Pukrop, Tobias

[["dc.bibliographiccitation.artnumber","135"],["dc.bibliographiccitation.journal","Frontiers in Oncology"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Bayerlová, Michaela"],["dc.contributor.author","Menck, Kerstin"],["dc.contributor.author","Klemm, Florian"],["dc.contributor.author","Wolff, Alexander"],["dc.contributor.author","Pukrop, Tobias"],["dc.contributor.author","Binder, Claudia"],["dc.contributor.author","Beißbarth, Tim"],["dc.contributor.author","Bleckmann, Annalen"],["dc.date.accessioned","2019-07-09T11:43:27Z"],["dc.date.available","2019-07-09T11:43:27Z"],["dc.date.issued","2017"],["dc.description.abstract","Breast cancer is a heterogeneous disease and has been classified into five molecular subtypes based on gene expression profiles. Signaling processes linked to different breast cancer molecular subtypes and different clinical outcomes are still poorly understood. Aberrant regulation of Wnt signaling has been implicated in breast cancer progression. In particular Ror1/2 receptors and several other members of the non-canonical Wnt signaling pathway were associated with aggressive breast cancer behavior. However, Wnt signals are mediated via multiple complex pathways, and it is clinically important to determine which particular Wnt cascades, including their domains and targets, are deregulated in poor prognosis breast cancer. To investigate activation and outcome of the Ror2-dependent non-canonical Wnt signaling pathway, we overexpressed the Ror2 receptor in MCF-7 and MDA-MB231 breast cancer cells, stimulated the cells with its ligand Wnt5a, and we knocked-down Ror1 in MDA-MB231 cells. We measured the invasive capacity of perturbed cells to assess phenotypic changes, and mRNA was profiled to quantify gene expression changes. Differentially expressed genes were integrated into a literature-based non-canonical Wnt signaling network. The results were further used in the analysis of an independent dataset of breast cancer patients with metastasis-free survival annotation. Overexpression of the Ror2 receptor, stimulation with Wnt5a, as well as the combination of both perturbations enhanced invasiveness of MCF-7 cells. The expression-responsive targets of Ror2 overexpression in MCF-7 induced a Ror2/Wnt module of the non-canonical Wnt signaling pathway. These targets alter regulation of other pathways involved in cell remodeling processing and cell metabolism. Furthermore, the genes of the Ror2/Wnt module were assessed as a gene signature in patient gene expression data and showed an association with clinical outcome. In summary, results of this study indicate a role of a newly defined Ror2/Wnt module in breast cancer progression and present a link between Ror2 expression and increased cell invasiveness."],["dc.identifier.doi","10.3389/fonc.2017.00135"],["dc.identifier.pmid","28695110"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14538"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58892"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.publisher","Frontiers Media S.A."],["dc.relation.eissn","2234-943X"],["dc.relation.issn","2234-943X"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","Ror2 Signaling and Its Relevance in Breast Cancer Progression."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","14"],["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","GMS Zeitschrift für medizinische Ausbildung"],["dc.bibliographiccitation.lastpage","14"],["dc.bibliographiccitation.volume","29"],["dc.contributor.author","Raupach, Tobias"],["dc.contributor.author","Schiekirka, Sarah"],["dc.contributor.author","Münscher, Christian"],["dc.contributor.author","Beißbarth, Tim"],["dc.contributor.author","Himmel, Wolfgang"],["dc.contributor.author","Burckhardt, Gerhard"],["dc.contributor.author","Pukrop, Tobias"],["dc.date.accessioned","2019-07-10T08:14:07Z"],["dc.date.available","2019-07-10T08:14:07Z"],["dc.date.issued","2012"],["dc.description.abstract","Zielsetzung: Aktuell werden an den deutschen medizinischen Fakultäten unterschiedliche Konzepte zur leistungsorientierten Mittelvergabe (LOM)in der Lehre diskutiert. Die Umsetzung scheitert mitunter am Mangel valider Messkriterien zur Beurteilung der Lehrqualität. Neben der Struktur und den Prozessen der Lehre sollte das Ergebnis der Lehre im Mittelpunkt der Qualitätsbewertung stehen. Ziele dieser Arbeit waren die Erprobung eines neuen, lernzielbezogenen Evaluationssystems im klinischen Abschnitt des Studiums der Humanmedizin und der Vergleich der Ergebnisse mit den Daten eines traditionellen Evaluationsverfahrens. Methodik: Aus studentischen Selbsteinschätzungen zu Beginn und Ende eines jeden Lehrmoduls wurde nach einer neu entwickelten Formel der lernzielbezogene, prozentuale Lernerfolg berechnet. Die Lernerfolgs- Mittelwerte pro Modul wurden mit traditionellen Evaluationsparametern, insbesondere mit Globalbewertungen, ins Verhältnis gesetzt. Ergebnisse: Der mittels vergleichender Selbsteinschätzungen berechnete Lernerfolg und die Globalbewertungen produzierten deutlich