite instability (MSI), an unfaithful replication of DNA at nucleotide repeats, occurs in about 15% of human colon tumors. MSI promotes a genetic frameshift and consequently a loss of HDAC2 in up to 43% of these tumors. We show that long-term and short-term cultures of colorectal cancers with MSI contain subpopulations of cells lacking HDAC2. These can be isolated as single cell-derived, proliferating populations. Xenografted patient-derived colon cancer tissues with MSI also show variable patterns of HDAC2 expression in mice. HDAC2-positive and HDAC2-negative RKO cells respond similarly to pharmacological inhibitors of the class I HDACs HDAC1/HDAC2/HDAC3. In contrast to this similarity, HDAC2-negative and HDAC2-positive RKO cells undergo differential cell cycle arrest and apoptosis induction in response to the frequently used chemotherapeutic 5-fluorouracil, which becomes incorporated into and damages RNA and DNA. 5-fluorouracil causes an enrichment of HDAC2-negative RKO cells in vitro and in a subset of primary colorectal tumors in mice. 5-fluorouracil induces the phosphorylation of KAP1, a target of the checkpoint kinase ataxia-telangiectasia mutated (ATM), stronger in HDAC2-negative cells than in their HDAC2-positive counterparts. Pharmacological inhibition of ATM sensitizes RKO cells to cytotoxic effects of 5-fluorouracil. These findings demonstrate that HDAC2 and ATM modulate the responses of colorectal cancer cells towards 5-FU. Graphical abstract"],["dc.description.sponsorship"," wilhelm sander-stiftung"],["dc.description.sponsorship","brigitte und dr. konstanze wegener-stiftung"],["dc.description.sponsorship"," deutsche forschungsgemeinschaft"],["dc.description.sponsorship"," Universitätsmedizin der Johannes Gutenberg-Universität Mainz 501100014584"],["dc.identifier.doi","10.1007/s10565-022-09731-3"],["dc.identifier.pii","9731"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/108600"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-572"],["dc.relation.eissn","1573-6822"],["dc.relation.issn","0742-2091"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","The epigenetic modifier HDAC2 and the checkpoint kinase ATM determine the responses of microsatellite instable colorectal cancer cells to 5-fluorouracil"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]Details DOI2010Journal Article [["dc.bibliographiccitation.firstpage","no"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","ChemInform"],["dc.bibliographiccitation.lastpage","no"],["dc.bibliographiccitation.volume","30"],["dc.contributor.author","BES, M. T."],["dc.contributor.author","WOELFLING, J."],["dc.contributor.author","USON, I."],["dc.contributor.author","PELIKAN, S."],["dc.contributor.author","TIETZE, L. F."],["dc.contributor.author","FRANK, E."],["dc.contributor.author","SCHNEIDER, G."],["dc.date.accessioned","2021-12-08T12:28:28Z"],["dc.date.available","2021-12-08T12:28:28Z"],["dc.date.issued","2010"],["dc.identifier.doi","10.1002/chin.199906166"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/95707"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-476"],["dc.relation.eissn","1522-2667"],["dc.relation.issn","0931-7597"],["dc.rights.uri","http://doi.wiley.com/10.1002/tdm_license_1.1"],["dc.title","ChemInform Abstract: A Hexacyclic Estrone Derivative."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]Details DOI2022Journal Article [["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Clinical and Translational Medicine"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Krämer, Oliver H."],["dc.contributor.author","Schneider, Günter"],["dc.date.accessioned","2022-06-01T09:40:15Z"],["dc.date.available","2022-06-01T09:40:15Z"],["dc.date.issued","2022"],["dc.identifier.doi","10.1002/ctm2.858"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/108681"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-572"],["dc.relation.eissn","2001-1326"],["dc.relation.issn","2001-1326"],["dc.title","Single‐cell profiling guided combination therapy of c‐Fos and histone deacetylase inhibitors in diffuse large B‐cell lymphoma"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]Details DOI2022Journal Article [["dc.bibliographiccitation.journal","Cancer Communications"],["dc.contributor.author","Schneeweis, Christian"],["dc.contributor.author","Hassan, Zonera"],["dc.contributor.author","Ascherl, Katja"],["dc.contributor.author","Wirth, Matthias"],["dc.contributor.author","Koutsouli, Stella"],["dc.contributor.author","Orben, Felix"],["dc.contributor.author","Krauß, Lukas"],["dc.contributor.author","Schneider, Carolin"],["dc.contributor.author","Öllinger, Rupert"],["dc.contributor.author","Krämer, Oliver