Grade, Marian

[["dc.bibliographiccitation.journal","Cancer Research"],["dc.bibliographiccitation.volume","72"],["dc.contributor.author","Spitzner, Melanie"],["dc.contributor.author","Roesler, Birte"],["dc.contributor.author","Bielfeld, Christian"],["dc.contributor.author","Gaedcke, Jochen"],["dc.contributor.author","Rave-Fränk, Margret"],["dc.contributor.author","Beißbarth, Tim"],["dc.contributor.author","Ried, Thomas"],["dc.contributor.author","Ghadimi, Michael B."],["dc.contributor.author","Grade, Marian"],["dc.date.accessioned","2018-11-07T09:11:10Z"],["dc.date.available","2018-11-07T09:11:10Z"],["dc.date.issued","2012"],["dc.identifier.doi","10.1158/1538-7445.AM2012-3446"],["dc.identifier.isi","000209701502014"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/26663"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Assoc Cancer Research"],["dc.publisher.place","Philadelphia"],["dc.title","Stat3 is a potential molecular target for chemoradiosensitization of colorectal cancer cells"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","1140"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","International Journal of Molecular Sciences"],["dc.bibliographiccitation.volume","18"],["dc.contributor.affiliation","Jo, Peter; \t\t \r\n\t\t Department of General-, Visceral-, and Pediatric Surgery, University Medical Center Goettingen, Robert-Koch-Str. 40, 37075 Goettingen, Germany, jo.peter@chirurgie-goettingen.de"],["dc.contributor.affiliation","Azizian, Azadeh; \t\t \r\n\t\t Department of General-, Visceral-, and Pediatric Surgery, University Medical Center Goettingen, Robert-Koch-Str. 40, 37075 Goettingen, Germany, azadeh.azizian@med.uni-goettingen.de"],["dc.contributor.affiliation","Salendo, Junius; \t\t \r\n\t\t Department of General-, Visceral-, and Pediatric Surgery, University Medical Center Goettingen, Robert-Koch-Str. 40, 37075 Goettingen, Germany, juniussalendo@gmail.com"],["dc.contributor.affiliation","Kramer, Frank; \t\t \r\n\t\t Department of Medical Statistics, University Medical Center Goettingen, Robert-Koch-Str. 40, 37075 Goettingen, Germany, frank.kramer@med.uni-goettingen.de"],["dc.contributor.affiliation","Bernhardt, Markus; \t\t \r\n\t\t Department of General-, Visceral-, and Pediatric Surgery, University Medical Center Goettingen, Robert-Koch-Str. 40, 37075 Goettingen, Germany, markus.bernhardt@med.uni-goettingen.de"],["dc.contributor.affiliation","Wolff, Hendrik; \t\t \r\n\t\t Department of Radiology, Nuclear Medicine and Radiotherapy, Radiology Munich, Burgstr. 7, 80333 Munich, Germany, drhawolff@googlemail.com"],["dc.contributor.affiliation","Gruber, Jens; \t\t \r\n\t\t German Primate Center, Medical RNA Biology, Kellnerweg 4, 37075 Goettingen, Germany, jgruber@dpz.eu"],["dc.contributor.affiliation","Grade, Marian; \t\t \r\n\t\t Department of General-, Visceral-, and Pediatric Surgery, University Medical Center Goettingen, Robert-Koch-Str. 40, 37075 Goettingen, Germany, marian.grade@med.uni-goettingen.de"],["dc.contributor.affiliation","Beißbarth, Tim; \t\t \r\n\t\t Department of Medical Statistics, University Medical Center Goettingen, Robert-Koch-Str. 40, 37075 Goettingen, Germany, tim.beissbarth@med.uni-goettingen.de"],["dc.contributor.affiliation","Ghadimi, B.; \t\t \r\n\t\t Department of General-, Visceral-, and Pediatric Surgery, University Medical Center Goettingen, Robert-Koch-Str. 40, 37075 Goettingen, Germany, mghadim@uni-goettingen.de"],["dc.contributor.affiliation","Gaedcke, Jochen; \t\t \r\n\t\t Department of General-, Visceral-, and Pediatric Surgery, University Medical Center Goettingen, Robert-Koch-Str. 40, 37075 Goettingen, Germany, jochen.gaedcke@med.uni-goettingen.de"],["dc.contributor.author","Jo, Peter"],["dc.contributor.author","Azizian, Azadeh"],["dc.contributor.author","Salendo, Junius"],["dc.contributor.author","Kramer, Frank"],["dc.contributor.author","Bernhardt, Markus"],["dc.contributor.author","Wolff, Hendrik Andreas"],["dc.contributor.author","Gruber, Jens"],["dc.contributor.author","Grade, Marian"],["dc.contributor.author","Beißbarth, Tim"],["dc.contributor.author","Ghadimi, Michael