Kramer, Frank

[["dc.bibliographiccitation.firstpage","123"],["dc.bibliographiccitation.lastpage","135"],["dc.bibliographiccitation.seriesnr","1525"],["dc.contributor.author","Kramer, Frank"],["dc.contributor.author","Beißbarth, Tim"],["dc.date.accessioned","2020-03-27T13:50:07Z"],["dc.date.available","2020-03-27T13:50:07Z"],["dc.date.issued","2017"],["dc.description.abstract","Ontologies are powerful and popular tools to encode data in a structured format and manage knowledge. A large variety of existing ontologies offer users access to biomedical knowledge. This chapter contains a short theoretical background of ontologies and introduces two notable examples: The Gene Ontology and the ontology for Biological Pathways Exchange. For both ontologies a short overview and working bioinformatic applications, i.e., Gene Ontology enrichment analyses and pathway data visualization, are provided."],["dc.identifier.doi","10.1007/978-1-4939-6622-6_6"],["dc.identifier.pmid","27896720"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/63396"],["dc.language.iso","en"],["dc.relation.crisseries","Methods in Molecular Biology"],["dc.relation.eissn","1940-6029"],["dc.relation.isbn","978-1-4939-6620-2"],["dc.relation.isbn","978-1-4939-6622-6"],["dc.relation.ispartof","Working with Ontologies"],["dc.relation.ispartofseries","Methods in molecular biology;1525"],["dc.relation.issn","1064-3745"],["dc.relation.issn","1940-6029"],["dc.title","Working with Ontologies"],["dc.type","book_chapter"],["dc.type.internalPublication","unknown"],["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.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","5739"],["dc.bibliographiccitation.issue","17"],["dc.bibliographiccitation.journal","Cancer Research"],["dc.bibliographiccitation.lastpage","5753"],["dc.bibliographiccitation.volume","71"],["dc.contributor.author","Prenzel, Tanja"],["dc.contributor.author","Begus-Nahrmann, Yvonne"],["dc.contributor.author","Kramer, Frank"],["dc.contributor.author","Hennion, Magali"],["dc.contributor.author","Hsu, Chieh"],["dc.contributor.author","Gorsler, Theresa"],["dc.contributor.author","Hintermair, Corinna"],["dc.contributor.author","Eick, Dirk"],["dc.contributor.author","Kremmer, Elisabeth"],["dc.contributor.author","Simons, Mikael"],["dc.contributor.author","Beißbarth, Tim"],["dc.contributor.author","Johnsen, Steven Arthur"],["dc.date.accessioned","2018-11-07T08:52:42Z"],["dc.date.available","2018-11-07T08:52:42Z"],["dc.date.issued","2011"],["dc.description.abstract","The estrogen receptor-alpha (ER alpha) determines the phenotype of breast cancers where it serves as a positive prognostic indicator. ER alpha is a well-established target for breast cancer therapy, but strategies to target its function remain of interest to address therapeutic resistance and further improve treatment. Recent findings indicate that proteasome inhibition can regulate estrogen-induced transcription, but how ER alpha function might be regulated was uncertain. In this study, we investigated the transcriptome-wide effects of the proteasome inhibitor bortezomib on estrogen-regulated transcription in MCF7 human breast cancer cells and showed that bortezomib caused a specific global decrease in estrogen-induced gene expression. This effect was specific because gene expression induced by the glucocorticoid receptor was unaffected by bortezomib. Surprisingly, we observed no changes in ERa recruitment or assembly of its transcriptional activation complex on ERa target genes. Instead, we found that proteasome inhibition caused a global decrease in histone H2B monoubiquitination (H2Bub1), leading to transcriptional elongation defects on estrogen target genes and to decreased chromatin dynamics overall. In confirming the functional significance of this link, we showed that RNA interference-mediated knockdown of the H2B ubiquitin ligase RNF40 decreased ER alpha-induced gene transcription. Surprisingly, RNF40 knockdown also supported estrogen-independent cell proliferation and activation of cell survival signaling pathways. Most importantly, we found that H2Bub1 levels decrease during tumor progression. H2Bub1 was abundant in normal mammary epithelium and benign breast tumors but absent in most malignant and metastatic breast cancers. Taken together, our findings show how ERa activity is blunted by bortezomib treatment as a result of reducing the downstream ubiquitin-dependent function of H2Bub1. In supporting a tumor suppressor role for H2Bub1 in breast cancer, our findings offer a rational basis to pursue H2Bub1-based therapies for future management of breast cancer. Cancer Res; 71(17); 5739-53. (C)2011 