Now showing 1 - 10 of 19
  • 2008Conference Abstract
    [["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Cellular Oncology"],["dc.bibliographiccitation.volume","30"],["dc.contributor.author","Ried, Thomas"],["dc.contributor.author","Grade, Marian"],["dc.contributor.author","Heselmeyer-Haddad, Kerstin"],["dc.contributor.author","Camps, Jordi"],["dc.contributor.author","Hummon, Amanda"],["dc.contributor.author","Emons, Georg"],["dc.contributor.author","Auer, Gert"],["dc.contributor.author","Liersch, Torsten"],["dc.contributor.author","Difilippantonio, Michael J."],["dc.contributor.author","Ghadimi, B. Michael"],["dc.date.accessioned","2018-11-07T11:19:37Z"],["dc.date.available","2018-11-07T11:19:37Z"],["dc.date.issued","2008"],["dc.format.extent","91"],["dc.identifier.isi","000254301100002"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/55325"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Ios Press"],["dc.publisher.place","Amsterdam"],["dc.relation.conference","Meeting of the International-Society-for-Cellular-Oncology (ISCO 2008)"],["dc.relation.eventlocation","Amsterdam, NETHERLANDS"],["dc.relation.issn","1570-5870"],["dc.title","Exploiting the genome and transcriptome for individualized cancer diagnosis and treatment stratification"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]
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  • 2011Conference Abstract
    [["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"]]
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  • 2017Journal 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"]]
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  • 2008Conference Abstract
    [["dc.bibliographiccitation.firstpage","149"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Cellular Oncology"],["dc.bibliographiccitation.lastpage","150"],["dc.bibliographiccitation.volume","30"],["dc.contributor.author","Emons, Georg"],["dc.contributor.author","Camps, Jordi"],["dc.contributor.author","Grade, Marian"],["dc.contributor.author","Hummon, Amanda"],["dc.contributor.author","Nguyen, Quang"],["dc.contributor.author","Gaedcke, Jochen"],["dc.contributor.author","Difilippantonio, Michael J."],["dc.contributor.author","Ghadimi, Michael B."],["dc.contributor.author","Ried, Thomas"],["dc.date.accessioned","2018-11-07T11:19:37Z"],["dc.date.available","2018-11-07T11:19:37Z"],["dc.date.issued","2008"],["dc.identifier.isi","000254301100112"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/55327"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Ios Press"],["dc.publisher.place","Amsterdam"],["dc.relation.conference","Meeting of the International-Society-for-Cellular-Oncology (ISCO 2008)"],["dc.relation.eventlocation","Amsterdam, NETHERLANDS"],["dc.relation.issn","1570-5870"],["dc.title","Identification and functional validation of candidate oncogenes in colorectal cancer"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]
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  • 2012Conference Abstract
    [["dc.bibliographiccitation.journal","Cancer Research"],["dc.bibliographiccitation.volume","72"],["dc.contributor.author","Grade, Marian"],["dc.contributor.author","Eimer, Christine"],["dc.contributor.author","Emons, Georg"],["dc.contributor.author","Kendziorra, Emil"],["dc.contributor.author","Spitzner, Melanie"],["dc.contributor.author","Gaedcke, Jochen"],["dc.contributor.author","Wolff, Hendrik Andreas"],["dc.contributor.author","Beißbarth, Tim"],["dc.contributor.author","Ried, Thomas"],["dc.contributor.author","Pukrop, Tobias"],["dc.contributor.author","Ghadimi, Michael B."],["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.AM2012-5729"],["dc.identifier.isi","209701500032"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/26661"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Assoc Cancer Research"],["dc.publisher.place","Philadelphia"],["dc.title","The Wnt transcription factor TCF4 mediates resistance of colorectal cancer cells to (chemo-) radiotherapy in a beta-catenin independent manner"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]
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  • 2010Journal Article
    [["dc.bibliographiccitation.artnumber","36"],["dc.bibliographiccitation.journal","BMC Medical Genomics"],["dc.bibliographiccitation.volume","3"],["dc.contributor.author","Opitz, Lennart"],["dc.contributor.author","Salinas-Riester, Gabriela"],["dc.contributor.author","Grade, Marian"],["dc.contributor.author","Jung, Klaus"],["dc.contributor.author","Jo, Peter"],["dc.contributor.author","Emons, Georg"],["dc.contributor.author","Ghadimi, Michael B."],["dc.contributor.author","Beißbarth, Tim"],["dc.contributor.author","Gaedcke, Jochen"],["dc.date.accessioned","2018-11-07T08:40:26Z"],["dc.date.available","2018-11-07T08:40:26Z"],["dc.date.issued","2010"],["dc.description.abstract","Background: Gene expression profiling is a highly sensitive technique which is used for profiling tumor samples for medical prognosis. RNA quality and degradation influence the analysis results of gene expression profiles. The impact of this influence on the profiles and its medical impact is not fully understood. As patient samples are very valuable for clinical studies, it is necessary to establish criteria for the RNA quality to be able to use these samples in later analysis. Methods: To investigate the effects of RNA integrity on gene expression profiling, whole genome expression arrays were used. We used tumor biopsies from patients diagnosed with locally advanced rectal cancer. To simulate degradation, the isolated total RNA of all patients was subjected to heat-induced degradation in a time-dependent manner. Expression profiling was then performed and data were analyzed