B."],["dc.contributor.author","Gaedcke, Jochen"],["dc.date.accessioned","2018-11-07T10:22:50Z"],["dc.date.available","2018-11-07T10:22:50Z"],["dc.date.issued","2017"],["dc.date.updated","2022-09-06T05:14:56Z"],["dc.description.abstract","Since the response to chemoradiotherapy in patients with locally advanced rectal cancer is heterogeneous, valid biomarkers are needed to monitor tumor response. Circulating microRNAs are promising candidates, however analyses of circulating microRNAs in rectal cancer are still rare. 111 patients with rectal cancer and 46 age-matched normal controls were enrolled. The expression levels of 30 microRNAs were analyzed in 17 pre-treatment patients' plasma samples. Differentially regulated microRNAs were validated in 94 independent patients. For 52 of the 94 patients a paired comparison between pre-treatment and post-treatment samples was performed. miR-17, miR-18b, miR-20a, miR-31, and miR-193a_3p, were significantly downregulated in pre-treatment plasma samples of patients with rectal cancer (p < 0.05). miR-29c, miR-30c, and miR-195 showed a trend of differential regulation. After validation, miR-31 and miR-30c were significantly deregulated by a decrease of expression. In 52 patients expression analyses of the 8 microRNAs in matched pre-treatment and post-treatment samples showed a significant decrease for all microRNAs (p < 0.05) after treatment. Expression levels of miR-31 and miR-30c could serve as valid biomarkers if validated in a prospective study. Plasma microRNA expression levels do not necessarily represent miRNA expression levels in tumor tissue. Also, expression levels of microRNAs change during multimodal therapy."],["dc.description.sponsorship","DFG (German Research Foundation)"],["dc.identifier.doi","10.3390/ijms18061140"],["dc.identifier.isi","000404581500040"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14793"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42349"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Mdpi Ag"],["dc.relation.eissn","1422-0067"],["dc.relation.issn","1422-0067"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Changes of Microrna Levels in Plasma of Patients with Rectal Cancer during Chemoradiotherapy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Cancer Research"],["dc.bibliographiccitation.volume","71"],["dc.contributor.author","Grade, Marian"],["dc.contributor.author","Spitzner, Melanie"],["dc.contributor.author","Emons, Georg"],["dc.contributor.author","Kramer, Frank"],["dc.contributor.author","Gaedcke, Jochen"],["dc.contributor.author","Rave-Fränk, Margret"],["dc.contributor.author","Scharf, Jens-Gerd"],["dc.contributor.author","Burfeind, Peter"],["dc.contributor.author","Becker, Heinz"],["dc.contributor.author","Beißbarth, Tim"],["dc.contributor.author","Ghadimi, Michael B."],["dc.contributor.author","Ried, Thomas"],["dc.date.accessioned","2018-11-07T08:57:01Z"],["dc.date.available","2018-11-07T08:57:01Z"],["dc.date.issued","2011"],["dc.identifier.doi","10.1158/1538-7445.AM2011-2508"],["dc.identifier.isi","000209701302047"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/23286"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Assoc Cancer Research"],["dc.publisher.place","Philadelphia"],["dc.relation.issn","1538-7445"],["dc.relation.issn","0008-5472"],["dc.title","Identification of potential relevant pathways and genes for resistance to chemoradiotherapy in colorectal cancer cells"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e1411"],["dc.bibliographiccitation.journal","Cell Death and Disease"],["dc.bibliographiccitation.volume","5"],["dc.contributor.author","Landmann, H."],["dc.contributor.author","Proia, D. A."],["dc.contributor.author","He, S."],["dc.contributor.author","Ogden, F. L."],["dc.contributor.author","Kramer, Franz-Josef"],["dc.contributor.author","Beißbarth, Tim"],["dc.contributor.author","Grade, Marian"],["dc.contributor.author","Gaedcke, Jochen"],["dc.contributor.author","Ghadimi, Michael B."],["dc.contributor.author","Moll, U."],["dc.contributor.author","Dobbelstein, Matthias"],["dc.date.accessioned","2018-11-07T09:35:41Z"],["dc.date.available","2018-11-07T09:35:41Z"],["dc.date.issued","2014"],["dc.description.abstract","HSP90 inhibition represents a