H."],["dc.contributor.author","Schneider, Günter"],["dc.date.accessioned","2022-04-01T10:01:19Z"],["dc.date.available","2022-04-01T10:01:19Z"],["dc.date.issued","2022"],["dc.identifier.doi","10.1002/cac2.12280"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/105649"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-530"],["dc.relation.eissn","2523-3548"],["dc.relation.issn","2523-3548"],["dc.title","Indirect targeting of MYC sensitizes pancreatic cancer cells to mechanistic target of rapamycin (mTOR) inhibition"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]Details DOI2021Journal Article [["dc.bibliographiccitation.firstpage","2520"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","Cells"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Nguyen, Alexandra"],["dc.contributor.author","Dzulko, Melanie"],["dc.contributor.author","Murr, Janine"],["dc.contributor.author","Yen, Yun"],["dc.contributor.author","Schneider, Günter"],["dc.contributor.author","Krämer, Oliver H."],["dc.date.accessioned","2021-12-01T09:22:47Z"],["dc.date.available","2021-12-01T09:22:47Z"],["dc.date.issued","2021"],["dc.description.abstract","Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive disease with a dismal prognosis. Here, we show how an inhibition of de novo dNTP synthesis by the ribonucleotide reductase (RNR) inhibitor hydroxyurea and an inhibition of epigenetic modifiers of the histone deacetylase (HDAC) family affect short-term cultured primary murine PDAC cells. We used clinically relevant doses of hydroxyurea and the class 1 HDAC inhibitor entinostat. We analyzed the cells by flow cytometry and immunoblot. Regarding the induction of apoptosis and DNA replication stress, hydroxyurea and the novel RNR inhibitor COH29 are superior to the topoisomerase-1 inhibitor irinotecan which is used to treat PDAC. Entinostat promotes the induction of DNA replication stress by hydroxyurea. This is associated with an increase in the PP2A subunit PR130/PPP2R3A and a reduction of the ribonucleotide reductase subunit RRM2 and the DNA repair protein RAD51. We further show that class 1 HDAC activity promotes the hydroxyurea-induced activation of the checkpoint kinase ataxia-telangiectasia mutated (ATM). Unlike in other cell systems, ATM is pro-apoptotic in hydroxyurea-treated murine PDAC cells. These data reveal novel insights into a cytotoxic, ATM-regulated, and HDAC-dependent replication stress program in PDAC cells."],["dc.description.abstract","Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive disease with a dismal prognosis. Here, we show how an inhibition of de novo dNTP synthesis by the ribonucleotide reductase (RNR) inhibitor hydroxyurea and an inhibition of epigenetic modifiers of the histone deacetylase (HDAC) family affect short-term cultured primary murine PDAC cells. We used clinically relevant doses of hydroxyurea and the class 1 HDAC inhibitor entinostat. We analyzed the cells by flow cytometry and immunoblot. Regarding the induction of apoptosis and DNA replication stress, hydroxyurea and the novel RNR inhibitor COH29 are superior to the topoisomerase-1 inhibitor irinotecan which is used to treat PDAC. Entinostat promotes the induction of DNA replication stress by hydroxyurea. This is associated with an increase in the PP2A subunit PR130/PPP2R3A and a reduction of the ribonucleotide reductase subunit RRM2 and the DNA repair protein RAD51. We further show that class 1 HDAC activity promotes the hydroxyurea-induced activation of the checkpoint kinase ataxia-telangiectasia mutated (ATM). Unlike in other cell systems, ATM is pro-apoptotic in hydroxyurea-treated murine PDAC cells. These data reveal novel insights into a cytotoxic, ATM-regulated, and HDAC-dependent replication stress program in PDAC cells."],["dc.identifier.doi","10.3390/cells10102520"],["dc.identifier.pii","cells10102520"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/94483"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-478"],["dc.relation.eissn","2073-4409"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0/"],["dc.title","Class 1 Histone Deacetylases and Ataxia-Telangiectasia Mutated Kinase Control the Survival of Murine Pancreatic Cancer Cells upon dNTP Depletion"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]Details DOI2010Journal Article [["dc.bibliographiccitation.firstpage","no"],["dc.bibliographiccitation.issue","29"],["dc.bibliographiccitation.journal","ChemInform"],["dc.bibliographiccitation.lastpage","no"],["dc.bibliographiccitation.volume","29"],["dc.contributor.author","BES, T."],["dc.contributor.author","HAJNAL, A."],["dc.contributor.author","SCHNEIDER, G."],["dc.contributor.author","NOLTEMEYER, M."],["dc.contributor.author","WOELFLING, J."],["dc.date.accessioned","2021-12-08T12:28:21Z"],["dc.date.available","2021-12-08T12:28:21Z"],["dc.date.issued","2010"],["dc.identifier.doi","10.1002/chin.199829232"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/95656"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-476"],["dc.relation.eissn","1522-2667"],["dc.relation.issn","0931-7597"],["dc.rights.uri","http://doi.wiley.com/10.1002/tdm_license_1.1"],["dc.title","ChemInform Abstract: A Steroidal Dihydro-1,3-oxazine Derivative."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]Details DOI2021Journal Article [["dc.bibliographiccitation.firstpage","canres.3209.2020"],["dc.bibliographiccitation.journal","Cancer Research"],["dc.contributor.author","Krauß, Lukas"],["dc.contributor.author","Urban, Bettina C."],["dc.contributor.author","Hastreiter, Sieglinde"],["dc.contributor.author","Schneider, Carolin"],["dc.contributor.author","Wenzel, Patrick"],["dc.contributor.author","Hassan, Zonera"],["dc.contributor.author","Wirth, Matthias"],["dc.contributor.author","Lankes, Katharina"],["dc.contributor.author","Terrasi, Andrea"],["dc.contributor.author","Klement, Christine"],["dc.contributor.author","Schneider, Günter"],["dc.date.accessioned","2022-01-11T14:06:12Z"],["dc.date.available","2022-01-11T14:06:12Z"],["dc.date.issued","2021"],["dc.identifier.doi","10.1158/0008-5472.CAN-20-3209"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/97850"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-507"],["dc.relation.eissn","1538-7445"],["dc.relation.issn","0008-5472"],["dc.title","HDAC2 facilitates pancreatic cancer metastasis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]Details DOI2022Journal Article [["dc.bibliographiccitation.artnumber","e151353"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","JCI Insight"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Orben, Felix"],["dc.contributor.author","Lankes, Katharina"],["dc.contributor.author","Schneeweis, Christian"],["dc.contributor.author","Hassan, Zonera"],["dc.contributor.author","Jakubowsky, Hannah"],["dc.contributor.author","Krauß, Lukas"],["dc.contributor.author","Boniolo, Fabio"],["dc.contributor.author","Schneider, Carolin"],["dc.contributor.author","Schäfer, Arlett"],["dc.contributor.author","Murr, Janine"],["dc.contributor.author","Schneider, Günter"],["dc.date.accessioned","2022-07-01T07:35:20Z"],["dc.date.available","2022-07-01T07:35:20Z"],["dc.date.issued","2022"],["dc.identifier.doi","10.1172/jci.insight.151353"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/112141"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-581"],["dc.relation.eissn","2379-3708"],["dc.title","Epigenetic drug screening defines a PRMT5 inhibitor–sensitive pancreatic cancer subtype"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]Details DOI2023Book Chapter [["dc.bibliographiccitation.firstpage","145"],["dc.bibliographiccitation.lastpage","155"],["dc.bibliographiccitation.seriesnr","2589"],["dc.contributor.author","Abdelsalam, Mohamed"],["dc.contributor.author","Ibrahim, Hany S."],["dc.contributor.author","Krauss, Lukas"],["dc.contributor.author","Zessin, Matthes"],["dc.contributor.author","Vecchio, Anita"],["dc.contributor.author","Hastreiter, Sieglinde"],["dc.contributor.author","Schutkowski, Mike"],["dc.contributor.author","Schneider, Günter"],["dc.contributor.author","Sippl, Wolfgang"],["dc.contributor.editor","Krämer, Oliver H."],["dc.date.accessioned","2022-11-01T10:17:17Z"],["dc.date.available","2022-11-01T10:17:17Z"],["dc.date.issued","2023"],["dc.identifier.doi","10.1007/978-1-0716-2788-4_10"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/116775"],["dc.notes.intern","DOI-Import GROB-605"],["dc.publisher","Springer US"],["dc.publisher.place","New York, NY"],["dc.relation.crisseries","Methods in Molecular Biology"],["dc.relation.eisbn","978-1-0716-2788-4"],["dc.relation.isbn","978-1-0716-2787-7"],["dc.relation.ispartof","HDAC/HAT Function Assessment and Inhibitor Development : Methods and Protocols"],["dc.title","Development of Pyrazine-Anilinobenzamides as Histone Deacetylase HDAC1–3 Selective Inhibitors and Biological Testing Against Pancreas Cancer Cell Lines"],["dc.type","book_chapter"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]Details DOI