Emons, Georg

[["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"]]

[["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","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"]]

[["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"]]

[["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","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"]]

[["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"]]

[["dc.bibliographiccitation.journal","Cancer Research"],["dc.bibliographiccitation.volume","71"],["dc.contributor.author","Kendziorra, Emil"],["dc.contributor.author","Ahlborn, Kerstin"],["dc.contributor.author","Spitzner, Melanie"],["dc.contributor.author","Rave-Fränk, Margret"],["dc.contributor.author","Gaedcke, Jochen"],["dc.contributor.author","Emons, Georg"],["dc.contributor.author","Kramer, Frank"],["dc.contributor.author","Beißbarth, Tim"],["dc.contributor.author","Ebner, Reinhard"],["dc.contributor.author","Becker, Heinz"],["dc.contributor.author","Ghadimi, Michael B."],["dc.contributor.author","Pukrop, Tobias"],["dc.contributor.author","Ried, Thomas"],["dc.contributor.author","Grade, Marian"],["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.AM2011-2490"],["dc.identifier.isi","000209701302028"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/23287"],["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","Silencing of TCF7L2 sensitizes Wnt/beta-catenin signaling-dependent colorectal cancer cells to radiation"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1024"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Genes Chromosomes and Cancer"],["dc.bibliographiccitation.lastpage","1034"],["dc.bibliographiccitation.volume","49"],["dc.contributor.author","Gaedcke, Jochen"],["dc.contributor.author","Grade, Marian"],["dc.contributor.author","Jung, Klaus"],["dc.contributor.author","Camps, Jordi"],["dc.contributor.author","Jo, Peter"],["dc.contributor.author","Emons, Georg"],["dc.contributor.author","Gehoff, Anastasia"],["dc.contributor.author","Sax, Ulrich"],["dc.contributor.author","Schirmer, Markus Anton"],["dc.contributor.author","Becker, Heinz"],["dc.contributor.author","Beißbarth, Tim"],["dc.contributor.author","Ried, Thomas"],["dc.contributor.author","Ghadimi, Michael B."],["dc.date.accessioned","2018-11-07T08:37:31Z"],["dc.date.available","2018-11-07T08:37:31Z"],["dc.date.issued","2010"],["dc.description.abstract","Mutations of the KRAS oncogene are predictive for resistance to treatment with antibodies against the epithelial growth factor receptor in patients with colorectal cancer. Overcoming this therapeutic dilemma could potentially be achieved by the introduction of drugs that inhibit signaling pathways that are activated by KRAS mutations. To identify comprehensively such signaling pathways, we profiled pretreatment biopsies and normal mucosa from 65 patients with locally advanced rectal cancer-30 of which carried mutated KRAS-using global gene expression microarrays. By comparing all tumor tissues exclusively to matched normal mucosa, we could improve assay sensitivity, and identified a total of 22,297 features that were differentially expressed (adjusted P-value <0.05) between normal mucosa and cancer, including several novel potential rectal cancer genes. We then used this comprehensive description of the rectal cancer transcriptome as the baseline for identifying KRAS-dependent alterations. The presence of activating KRAS mutations is significantly correlated to an upregulation of 13 genes (adjusted P-value <0.05), among them DUSP4, a MAP-kinase phosphatase, and SMYD3, a histone methyltransferase. Inhibition of the expression of both genes has previously been shown using the MEK1-inhibitor PD98059 and the antibacterial compound Novobiocin, respectively. These findings suggest a potential approach to overcome resistance to treatment with antibodies against the epithelial growth factor receptor in patients with KRAS-mutant rectal carcinomas. (C) 2010 Wiley-Liss, Inc."],["dc.identifier.doi","10.1002/gcc.20811"],["dc.identifier.isi","000282188000006"],["dc.identifier.pmid","20725992"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/18554"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-liss"],["dc.relation.issn","1045-2257"],["dc.title","Mutated KRAS Results in Overexpression of DUSP4, a MAP-Kinase Phosphatase, and SMYD3, a Histone Methyltransferase, in Rectal Carcinomas"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]