promising route to cancer therapy, taking advantage of cancer cell-inherent proteotoxic stress. The HSP90-inhibitor ganetespib showed benefit in advanced clinical trials. This raises the need to identify the molecular determinants of treatment response. We tested the efficacy of ganetespib on a series of colorectal cancer (CRC)-derived cell lines and correlated their sensitivities with comprehensive gene expression analysis. Notably, the drug concentration required for 50% growth inhibition (IC50) varied up to 70-fold (from 36 to 2500 nM) between different cell lines. Correlating cell line-specific IC(50)s with the corresponding gene expression patterns revealed a strong association between ganetespib resistance (IC50 > 500 nM) and high expression of the UDP glucuronosyltransferase 1A (UGT1A) gene cluster. Moreover, CRC tumor samples showed a comparable distribution of UGT1A expression levels. The members of the UGT1A gene family are known as drug-conjugating liver enzymes involved in drug excretion, but their function in tumor cells is hardly understood. Chemically unrelated HSP90 inhibitors, for example, 17-N-allylamino-17-demethoxygeldanamycin (17-AAG), did not show correlation of drug sensitivities with UGT1A levels, whereas the ganetespib-related compound NVP-AUY922 did. When the most ganetespib-resistant cell line, HT29, was treated with ganetespib, the levels of HSP90 clients were unaffected. However, HT29 cells became sensitized to the drug, and HSP90 client proteins were destabilized by ganetespib upon siRNA-mediated UGT1A knockdown. Conversely, the most ganetespib-sensitive cell lines HCT116 and SW480 became more tolerant toward ganetespib upon UGT1A overexpression. Mechanistically, ganetespib was rapidly glucuronidated and excreted in resistant but not in sensitive CRC lines. We conclude that CRC cell-expressed UGT1A inactivates ganetespib and other resorcinolic Hsp90 inhibitors by glucuronidation, which renders the drugs unable to inhibit Hsp90 and thereby abrogates their biological activity. UGT1A levels in tumor tissues may be a suitable predictive biomarker to stratify CRC patients for ganetespib treatment."],["dc.description.sponsorship","Open-Access Publikationsfonds 2014"],["dc.identifier.doi","10.1038/cddis.2014.378"],["dc.identifier.isi","000343162000012"],["dc.identifier.pmid","25210794"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/10891"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/32445"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.notes.submitter","Najko"],["dc.relation.issn","2041-4889"],["dc.rights","CC BY-NC-ND 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/3.0"],["dc.title","UDP glucuronosyltransferase 1A expression levels determine the response of colorectal cancer cells to the heat shock protein 90 inhibitor ganetespib"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["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"]]

[["dc.bibliographiccitation.firstpage","451"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Radiotherapy and Oncology"],["dc.bibliographiccitation.lastpage","457"],["dc.bibliographiccitation.volume","108"],["dc.contributor.author","Salendo, Junius"],["dc.contributor.author","Spitzner, Melanie"],["dc.contributor.author","Kramer, Frank"],["dc.contributor.author","Zhang, X."],["dc.contributor.author","Jo, Peter"],["dc.contributor.author","Wolff, Hendrik Andreas"],["dc.contributor.author","Kitz, Julia"],["dc.contributor.author","Kaulfuß, Silke"],["dc.contributor.author","Beißbarth, Tim"],["dc.contributor.author","Dobbelstein, Matthias"],["dc.contributor.author","Ghadimi, Michael B."],["dc.contributor.author","Grade, Marian"],["dc.contributor.author","Gaedcke, Jochen"],["dc.date.accessioned","2018-11-07T09:20:18Z"],["dc.date.available","2018-11-07T09:20:18Z"],["dc.date.issued","2013"],["dc.description.abstract","Background and purpose: Preoperative chemoradiotherapy (CRT) represents the standard treatment for locally advanced rectal cancer. Tumor response and progression vary considerably. MicroRNAs represent master regulators of gene expression, and may therefore contribute to this diversity. Material and methods: Genome-wide