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Spitzner, Melanie
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Spitzner, Melanie
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Spitzner, Melanie
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Spitzner, M.
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2008Conference Abstract [["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","EJC SUPPLEMENTS"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Grade, Marian"],["dc.contributor.author","Hummon, Amanda B."],["dc.contributor.author","Camps, Jordi"],["dc.contributor.author","Emons, G."],["dc.contributor.author","Spitzner, Melanie"],["dc.contributor.author","Gaedcke, Jochen"],["dc.contributor.author","Difilippantonio, Michael J."],["dc.contributor.author","Ghadimi, B. Michael"],["dc.contributor.author","Caplen, Natasha J."],["dc.contributor.author","Ried, Thomas"],["dc.date.accessioned","2018-11-07T11:10:28Z"],["dc.date.available","2018-11-07T11:10:28Z"],["dc.date.issued","2008"],["dc.format.extent","174"],["dc.identifier.doi","10.1016/S1359-6349(08)72485-6"],["dc.identifier.isi","000261221200548"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53216"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Pergamon-elsevier Science Ltd"],["dc.publisher.place","Oxford"],["dc.relation.conference","20th EORTC-NCI-AACR Symposium on Molecular Targets and Cancer Therapeutics"],["dc.relation.eventlocation","Geneva, SWITZERLAND"],["dc.relation.issn","1359-6349"],["dc.title","RNAi-based identification of potential targets in colorectal cancers"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details DOI WOS2017Journal Article [["dc.bibliographiccitation.firstpage","1481"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Molecular Cancer Research"],["dc.bibliographiccitation.lastpage","1490"],["dc.bibliographiccitation.volume","15"],["dc.contributor.author","Emons, Georg"],["dc.contributor.author","Spitzner, Melanie"],["dc.contributor.author","Reineke, Sebastian"],["dc.contributor.author","Möller, Janneke"],["dc.contributor.author","Auslander, Noam"],["dc.contributor.author","Kramer, Frank"],["dc.contributor.author","Hu, Yue"],["dc.contributor.author","Beissbarth, Tim"],["dc.contributor.author","Wolff, Hendrik A."],["dc.contributor.author","Rave-Fränk, Margret"],["dc.contributor.author","Heßmann, Elisabeth"],["dc.contributor.author","Gaedcke, Jochen"],["dc.contributor.author","Ghadimi, B. Michael"],["dc.contributor.author","Johnsen, Steven A."],["dc.contributor.author","Ried, Thomas"],["dc.contributor.author","Grade, Marian"],["dc.date.accessioned","2020-12-10T18:37:47Z"],["dc.date.available","2020-12-10T18:37:47Z"],["dc.date.issued","2017"],["dc.description.abstract","Activation of Wnt/β-catenin signaling plays a central role in the development and progression of colorectal cancer. The Wnt-transcription factor, TCF7L2, is overexpressed in primary rectal cancers that are resistant to chemoradiotherapy and TCF7L2 mediates resistance to chemoradiotherapy. However, it is unclear whether the resistance is mediated by a TCF7L2 inherent mechanism or Wnt/β-catenin signaling in general. Here, inhibition of β-catenin by siRNAs or a small-molecule inhibitor (XAV-939) resulted in sensitization of colorectal cancer cells to chemoradiotherapy. To investigate the potential role of Wnt/β-catenin signaling in controlling therapeutic responsiveness, nontumorigenic RPE-1 cells were stimulated with Wnt-3a, a physiologic ligand of Frizzled receptors, which increased resistance to chemoradiotherapy. This effect could be recapitulated by overexpression of a degradation-resistant mutant of β-catenin (S33Y), also boosting resistance of RPE-1 cells to chemoradiotherapy, which was, conversely, abrogated by siRNA-mediated silencing of β-catenin. Consistent with these findings, higher expression levels of active β-catenin were observed as well as increased TCF/LEF reporter activity in SW1463 cells that evolved radiation resistance due to repeated radiation treatment. Global gene expression profiling identified