AACR."],["dc.identifier.doi","10.1158/0008-5472.CAN-11-1896"],["dc.identifier.isi","000294454700017"],["dc.identifier.pmid","21862633"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/22232"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Assoc Cancer Research"],["dc.relation.issn","0008-5472"],["dc.title","Estrogen-Dependent Gene Transcription in Human Breast Cancer Cells Relies upon Proteasome-Dependent Monoubiquitination of Histone H2B"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["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","401"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Statistical Applications in Genetics and Molecular Biology"],["dc.bibliographiccitation.lastpage","414"],["dc.bibliographiccitation.volume","15"],["dc.contributor.author","Kruppa, Jochen"],["dc.contributor.author","Kramer, Frank"],["dc.contributor.author","Beißbarth, Tim"],["dc.contributor.author","Jung, Klaus"],["dc.date.accessioned","2018-11-07T10:07:53Z"],["dc.date.available","2018-11-07T10:07:53Z"],["dc.date.issued","2016"],["dc.description.abstract","As part of the data processing of high-throughput-sequencing experiments count data are produced representing the amount of reads that map to specific genomic regions. Count data also arise in mass spectrometric experiments for the detection of protein-protein interactions. For evaluating new computational methods for the analysis of sequencing count data or spectral count data from proteomics experiments artificial count data is thus required. Although, some methods for the generation of artificial sequencing count data have been proposed, all of them simulate single sequencing runs, omitting thus the correlation structure between the individual genomic features, or they are limited to specific structures. We propose to draw correlated data from the multivariate normal distribution and round these continuous data in order to obtain discrete counts. In our approach, the required distribution parameters can either be constructed in different ways or estimated from real count data. Because rounding affects the correlation structure we evaluate the use of shrinkage estimators that have already been used in the context of artificial expression data from DNA microarrays. Our approach turned out to be useful for the simulation of counts for defined subsets of features such as individual pathways or GO categories."],["dc.identifier.doi","10.1515/sagmb-2015-0082"],["dc.identifier.isi","000385368900003"],["dc.identifier.pmid","27655448"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/39364"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Walter De Gruyter Gmbh"],["dc.relation.issn","1544-6115"],["dc.relation.issn","2194-6302"],["dc.title","A simulation framework for correlated count data of features subsets in high-throughput sequencing or proteomics experiments"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","13"],["dc.bibliographiccitation.journal","Epigenetics & Chromatin"],["dc.bibliographiccitation.volume","5"],["dc.contributor.author","Prenzel, Tanja"],["dc.contributor.author","Kramer, Frank"],["dc.contributor.author","Bedi, Upasana"],["dc.contributor.author","Nagarajan, Sankari"],["dc.contributor.author","Beißbarth, Tim"],["dc.contributor.author","Johnsen, Steven Arthur"],["dc.date.accessioned","2018-11-07T09:07:07Z"],["dc.date.available","2018-11-07T09:07:07Z"],["dc.date.issued","2012"],["dc.description.abstract","Background: In conjunction with posttranslational chromatin modifications, proper arrangement of higher order chromatin structure appears to be important for controlling transcription in the nucleus. Recent genome-wide studies have shown that the Estrogen Receptor-alpha (ER alpha), encoded by the ESR1 gene, nucleates tissue-specific long-range chromosomal interactions in collaboration with the cohesin complex. Furthermore, the Mediator complex not only regulates ERa activity, but also interacts with the cohesin complex to facilitate long-range chromosomal interactions. However, whether the cohesin and Mediator complexes function together to contribute to estrogen-regulated gene transcription remains unknown. Results: In this study we show that depletion of the cohesin subunit SMC3 or the Mediator subunit MED12 significantly impairs the ER alpha-regulated transcriptome. Surprisingly, SMC3 depletion appears to elicit this effect indirectly by rapidly decreasing ESR1 transcription and ER alpha protein levels. Moreover, we provide evidence that both SMC3 and MED12 colocalize on the ESR1 gene and are mutually required for their own occupancy as well as for RNAPII occupancy across the ESR1 gene. Finally, we show that extended proteasome inhibition decreases the mRNA expression of cohesin subunits which accompanies a decrease in ESR1 mRNA and ERa protein levels as well as estrogen-regulated transcription. Conclusions: These results identify the ESR1 gene as a cohesin/Mediator-dependent gene and indicate that this regulation may potentially be exploited for the treatment of estrogen-dependent breast cancer."],["dc.identifier.doi","10.1186/1756-8935-5-13"],["dc.identifier.isi","000310834100001"],["dc.identifier.pmid","22913342"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12877"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/25716"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Biomed Central Ltd"],["dc.relation.issn","1756-8935"],["dc.rights","CC BY 2.