microRNA (miRNA) profiling was performed for 12 colorectal cancer (CRC) cell lines and an individual in vitro signature of chemoradiosensitivity was established. Functional relevance of selected miRNAs was established by transfecting miRNA-mimics into SW480 and SW837 cells. The prognostic value of selected miRNAs was assessed in 128 pretherapeutic patient biopsies. Results: Thirty-six miRNAs were identified to significantly correlate with sensitivity to CRT (Q < 0.05) including miR-320a and other miRNAs involved in the MAPK-, TGF- and Wnt-pathway. Transfection of selected miRNAs (let-7g, miR-132, miR-224, miR-320a) each induced a shift of sensitivity. High expression of let-7g was associated with a good prognosis in rectal cancer patients (P = 0.03). Conclusions: This is the first report of a miRNA expression signature for in vitro chemoradiosensitivity of cell lines. Many of the identified miRNAs have not been linked to the response to CRT and may represent potential molecular targets to sensitize resistant cancers. If further validated, let7g expression may serve as predictive biomarker. (C) 2013 Elsevier Ireland Ltd. All rights reserved. Radiotherapy and Oncology 108 (2013) 451-457"],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft [KFO 179]"],["dc.identifier.doi","10.1016/j.radonc.2013.06.032"],["dc.identifier.isi","000327004700015"],["dc.identifier.pmid","23932154"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/28850"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Ireland Ltd"],["dc.publisher.place","Clare"],["dc.relation.conference","13th International Wolfsberg Meeting on Molecular Radiation Biology/Oncology"],["dc.relation.eventlocation","Ermatingen, SWITZERLAND"],["dc.relation.issn","0167-8140"],["dc.title","Identification of a microRNA expression signature for chemoradiosensitivity of colorectal cancer cells, involving miRNAs-320a,-224,-132 and let7g"],["dc.type","conference_paper"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","5640"],["dc.bibliographiccitation.lastpage","5640"],["dc.contributor.author","Gaedcke, Jochen"],["dc.contributor.author","Grade, Marian"],["dc.contributor.author","Jung, Klaus"],["dc.contributor.author","Wolff, Hendrik A."],["dc.contributor.author","Beissbarth, Tim"],["dc.contributor.author","Becker, Heinz"],["dc.contributor.author","Ried, Thomas"],["dc.contributor.author","Ghadimi, Michael"],["dc.date.accessioned","2022-06-08T07:57:08Z"],["dc.date.available","2022-06-08T07:57:08Z"],["dc.date.issued","2014"],["dc.identifier.doi","10.1158/1538-7445.AM10-5640"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/110007"],["dc.notes.intern","DOI-Import GROB-575"],["dc.publisher","American Association for Cancer Research"],["dc.relation.conference","Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC"],["dc.title","Abstract 5640: KRAS and BRAF in rectal cancer treated with preoperative chemoradiotherapy"],["dc.type","conference_paper"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","8318"],["dc.bibliographiccitation.issue","21"],["dc.bibliographiccitation.journal","International Journal of Molecular Sciences"],["dc.bibliographiccitation.volume","21"],["dc.contributor.affiliation","Mewes, Caspar; \t\t \r\n\t\t Department of Anesthesiology, University Medical Center, Georg August University, D-37075 Goettingen, Germany, caspar.mewes@med.uni-goettingen.de"],["dc.contributor.affiliation","Alexander, Tessa; \t\t \r\n\t\t Department of Anesthesiology, University Medical Center, Georg August University, D-37075 Goettingen, Germany, tessa.alexander@med.uni-goettingen.de"],["dc.contributor.affiliation","Büttner, Benedikt; \t\t \r\n\t\t Department of Anesthesiology, University Medical Center, Georg August University, D-37075 Goettingen, Germany, benedikt.buettner@med.uni-goettingen.de"],["dc.contributor.affiliation","Hinz, José; \t\t \r\n\t\t Department of Anesthesiology and Intensive Care Medicine, Klinikum Region Hannover, D-30459 Hannover, Germany, jose.hinz@krh.eu"],["dc.contributor.affiliation","Alpert, Ayelet; \t\t \r\n\t\t Department of Immunology, Rapport Faculty of Medicine, Technion-Israeli Institute of Technology, Haifa 