Schneider, Günter

[["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"]]

[["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"]]

[["dc.bibliographiccitation.artnumber","104"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","EJNMMI Research"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Schneider, Günter"],["dc.contributor.author","Wirth, Matthias"],["dc.contributor.author","Keller, Ulrich"],["dc.contributor.author","Saur, Dieter"],["dc.date.accessioned","2021-11-25T11:13:53Z"],["dc.date.accessioned","2022-08-16T12:43:40Z"],["dc.date.available","2021-11-25T11:13:53Z"],["dc.date.available","2022-08-16T12:43:40Z"],["dc.date.issued","2021-10-12"],["dc.date.updated","2022-07-29T12:18:23Z"],["dc.description.abstract","Abstract\r\n The incidence and lethality of pancreatic ductal adenocarcinoma (PDAC) will continue to increase in the next decade. For most patients, chemotherapeutic combination therapies remain the standard of care. The development and successful implementation of precision oncology in other gastrointestinal tumor entities point to opportunities also for PDAC. Therefore, markers linked to specific therapeutic responses and important subgroups of the disease are needed. The MYC oncogene is a relevant driver in PDAC and is linked to drug resistance and sensitivity. Here, we update recent insights into MYC biology in PDAC, summarize the connections between MYC and drug responses, and point to an opportunity to image MYC non-invasively. In sum, we propose MYC-associated biology as a basis for the development of concepts for precision oncology in PDAC."],["dc.identifier.citation","EJNMMI Research. 2021 Oct 12;11(1):104"],["dc.identifier.doi","10.1186/s13550-021-00843-1"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/93546"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/112742"],["dc.language.iso","en"],["dc.rights","CC BY 4.0"],["dc.rights.holder","The Author(s)"],["dc.subject","Pancreatic cancer"],["dc.subject","Precision oncology"],["dc.subject","MYC"],["dc.subject","Targeted therapies"],["dc.title","Rationale for MYC imaging and targeting in pancreatic 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","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"]]

[["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"]]

[["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"]]

[["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"]]