bioinformatically to assess the differences. Results: The differences introduced by RNA degradation were largely outweighed by the biological differences between the patients. Only a relatively small number of probes (275 out of 41,000) show a significant effect due to degradation. The genes that show the strongest effect due to RNA degradation were, especially, those with short mRNAs and probe positions near the 5' end. Conclusions: Degraded RNA from tumor samples (RIN > 5) can still be used to perform gene expression analysis. A much higher biological variance between patients is observed compared to the effect that is imposed by degradation of RNA. Nevertheless there are genes, very short ones and those with the probe binding side close to the 5' end that should be excluded from gene expression analysis when working with degraded RNA. These results are limited to the Agilent 44 k microarray platform and should be carefully interpreted when transferring to other settings."],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft [KFO 179]; BMBF [01GS0890]; BreastSys"],["dc.identifier.doi","10.1186/1755-8794-3-36"],["dc.identifier.isi","000283179600001"],["dc.identifier.pmid","20696062"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/5664"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/19230"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Biomed Central Ltd"],["dc.relation.issn","1755-8794"],["dc.rights","CC BY 2.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.0"],["dc.title","Impact of RNA degradation on gene expression profiling"],["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"]]
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  • 2014Conference Paper
    [["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"]]
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  • 2013Journal Article
    [["dc.bibliographiccitation.firstpage","2003"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Cancer Research"],["dc.bibliographiccitation.lastpage","2013"],["dc.bibliographiccitation.volume","73"],["dc.contributor.author","Camps, Jordi"],["dc.contributor.author","Pitt, Jason J."],["dc.contributor.author","Emons, Georg"],["dc.contributor.author","Hummon, Amanda B."],["dc.contributor.author","Case, Chanelle M."],["dc.contributor.author","Grade, Marian"],["dc.contributor.author","Jones, Tamara L."],["dc.contributor.author","Nguyen, Quang T."],["dc.contributor.author","Ghadimi, Michael B."],["dc.contributor.author","Beißbarth, Tim"],["dc.contributor.author","Difilippantonio, Michael J."],["dc.contributor.author","Caplen, Natasha J."],["dc.contributor.author","Ried, Thomas"],["dc.date.accessioned","2018-11-07T09:27:02Z"],["dc.date.available","2018-11-07T09:27:02Z"],["dc.date.issued","2013"],["dc.description.abstract","Chromosomal copy number alterations (aneuploidy) define the genomic landscape of most cancer cells, but identification of the oncogenic drivers behind these imbalances remains an unfinished task. In this study, we conducted a systematic analysis of colorectal carcinomas that integrated genomic copy number changes and gene expression profiles. This analysis revealed 44 highly overexpressed genes mapping to localized amplicons on chromosome 13, gains of which occur often in colorectal cancers (CRC). RNA interference (RNAi)-mediated silencing identified eight candidates whose loss-of-function reduced cell viability 20% or more in CRC cell lines. The functional space of the genes NUPL1, LNX2, POLR1D, POMP, SLC7A1, DIS3, KLF5, and GPR180 was established by global expression profiling after RNAi exposure. One candidate, LNX2, not previously known as an oncogene, was involved in regulating NOTCH signaling. Silencing LNX2 reduced NOTCH levels but also downregulated the transcription factor TCF7L2 and markedly reduced WNT signaling. LNX2 overexpression and chromosome 13 amplification therefore constitutively activates the WNT pathway, offering evidence of an aberrant NOTCH-WNT axis in CRC. Cancer Res; 73(6); 2003-13. (C)2012 AACR."],["dc.identifier.doi","10.1158/0008-5472.CAN-12-3159"],["dc.identifier.isi","000316187500035"],["dc.identifier.pmid","23319804"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/30442"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Assoc Cancer Research"],["dc.relation.issn","0008-5472"],["dc.title","Genetic Amplification of the NOTCH Modulator LNX2 Upregulates the WNT/beta-Catenin Pathway in Colorectal Cancer"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]
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  • 2010Journal Article
    [["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"]]
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  • 2009Conference Abstract
    [["dc.bibliographiccitation.journal","Cancer Research"],["dc.bibliographiccitation.volume","69"],["dc.contributor.author","Camps, Jordi"],["dc.contributor.author","Hummon, Amanda"],["dc.contributor.author","Grade, Marian"],["dc.contributor.author","Emons, Georg"],["dc.contributor.author","Quang Nguyen, Quang Nguyen"],["dc.contributor.author","Ghadimi, B. Michael"],["dc.contributor.author","Difilippantonio, Michael J."],["dc.contributor.author","Caplen, Natasha J."],["dc.contributor.author","Ried, Thomas"],["dc.date.accessioned","2018-11-07T08:30:09Z"],["dc.date.available","2018-11-07T08:30:09Z"],["dc.date.issued","2009"],["dc.identifier.isi","000209701804016"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/16828"],["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","Functional validation of deregulated genes on chromosome 13 identifies novel candidate oncogenes in colon cancer"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]
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