31096, Israel, ayelethappy@gmail.com"],["dc.contributor.affiliation","Popov, Aron-F.; \t\t \r\n\t\t Department of Thoracic and Cardiovascular Surgery, University Medical Center, Eberhard Karls University, D-72076 Tuebingen, Germany, aronf.popov@gmail.com"],["dc.contributor.affiliation","Ghadimi, Michael; \t\t \r\n\t\t Department of General and Visceral Surgery, University Medical Center, Georg August University, D-37075 Goettingen, Germany, mghadim@uni-goettingen.de"],["dc.contributor.affiliation","Beißbarth, Tim; \t\t \r\n\t\t Institute of Medical Bioinformatics, University Medical Center, Georg August University, D-37077 Goettingen, Germany, tim.beissbarth@ams.med.uni-goettingen.de"],["dc.contributor.affiliation","Tzvetkov, Mladen; \t\t \r\n\t\t Department of Pharmacology, University Medical Center, Ernst-Moritz-Arndt-University, D-17487 Greifswald, Germany, mladen.tzvetkov@uni-greifswald.de"],["dc.contributor.affiliation","Grade, Marian; \t\t \r\n\t\t Department of General and Visceral Surgery, University Medical Center, Georg August University, D-37075 Goettingen, Germany, marian.grade@med.uni-goettingen.de"],["dc.contributor.affiliation","Quintel, Michael; \t\t \r\n\t\t Department of Anesthesiology, University Medical Center, Georg August University, D-37075 Goettingen, Germany, mquintel@med.uni-goettingen.de"],["dc.contributor.affiliation","Bergmann, Ingo; \t\t \r\n\t\t Department of Anesthesiology, University Medical Center, Georg August University, D-37075 Goettingen, Germany, ingo.bergmann@med.uni-goettingen.de"],["dc.contributor.affiliation","Mansur, Ashham; \t\t \r\n\t\t Department of Anesthesiology, University Medical Center, Georg August University, D-37075 Goettingen, Germany, ashham.mansur@med.uni-goettingen.de\t\t \r\n\t\t Department of Anesthesiology, Asklepios Hospitals Schildautal, D-38723 Seesen, Germany, ashham.mansur@med.uni-goettingen.de"],["dc.contributor.author","Mewes, Caspar"],["dc.contributor.author","Alexander, Tessa"],["dc.contributor.author","Büttner, Benedikt"],["dc.contributor.author","Hinz, José"],["dc.contributor.author","Alpert, Ayelet"],["dc.contributor.author","Popov, Aron-F."],["dc.contributor.author","Ghadimi, Michael"],["dc.contributor.author","Beißbarth, Tim"],["dc.contributor.author","Tzvetkov, Mladen"],["dc.contributor.author","Grade, Marian"],["dc.contributor.author","Quintel, Michael"],["dc.contributor.author","Bergmann, Ingo"],["dc.contributor.author","Mansur, Ashham"],["dc.date.accessioned","2021-04-14T08:31:06Z"],["dc.date.available","2021-04-14T08:31:06Z"],["dc.date.issued","2020"],["dc.date.updated","2022-09-06T17:44:59Z"],["dc.description.sponsorship","Volkswagen Foundation"],["dc.identifier.doi","10.3390/ijms21218318"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17650"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/83484"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.notes.intern","Merged from goescholar"],["dc.relation.eissn","1422-0067"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","TIM-3 Genetic Variants Are Associated with Altered Clinical Outcome and Susceptibility to Gram-Positive Infections in Patients with Sepsis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Oncology Research and Treatment"],["dc.bibliographiccitation.volume","37"],["dc.contributor.author","Grade, Marian"],["dc.contributor.author","Spitzner, Melanie"],["dc.contributor.author","Roesler, Birte"],["dc.contributor.author","Bielfeld, Christian"],["dc.contributor.author","Gaedcke, Jochen"],["dc.contributor.author","Wolff, Hendrik Andreas"],["dc.contributor.author","Beißbarth, Tim"],["dc.contributor.author","Wienands, Juergen"],["dc.contributor.author","Ghadimi, Michael B."],["dc.date.accessioned","2018-11-07T09:44:11Z"],["dc.date.available","2018-11-07T09:44:11Z"],["dc.date.issued","2014"],["dc.identifier.isi","000332306700320"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/34336"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Karger"],["dc.publisher.place","Basel"],["dc.title","Targeting STAT3 as a therapeutic strategy to sensitize colorectal cancer to chemoradiotherapy"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

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