[["dc.bibliographiccitation.firstpage","1301"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Cancers"],["dc.bibliographiccitation.volume","14"],["dc.contributor.affiliation","Flebbe, Hannah; 1Department of General, Visceral and Pediatric Surgery, University Medical Center Goettingen, 37075 Goettingen, Germany; hannah.flebbe@med.uni-goettingen.de (H.F.); melanie.spitzner@med.uni-goettingen.de (M.S.); pmarquet@tabea-krankenhaus.de (P.E.M.); jochen.gaedcke@med.uni-goettingen.de (J.G.); mghadim@uni-goettingen.de (B.M.G.); guenter.schneider@med.uni-goettingen.de (G.S.)"],["dc.contributor.affiliation","Spitzner, Melanie; 1Department of General, Visceral and Pediatric Surgery, University Medical Center Goettingen, 37075 Goettingen, Germany; hannah.flebbe@med.uni-goettingen.de (H.F.); melanie.spitzner@med.uni-goettingen.de (M.S.); pmarquet@tabea-krankenhaus.de (P.E.M.); jochen.gaedcke@med.uni-goettingen.de (J.G.); mghadim@uni-goettingen.de (B.M.G.); guenter.schneider@med.uni-goettingen.de (G.S.)"],["dc.contributor.affiliation","Marquet, Philipp Enno; 1Department of General, Visceral and Pediatric Surgery, University Medical Center Goettingen, 37075 Goettingen, Germany; hannah.flebbe@med.uni-goettingen.de (H.F.); melanie.spitzner@med.uni-goettingen.de (M.S.); pmarquet@tabea-krankenhaus.de (P.E.M.); jochen.gaedcke@med.uni-goettingen.de (J.G.); mghadim@uni-goettingen.de (B.M.G.); guenter.schneider@med.uni-goettingen.de (G.S.)"],["dc.contributor.affiliation","Gaedcke, Jochen; 1Department of General, Visceral and Pediatric Surgery, University Medical Center Goettingen, 37075 Goettingen, Germany; hannah.flebbe@med.uni-goettingen.de (H.F.); melanie.spitzner@med.uni-goettingen.de (M.S.); pmarquet@tabea-krankenhaus.de (P.E.M.); jochen.gaedcke@med.uni-goettingen.de (J.G.); mghadim@uni-goettingen.de (B.M.G.); guenter.schneider@med.uni-goettingen.de (G.S.)"],["dc.contributor.affiliation","Ghadimi, B. Michael; 1Department of General, Visceral and Pediatric Surgery, University Medical Center Goettingen, 37075 Goettingen, Germany; hannah.flebbe@med.uni-goettingen.de (H.F.); melanie.spitzner@med.uni-goettingen.de (M.S.); pmarquet@tabea-krankenhaus.de (P.E.M.); jochen.gaedcke@med.uni-goettingen.de (J.G.); mghadim@uni-goettingen.de (B.M.G.); guenter.schneider@med.uni-goettingen.de (G.S.)"],["dc.contributor.affiliation","Rieken, Stefan; 3Department of Radiotherapy and Radiooncology, University Medical Center Goettingen, 37075 Goettingen, Germany; stefan.rieken@med.uni-goettingen.de"],["dc.contributor.affiliation","Schneider, Günter; 1Department of General, Visceral and Pediatric Surgery, University Medical Center Goettingen, 37075 Goettingen, Germany; hannah.flebbe@med.uni-goettingen.de (H.F.); melanie.spitzner@med.uni-goettingen.de (M.S.); pmarquet@tabea-krankenhaus.de (P.E.M.); jochen.gaedcke@med.uni-goettingen.de (J.G.); mghadim@uni-goettingen.de (B.M.G.); guenter.schneider@med.uni-goettingen.de (G.S.)"],["dc.contributor.affiliation","Koenig, Alexander O.; 4Department of Gastroenterology, Gastrointestinal Oncology and Endocrinology, University Medical Center Goettingen, 37075 Goettingen, Germany; alexander.koenig@med.uni-goettingen.de"],["dc.contributor.affiliation","Grade, Marian; 1Department of General, Visceral and Pediatric Surgery, University Medical Center Goettingen, 37075 Goettingen, Germany; hannah.flebbe@med.uni-goettingen.de (H.F.); melanie.spitzner@med.uni-goettingen.de (M.S.); pmarquet@tabea-krankenhaus.de (P.E.M.); jochen.gaedcke@med.uni-goettingen.de (J.G.); mghadim@uni-goettingen.de (B.M.G.); guenter.schneider@med.uni-goettingen.de (G.S.)"],["dc.contributor.author","Flebbe, Hannah"],["dc.contributor.author","Spitzner, Melanie"],["dc.contributor.author","Marquet, Philipp Enno"],["dc.contributor.author","Gaedcke, Jochen"],["dc.contributor.author","Ghadimi, B. Michael"],["dc.contributor.author","Rieken, Stefan"],["dc.contributor.author","Schneider, Günter"],["dc.contributor.author","Koenig, Alexander O."],["dc.contributor.author","Grade, Marian"],["dc.date.accessioned","2022-04-01T10:00:34Z"],["dc.date.available","2022-04-01T10:00:34Z"],["dc.date.issued","2022"],["dc.date.updated","2022-04-08T08:31:13Z"],["dc.description.abstract","The debate is ongoing regarding the potential role of preoperative chemoradiotherapy (CRT) for patients with pancreatic ductal adenocarcinoma (PDAC), and whether it should be reserved for borderline resectable or unresectable tumors. However, treatment response is heterogeneous, implicating the need to unveil and overcome the underlying mechanisms of resistance. Activation of the transcription factor STAT3 was recently linked to CRT resistance in other gastrointestinal cancers such as rectal and esophageal cancers, but its role in PDAC needs to be clarified. Protein expression and phosphorylation of STAT3 was determined in PDAC cell lines and connected to transcriptional activity measured by dual-luciferase reporter gene assays. Inhibition of STAT3 signaling was achieved by RNAi or the small-molecule inhibitor napabucasin. We observed a positive correlation between STAT3 signaling activity and CRT resistance. Importantly, genetical and pharmacological perturbation of the IL-6/STAT3 pathway resulted in CRT sensitization specifically in those cell lines, in which STAT3 activity was augmented by IL-6. In conclusion, our data underscore the general importance of IL-6/STAT3 signaling for CRT resistance and suggest that pathway inhibition may represents a putative treatment strategy in order to increase the fraction of patients with PDAC who are candidates for surgical approaches."],["dc.identifier.doi","10.3390/cancers14051301"],["dc.identifier.pii","cancers14051301"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/105459"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-530"],["dc.relation.eissn","2072-6694"],["dc.rights","Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/)."],["dc.title","Targeting STAT3 Signaling Facilitates Responsiveness of Pancreatic Cancer Cells to Chemoradiotherapy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["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"]]

[["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"]]