several altered pathways, including PPAR signaling and other metabolic pathways, associated with cellular response to radiation. In summary, aberrant activation of Wnt/β-catenin signaling not only regulates the development and progression of colorectal cancer, but also mediates resistance of rectal cancers to chemoradiotherapy.Implications: Targeting Wnt/β-catenin signaling or one of the downstream pathways represents a promising strategy to increase response to chemoradiotherapy. Mol Cancer Res; 15(11); 1481-90. ©2017 AACR."],["dc.identifier.doi","10.1158/1541-7786.MCR-17-0205"],["dc.identifier.eissn","1557-3125"],["dc.identifier.issn","1541-7786"],["dc.identifier.pmid","28811361"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77090"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.relation.eissn","1557-3125"],["dc.relation.issn","1541-7786"],["dc.title","Chemoradiotherapy Resistance in Colorectal Cancer Cells is Mediated by Wnt/β-catenin Signaling"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]Details DOI PMID PMC2010Conference Abstract [["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","EJC SUPPLEMENTS"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Grade, Marian"],["dc.contributor.author","Kendziorra, Emil"],["dc.contributor.author","Ahlborn, Kerstin"],["dc.contributor.author","Spitzner, Melanie"],["dc.contributor.author","Gaedcke, Jochen"],["dc.contributor.author","Rave-Fraenk, Margret"],["dc.contributor.author","Becker, H."],["dc.contributor.author","Ghadimi, B. Michael"],["dc.contributor.author","Pukrop, Tobias"],["dc.contributor.author","Ried, Thomas"],["dc.date.accessioned","2018-11-07T08:37:08Z"],["dc.date.available","2018-11-07T08:37:08Z"],["dc.date.issued","2010"],["dc.format.extent","97"],["dc.identifier.doi","10.1016/S1359-6349(10)72008-5"],["dc.identifier.isi","000288460100295"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/18461"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Pergamon-elsevier Science Ltd"],["dc.publisher.place","Oxford"],["dc.relation.conference","22nd EORTC-NCI-AACR Symposium on Molecular Targets and Cancer Therapeutics"],["dc.relation.eventlocation","Berlin, GERMANY"],["dc.relation.issn","1359-6349"],["dc.title","Silencing of TCF7L2 sensitizes colorectal cancer cells to radiation therapy"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details DOI WOS2014Review [["dc.bibliographiccitation.firstpage","1986"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","CANCERS"],["dc.bibliographiccitation.lastpage","2011"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Spitzner, Melanie"],["dc.contributor.author","Ebner, Reinhard"],["dc.contributor.author","Wolff, Hendrik Andreas"],["dc.contributor.author","Ghadimi, B. Michael"],["dc.contributor.author","Wienands, Juergen"],["dc.contributor.author","Grade, Marian"],["dc.date.accessioned","2018-11-07T09:32:22Z"],["dc.date.available","2018-11-07T09:32:22Z"],["dc.date.issued","2014"],["dc.description.abstract","Chemoradiotherapy (CRT) represents a standard treatment for many human cancers, frequently combined with radical surgical resection. However, a considerable percentage of primary cancers are at least partially resistant to CRT, which represents a substantial clinical problem, because it exposes cancer patients to the potential side effects of both irradiation and chemotherapy. It is therefore exceedingly important to determine the molecular characteristics underlying CRT-resistance and to identify novel molecular targets that can be manipulated to re-sensitize resistant tumors to CRT. In this review, we highlight much of the recent evidence suggesting that the signal transducer and activator of transcription 3 (STAT3) plays a prominent role in mediating CRT-resistance, and we outline why inhibition of STAT3 holds great promise for future multimodal treatment concepts in oncology."],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft [Klinische Forschergruppe 