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.0"],["dc.title","Cohesin is required for expression of the estrogen receptor-alpha (ESR1) gene"],["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","247"],["dc.bibliographiccitation.lastpage","247"],["dc.contributor.author","Camps, Jordi"],["dc.contributor.author","Hummon, Amanda H."],["dc.contributor.author","Emons, Georg"],["dc.contributor.author","Kramer, Frank"],["dc.contributor.author","Pitt, Jason J."],["dc.contributor.author","Grade, Marian"],["dc.contributor.author","Nguyen, Quang T."],["dc.contributor.author","Ghadimi, B. Michael"],["dc.contributor.author","Difilippantonio, Michael J."],["dc.contributor.author","Beissbarth, Tim"],["dc.contributor.author","Caplen, Natasha J."],["dc.contributor.author","Ried, Thomas"],["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.AM10-247"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/110005"],["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 247: A functional genomics and a systems biology approach identify POMP as a potential therapeutic target for colorectal cancer"],["dc.type","conference_paper"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1184"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","International Journal of Radiation Oncology*Biology*Physics"],["dc.bibliographiccitation.lastpage","1192"],["dc.bibliographiccitation.volume","78"],["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.contributor.author","Grade, Marian"],["dc.date.accessioned","2018-11-07T08:36:51Z"],["dc.date.available","2018-11-07T08:36:51Z"],["dc.date.issued","2010"],["dc.description.abstract","Purpose: The standard treatment of patients with locally advanced rectal cancers comprises preoperative 5-fluorouracil based chemoradiotherapy followed by standardized surgery. However, tumor response to multimodal treatment has varied greatly, ranging from complete resistance to complete pathologic regression. The prediction of the response is, therefore, an important clinical need. Methods and Materials: To establish in vitro models for studying the molecular basis of this heterogeneous tumor response, we exposed 12 colorectal cancer cell lines to 3 mu M of 5-fluorouracil and 2 Gy of radiation. The differences in treatment sensitivity were then correlated with the pretherapeutic gene expression profiles of these cell lines. Results: We observed a heterogeneous response, with surviving fractions ranging from 0.28 to 0.81, closely recapitulating clinical reality. Using a linear model analysis, we identified 4,796 features whose expression levels correlated significantly with the sensitivity to chemoradiotherapy (Q < .05), including many genes involved in the mitogen-activated protein kinase signaling pathway or cell cycle genes. These data have suggested a potential relevance of the insulin and Wnt signaling pathways for treatment response, and we identified STAT3, RASSF1, DOK3, and ERBB2 as potential therapeutic targets. The microarray measurements were independently validated for a subset of these genes using real-time polymerase chain reactions. Conclusion: We are the first to report a gene expression signature for the in vitro chemoradiosensitivity of colorectal cancer cells. We anticipate that this analysis will unveil molecular biomarkers predictive of the response of rectal cancers to chemoradiotherapy and enable the identification of genes that could serve as targets to sensitize a priori resistant primary tumors. (C) 2010 Elsevier Inc."],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft [KFO 179]"],["dc.identifier.doi","10.1016/j.ijrobp.2010.06.023"],["dc.identifier.isi","000283963100030"],["dc.identifier.pmid","20970032"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6106"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/18405"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Inc"],["dc.relation.issn","0360-3016"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","A GENE EXPRESSION SIGNATURE FOR CHEMORADIOSENSITIVITY OF COLORECTAL CANCER CELLS"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]