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.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.firstpage","51"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","EJC SUPPLEMENTS"],["dc.bibliographiccitation.lastpage","52"],["dc.bibliographiccitation.volume","4"],["dc.contributor.author","Grade, Marian"],["dc.contributor.author","Liersch, Torsten"],["dc.contributor.author","Varma, Sudhir"],["dc.contributor.author","Difilippantonio, Michael J."],["dc.contributor.author","Langer, Claus"],["dc.contributor.author","Simon, Richard"],["dc.contributor.author","Ried, Thomas"],["dc.contributor.author","Becker, Heinz"],["dc.contributor.author","Ghadimi, B. Michael"],["dc.date.accessioned","2018-11-07T09:44:37Z"],["dc.date.available","2018-11-07T09:44:37Z"],["dc.date.issued","2006"],["dc.identifier.doi","10.1016/j.ejcsup.2006.04.127"],["dc.identifier.isi","000238969500127"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/34435"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Pergamon-elsevier Science Ltd"],["dc.publisher.place","Oxford"],["dc.relation.issn","1359-6349"],["dc.title","Pretherapeutical gene expression profiling for response prediction of rectal adenocarcinomas to preoperative chemoradiotherapy and its impact on disease free survival"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1607"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Laboratory Investigation"],["dc.bibliographiccitation.lastpage","1622"],["dc.bibliographiccitation.volume","92"],["dc.contributor.author","Peickert, Susann"],["dc.contributor.author","Waurig, Julia"],["dc.contributor.author","Dittfeld, Claudia"],["dc.contributor.author","Dietrich, Antje"],["dc.contributor.author","Garbe, Yvette"],["dc.contributor.author","Kabus, Lydia"],["dc.contributor.author","Baumann, Michael"],["dc.contributor.author","Grade, Marian"],["dc.contributor.author","Ried, Thomas"],["dc.contributor.author","Kunz-Schughart, Leoni A."],["dc.date.accessioned","2018-11-07T09:04:05Z"],["dc.date.available","2018-11-07T09:04:05Z"],["dc.date.issued","2012"],["dc.description.abstract","Studies related to the cancer stem cell hypothesis are challenging because of the imperfect tools to identify cell populations of interest and controversy on the usefulness of established cancer cell lines. We previously found CD133 to not be selective for a tumor-propagating or radioresistant population in a near-diploid, microsatellite-instable colorectal carcinoma (CRC) cell line. Because of discrepant literature data, we herein systematically analyzed the behavior of microsatellite-stable cell line subpopulations reflecting the more frequent carcinogenesis pathway in spontaneous CRC. CD133(+) and CD133(-/low) populations were isolated by fluorescence-activated cell sorting and further processed. HT29 and SW620 cells were studied in detail in monolayer and/or spheroid culture assays and upon subcutaneous injection in NMRI (nu/nu) mice using a limiting dilution approach. CD133(-/low) HT29 cells showed a significantly lower clonogenic survival and reduced spheroid formation capacity than their CD133+ counterparts. However, the cell populations neither differed in growth kinetics and response to treatment in vitro nor in tumor formation capacity when injecting as low as 10 cells. CD 133(-/low) HT29 cells rapidly re-expressed CD 133 protein in vitro and in vivo as shown by flow cytometry and/or western blot analyses, and they also showed a particular survival benefit under tissue normoxic conditions. In contrast, CD133 protein in the CD133(+) population was quite stable throughout culturing. The observation of CD133 re-expression and lack of difference in tumor take rate of subpopulations was confirmed in SW620 cells. Here, we found cell density to affect CD133 re-expression in the CD133(-)-sorted population. And even SW480 cells, classified as a CD133(-) cell line, presented some CD133 protein on their surface upon in vivo engraftment. We conclude that (i) CD133 protein expression shows high plasticity in CRC cell lines, and (ii) in vitro CD133 status on the cell surface neither determines tumorigenic potential nor CD133 profile in vivo. Laboratory Investigation (2012) 92, 1607-1622; doi:10.1038/labinvest.2012.124; published online 10 September 2012"],["dc.identifier.doi","10.1038/labinvest.2012.124"],["dc.identifier.isi","000310761800009"],["dc.identifier.pmid","22964855"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/25033"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","0023-6837"],["dc.title","Rapid re-expression of CD133 protein in colorectal cancer cell lines in vitro and in vivo"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","EJC SUPPLEMENTS"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Grade, Marian"],["dc.contributor.author","Hummon, Amanda B."],["dc.contributor.author","Camps, Jordi"],["dc.contributor.author","Emons, G."],["dc.contributor.author","Spitzner, Melanie"],["dc.contributor.author","Gaedcke, Jochen"],["dc.contributor.author","Difilippantonio, Michael