unterschiedliche Rangfolgen der 21 klinischen Module. Zwischen dem Lernerfolg und den Globalbewertungen fand sich keine statistisch signifikante Korrelation. Allerdings korrelierten die Globalbewertungen stark mit den studentischen Erwartungen vor Modulbeginn und mit strukturellen und prozeduralen Parametern der Lehre (Pearson’s r zwischen 0,7 und 0,9). Schlussfolgerung: Die Messung des Lernzuwachses mittels vergleichender studentischer Selbsteinschätzungen kann die traditionelle Evaluation um eine wichtige Dimension erweitern. Im Unterschied zu studentischen Globalbewertungen ist das neue Instrument lernzielbezogen und unabhängiger vom Einfluss Konstrukt-irrelevanter Parameter. Hinsichtlich der Entwicklung eines LOM-Algorithmus eignet sich das neue Instrument gut zur Beurteilung der Lehrqualität."],["dc.identifier.fs","591967"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/9538"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/61439"],["dc.language.iso","de"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1860-3572"],["dc.relation.orgunit","Universitätsmedizin Göttingen"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.ddc","610"],["dc.title","Implementierung und Erprobung eines Lernziel-basierten Evaluationssystems im Studium der Humanmedizin"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","3170"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","International Journal of Cancer"],["dc.bibliographiccitation.lastpage","3183"],["dc.bibliographiccitation.volume","146"],["dc.contributor.author","Blazquez, Raquel"],["dc.contributor.author","Rietkötter, Eva"],["dc.contributor.author","Wenske, Britta"],["dc.contributor.author","Wlochowitz, Darius"],["dc.contributor.author","Sparrer, Daniela"],["dc.contributor.author","Vollmer, Elena"],["dc.contributor.author","Müller, Gunnar"],["dc.contributor.author","Seegerer, Julia"],["dc.contributor.author","Sun, Xueni"],["dc.contributor.author","Dettmer, Katja"],["dc.contributor.author","Barrantes‐Freer, Alonso"],["dc.contributor.author","Stange, Lena"],["dc.contributor.author","Utpatel, Kirsten"],["dc.contributor.author","Bleckmann, Annalen"],["dc.contributor.author","Treiber, Hannes"],["dc.contributor.author","Bohnenberger, Hanibal"],["dc.contributor.author","Lenz, Christof"],["dc.contributor.author","Schulz, Matthias"],["dc.contributor.author","Reimelt, Christian"],["dc.contributor.author","Hackl, Christina"],["dc.contributor.author","Grade, Marian"],["dc.contributor.author","Büyüktas, Deram"],["dc.contributor.author","Siam, Laila"],["dc.contributor.author","Balkenhol, Marko"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Kube, Dieter"],["dc.contributor.author","Krahn, Michael P."],["dc.contributor.author","Proescholdt, Martin A."],["dc.contributor.author","Riemenschneider, Markus J."],["dc.contributor.author","Evert, Matthias"],["dc.contributor.author","Oefner, Peter J."],["dc.contributor.author","Klein, Chistoph A."],["dc.contributor.author","Hanisch, Uwe K."],["dc.contributor.author","Binder, Claudia"],["dc.contributor.author","Pukrop, Tobias"],["dc.date.accessioned","2019-12-09T11:26:05Z"],["dc.date.accessioned","2021-10-27T13:21:49Z"],["dc.date.available","2019-12-09T11:26:05Z"],["dc.date.available","2021-10-27T13:21:49Z"],["dc.date.issued","2020"],["dc.description.abstract","More than half of all brain metastases show infiltrating rather than displacing growth at the macro-metastasis/organ parenchyma interface (MMPI), a finding associated with shorter survival. The lymphoid enhancer-binding factor-1 (LEF1) is an epithelial-mesenchymal transition (EMT) transcription factor that is commonly overexpressed in brain-colonizing cancer cells. Here, we overexpressed LEF1 in an in vivo breast cancer brain colonization model. It shortened survival, albeit without engaging EMT at the MMPI. By differential proteome analysis, we identified a novel function of LEF1 as a regulator of the glutathione (GSH) system, the principal cellular redox buffer. LEF1 overexpression also conferred resistance against therapeutic GSH depletion during brain colonization and improved management of intracellular ROS. We conclude that besides EMT, LEF1 facilitates metastasis by improving the antioxidative capacity of epithelial breast cancer cells, in particular during colonization of the brain parenchyma."],["dc.identifier.doi","10.1002/ijc.32742"],["dc.identifier.eissn","1097-0215"],["dc.identifier.issn","0020-7136"],["dc.identifier.pmid","31626715"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16874"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/92047"],["dc.language.iso","en"],["dc.notes.intern","Migrated from goescholar"],["dc.relation.eissn","1097-0215"],["dc.relation.issn","1097-0215"],["dc.relation.issn","0020-7136"],["dc.relation.orgunit","Universitätsmedizin Göttingen"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","LEF1 supports metastatic brain colonization by regulating glutathione metabolism and increasing ROS resistance in breast cancer"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]