179]"],["dc.identifier.doi","10.3390/cancers6041986"],["dc.identifier.isi","000209950800006"],["dc.identifier.pmid","25268165"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12173"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/31743"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Mdpi Ag"],["dc.relation.issn","2072-6694"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","STAT3: A Novel Molecular Mediator of Resistance to Chemoradiotherapy"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS2022Journal Article Research Paper [["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"]]Details DOI2021Journal Article [["dc.bibliographiccitation.firstpage","455"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Cancers"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Koerdel, Kristin"],["dc.contributor.author","Spitzner, Melanie"],["dc.contributor.author","Meyer, Thomas"],["dc.contributor.author","Engels, Niklas"],["dc.contributor.author","Krause, Florian"],["dc.contributor.author","Gaedcke, Jochen"],["dc.contributor.author","Conradi, Lena-Christin"],["dc.contributor.author","Haubrock, Martin"],["dc.contributor.author","Beißbarth, Tim"],["dc.contributor.author","Leha, Andreas"],["dc.contributor.author","Johnsen, Steven A."],["dc.contributor.author","Ghadimi, B. Michael"],["dc.contributor.author","Rose-John, Stefan"],["dc.contributor.author","Grade, Marian"],["dc.contributor.author","Wienands, Jürgen"],["dc.date.accessioned","2021-04-14T08:29:46Z"],["dc.date.available","2021-04-14T08:29:46Z"],["dc.date.issued","2021"],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft"],["dc.identifier.doi","10.3390/cancers13030455"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/82985"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.publisher","MDPI"],["dc.relation.eissn","2072-6694"],["dc.rights","https://creativecommons.org/licenses/by/4.0/"],["dc.title","NOTCH Activation via gp130/STAT3 Signaling Confers Resistance to Chemoradiotherapy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]Details DOI2021Journal Article Research Paper [["dc.bibliographiccitation.firstpage","10301"],["dc.bibliographiccitation.issue","19"],["dc.bibliographiccitation.journal","International Journal of Molecular Sciences"],["dc.bibliographiccitation.volume","22"],["dc.contributor.affiliation","Spitzner, Melanie; 1Department of General, Visceral and Pediatric Surgery, University Medical Center Goettingen, 37075 Goettingen, Germany; melanie.spitzner@med.uni-goettingen.de (M.S.); georg.emons@med.uni-goettingen.de (G.E.); karlburkhard.schuetz@sanktgeorg.de (K.B.S.); mghadim@uni-goettingen.de (B.M.G.); guenter.schneider@med.uni-goettingen.de (G.S.)"],["dc.contributor.affiliation","Emons, Georg; 1Department of General, Visceral and Pediatric Surgery, University Medical Center Goettingen, 37075 Goettingen, Germany; melanie.spitzner@med.uni-goettingen.de (M.S.); georg.emons@med.uni-goettingen.de (G.E.); karlburkhard.schuetz@sanktgeorg.de (K.B.S.); mghadim@uni-goettingen.de (B.M.G.); guenter.schneider@med.uni-goettingen.de (G.S.)"],["dc.contributor.affiliation","Schütz, Karl Burkhard; 1Department of General, Visceral and Pediatric Surgery, University Medical Center Goettingen, 37075 Goettingen, Germany; melanie.spitzner@med.uni-goettingen.de (M.S.); georg.emons@med.uni-goettingen.de (G.E.); karlburkhard.schuetz@sanktgeorg.de (K.B.S.); mghadim@uni-goettingen.de (B.M.G.); guenter.schneider@med.uni-goettingen.de (G.S.)"],["dc.contributor.affiliation","Wolff, Hendrik A.; 3Department of Radiotherapy and Radiooncology, University Medical Center Goettingen, 37075 Goettingen, Germany; h.wolff@strahlentherapie-muenchen.eu (H.A.W.); stefan.rieken@med.uni-goettingen.de (S.R.)"],["dc.contributor.affiliation","Rieken, Stefan; 3Department of Radiotherapy and Radiooncology, University Medical Center Goettingen, 37075 Goettingen, Germany; h.wolff@strahlentherapie-muenchen.eu (H.A.W.); stefan.rieken@med.uni-goettingen.de (S.R.)"],["dc.contributor.affiliation","Ghadimi, B. Michael; 1Department of General, Visceral and Pediatric Surgery, University Medical Center Goettingen, 37075 Goettingen, Germany; melanie.spitzner@med.uni-goettingen.de (M.S.); georg.emons@med.uni-goettingen.de (G.E.); karlburkhard.schuetz@sanktgeorg.de (K.B.S.); mghadim@uni-goettingen.de (B.M.G.); guenter.schneider@med.uni-goettingen.de (G.S.)"],["dc.contributor.affiliation","Schneider, Günter; 1Department of General, Visceral and Pediatric Surgery, University Medical Center Goettingen, 37075 Goettingen, Germany; melanie.spitzner@med.uni-goettingen.de (M.S.); georg.emons@med.uni-goettingen.de (G.E.); karlburkhard.schuetz@sanktgeorg.de (K.B.S.); mghadim@uni-goettingen.de (B.M.G.); guenter.schneider@med.uni-goettingen.de (G.S.)"],["dc.contributor.affiliation","Grade, Marian; 1Department of General, Visceral and Pediatric Surgery, University Medical Center Goettingen, 37075 Goettingen, Germany; melanie.spitzner@med.uni-goettingen.de (M.S.); georg.emons@med.uni-goettingen.de (G.E.); karlburkhard.schuetz@sanktgeorg.de (K.B.S.); mghadim@uni-goettingen.de (B.M.G.); guenter.schneider@med.uni-goettingen.de (G.S.)"],["dc.contributor.author","Spitzner, Melanie"],["dc.contributor.author","Emons, Georg"],["dc.contributor.author","Schütz, Karl Burkhard"],["dc.contributor.author","Wolff, Hendrik A."],["dc.contributor.author","Rieken, Stefan"],["dc.contributor.author","Ghadimi, B. Michael"],["dc.contributor.author","Schneider, Günter"],["dc.contributor.author","Grade, Marian"],["dc.date.accessioned","2021-12-01T09:23:14Z"],["dc.date.available","2021-12-01T09:23:14Z"],["dc.date.issued","2021"],["dc.date.updated","2022-09-03T10:10:11Z"],["dc.description.abstract","The standard treatment of locally advanced esophageal cancer comprises multimodal treatment concepts including preoperative chemoradiotherapy (CRT) followed by radical surgical resection. However, despite intensified treatment approaches, 5-year survival rates are still low. Therefore, new strategies are required to overcome treatment resistance, and to improve patients’ outcome. In this study, we investigated the impact of Wnt/β-catenin signaling on CRT resistance in esophageal cancer cells. Experiments were conducted in adenocarcinoma and squamous cell carcinoma cell lines with varying expression levels of Wnt proteins and Wnt/β-catenin signaling activities. To investigate the effect of Wnt/β-catenin signaling on CRT responsiveness, we genetically or pharmacologically inhibited Wnt/β-catenin signaling. Our experiments revealed that inhibition of Wnt/β-catenin signaling sensitizes cell lines with robust pathway activity to CRT. In conclusion, Wnt/β-catenin activity may guide precision therapies in esophageal carcinoma patients."],["dc.description.abstract","The standard treatment of locally advanced esophageal cancer comprises multimodal treatment concepts including preoperative chemoradiotherapy (CRT) followed by radical surgical resection. However, despite intensified treatment approaches, 5-year survival rates are still low. Therefore, new strategies are required to overcome treatment resistance, and to improve patients’ outcome. In this study, we investigated the impact of Wnt/β-catenin signaling on CRT resistance in esophageal cancer cells. Experiments were conducted in adenocarcinoma and squamous cell carcinoma cell lines with varying expression levels of Wnt proteins and Wnt/β-catenin signaling activities. To investigate the effect of Wnt/β-catenin signaling on CRT responsiveness, we genetically or pharmacologically inhibited Wnt/β-catenin signaling. Our experiments revealed that inhibition of Wnt/β-catenin signaling sensitizes cell lines with robust pathway activity to CRT. In conclusion, Wnt/β-catenin activity may guide precision therapies in esophageal carcinoma patients."],["dc.identifier.doi","10.3390/ijms221910301"],["dc.identifier.pii","ijms221910301"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/94598"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-478"],["dc.relation.eissn","1422-0067"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0/"],["dc.title","Inhibition of Wnt/β-Catenin Signaling Sensitizes Esophageal Cancer Cells to Chemoradiotherapy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]Details DOI