J."],["dc.contributor.author","Ghadimi, B. Michael"],["dc.contributor.author","Caplen, Natasha J."],["dc.contributor.author","Ried, Thomas"],["dc.date.accessioned","2018-11-07T11:10:28Z"],["dc.date.available","2018-11-07T11:10:28Z"],["dc.date.issued","2008"],["dc.format.extent","174"],["dc.identifier.doi","10.1016/S1359-6349(08)72485-6"],["dc.identifier.isi","000261221200548"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53216"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Pergamon-elsevier Science Ltd"],["dc.publisher.place","Oxford"],["dc.relation.conference","20th EORTC-NCI-AACR Symposium on Molecular Targets and Cancer Therapeutics"],["dc.relation.eventlocation","Geneva, SWITZERLAND"],["dc.relation.issn","1359-6349"],["dc.title","RNAi-based identification of potential targets in colorectal cancers"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["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","784"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Biochimica et Biophysica Acta (BBA) - Gene Regulatory Mechanisms"],["dc.bibliographiccitation.lastpage","793"],["dc.bibliographiccitation.volume","1819"],["dc.contributor.author","Ried, Thomas"],["dc.contributor.author","Hu, Yue"],["dc.contributor.author","Difilippantonio, Michael J."],["dc.contributor.author","Ghadimi, B. Michael"],["dc.contributor.author","Grade, Marian"],["dc.contributor.author","Camps, Jordi"],["dc.date.accessioned","2018-11-07T09:08:35Z"],["dc.date.available","2018-11-07T09:08:35Z"],["dc.date.issued","2012"],["dc.description.abstract","Chromosomal aneuploidies are a defining feature of carcinomas, i.e., tumors of epithelial origin. Such aneuploidies result in tumor specific genomic copy number alterations. The patterns of genomic imbalances are tumor specific, and to a certain extent specific for defined stages of tumor development. Genomic imbalances occur already in premalignant precursor lesions. i.e., before the transition to invasive disease, and their distribution is maintained in metastases, and in cell lines derived from primary tumors. These observations are consistent with the interpretation that tumor specific genomic imbalances are drivers of malignant transformation. Naturally, this precipitates the question of how such imbalances influence the expression of resident genes. A number of laboratories have systematically integrated copy number alterations with gene expression changes in primary tumors and metastases, cell lines, and experimental models of aneuploidy to address the question as to whether genomic imbalances deregulate the expression of one or few key genes, or rather affect the cancer transcriptome more globally. The majority of these studies showed that gene expression levels follow genomic copy number. Therefore, gross genomic copy number changes, including aneuploidies of entire chromosome arms and chromosomes, result in a massive deregulation of the transcriptome of cancer cells. This article is part of a Special Issue entitled: Chromatin in time and space. Published by Elsevier B.V."],["dc.identifier.doi","10.1016/j.bbagrm.2012.02.020"],["dc.identifier.isi","000306265100023"],["dc.identifier.pmid","22426433"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/26067"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","1874-9399"],["dc.title","The consequences of chromosomal aneuploidy on the transcriptome of cancer cells"],["dc.type","review"],["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.issue","7"],["dc.bibliographiccitation.journal","EJC SUPPLEMENTS"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Grade, Marian"],["dc.contributor.author","Kendziorra, Emil"],["dc.contributor.author","Ahlborn, Kerstin"],["dc.contributor.author","Spitzner, Melanie"],["dc.contributor.author","Gaedcke, Jochen"],["dc.contributor.author","Rave-Fraenk, Margret"],["dc.contributor.author","Becker, H."],["dc.contributor.author","Ghadimi, B. Michael"],["dc.contributor.author","Pukrop, Tobias"],["dc.contributor.author","Ried, Thomas"],["dc.date.accessioned","2018-11-07T08:37:08Z"],["dc.date.available","2018-11-07T08:37:08Z"],["dc.date.issued","2010"],["dc.format.extent","97"],["dc.identifier.doi","10.1016/S1359-6349(10)72008-5"],["dc.identifier.isi","000288460100295"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/18461"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Pergamon-elsevier Science Ltd"],["dc.publisher.place","Oxford"],["dc.relation.conference","22nd EORTC-NCI-AACR Symposium on Molecular Targets and Cancer Therapeutics"],["dc.relation.eventlocation","Berlin, GERMANY"],["dc.relation.issn","1359-6349"],["dc.title","Silencing of TCF7L2 sensitizes colorectal cancer cells to radiation therapy"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["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"]]