Linke, Franziska

[["dc.bibliographiccitation.journal","Oncology Research and Treatment"],["dc.bibliographiccitation.volume","38"],["dc.contributor.author","Linke, F."],["dc.contributor.author","Zaunig, S."],["dc.contributor.author","von Bonin, Frederike"],["dc.contributor.author","Wilting, J."],["dc.contributor.author","Bryja, V."],["dc.contributor.author","Pukrop, Tobias"],["dc.contributor.author","Truemper, Lorenz H."],["dc.contributor.author","Kube, Dieter"],["dc.date.accessioned","2018-11-07T09:50:39Z"],["dc.date.available","2018-11-07T09:50:39Z"],["dc.date.issued","2015"],["dc.format.extent","211"],["dc.identifier.isi","364268800509"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/35748"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Karger"],["dc.publisher.place","Basel"],["dc.relation.issn","2296-5262"],["dc.relation.issn","2296-5270"],["dc.title","Wnt5a signaling mediates cell migration and invasion of Hodgkin Lymphoma in vitro and in xenograft models"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","International Journal of Medical Microbiology"],["dc.bibliographiccitation.volume","302"],["dc.contributor.author","van Oordt, T."],["dc.contributor.author","Strohmeier, Oliver"],["dc.contributor.author","Mark, D."],["dc.contributor.author","Kosse, D."],["dc.contributor.author","Roth, G."],["dc.contributor.author","Achazi, Katharina"],["dc.contributor.author","Patel, Pranav"],["dc.contributor.author","Linke, S."],["dc.contributor.author","Paust, N."],["dc.contributor.author","Weidmann, Manfred"],["dc.contributor.author","Drexler, Josef"],["dc.contributor.author","Hufert, Frank T."],["dc.contributor.author","Zengerle, R."],["dc.contributor.author","Eberhard, Michael"],["dc.contributor.author","Niedrig, M."],["dc.contributor.author","von Stetten, Felix"],["dc.date.accessioned","2018-11-07T09:06:01Z"],["dc.date.available","2018-11-07T09:06:01Z"],["dc.date.issued","2012"],["dc.format.extent","7"],["dc.identifier.isi","000311593300019"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/25458"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Gmbh, Urban & Fischer Verlag"],["dc.publisher.place","Jena"],["dc.relation.conference","64th Annual Meeting of the German-Society-for-Hygiene-and-Microbiology (DGHM)"],["dc.relation.eventlocation","Hamburg, GERMANY"],["dc.relation.issn","1438-4221"],["dc.title","A Functional Blister-Pack LabDisk System for Point of Care Testing"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","13"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Oncogene"],["dc.bibliographiccitation.lastpage","23"],["dc.bibliographiccitation.volume","36"],["dc.contributor.author","Linke, F."],["dc.contributor.author","Zaunig, S."],["dc.contributor.author","Nietert, M. M."],["dc.contributor.author","Bonin, F. von"],["dc.contributor.author","Lutz, S."],["dc.contributor.author","Dullin, C."],["dc.contributor.author","Janovská, P."],["dc.contributor.author","Beissbarth, T."],["dc.contributor.author","Alves, F."],["dc.contributor.author","Klapper, W."],["dc.contributor.author","Bryja, V."],["dc.contributor.author","Pukrop, T."],["dc.contributor.author","Trümper, L."],["dc.contributor.author","Wilting, J."],["dc.contributor.author","Kube, D."],["dc.date.accessioned","2018-10-19T06:32:50Z"],["dc.date.available","2018-10-19T06:32:50Z"],["dc.date.issued","2017"],["dc.description.abstract","Classical Hodgkin lymphoma (cHL) has a typical clinical manifestation, with dissemination involving functionally neighboring lymph nodes. The factors involved in the spread of lymphoma cells are poorly understood. Here we show that cHL cell lines migrate with higher rates compared with non-Hodgkin lymphoma cell lines. cHL cell migration, invasion and adhesion depend on autocrine WNT signaling as revealed by the inhibition of WNT secretion with the porcupine inhibitors Wnt-C59/IWP-2, but did not affect cell proliferation. While application of recombinant WNT5A or WNT5A overexpression stimulates HL cell migration, neither WNT10A, WNT10B nor WNT16 did so. Time-lapse studies revealed an amoeboid type of cell migration modulated by WNT5A. Reduced migration distances and velocity of cHL cells, as well as altered movement patterns, were observed using porcupine inhibitor or WNT5A antagonist. Knockdown of Frizzled5 and Dishevelled3 disrupted the WNT5A-mediated RHOA activation and cell migration. Overexpression of DVL3-K435M or inhibition of ROCK (Rho-associated protein kinase) by Y-27632/H1152P disrupted cHL cell migration. In addition to these mechanistic insights into the role of WNT5A in vitro, global gene expression data revealed an increased WNT5A expression in primary HL cells in comparison with normal B-cell subsets and other lymphomas. Furthermore, the activity of both porcupine and WNT5A in cHL cells had an impact on lymphoma development in the chick chorionallantoic membrane assay. Massive bleeding of these lymphomas was significantly reduced after inhibition of WNT secretion by Wnt-C59. Therefore, a model is proposed where WNT signaling has an important role in regulating tumor-promoting processes."],["dc.fs.pkfprnr","66887"],["dc.identifier.doi","10.1038/onc.2016.183"],["dc.identifier.fs","626468"],["dc.identifier.pmid","27270428"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/16088"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.eissn","1476-5594"],["dc.title","WNT5A: a motility-promoting factor in Hodgkin lymphoma"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","571"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Molecular Oncology"],["dc.bibliographiccitation.lastpage","589"],["dc.bibliographiccitation.volume","14"],["dc.contributor.author","Arlt, Annekatrin"],["dc.contributor.author","Bonin, Frederike"],["dc.contributor.author","Rehberg, Thorsten"],["dc.contributor.author","Perez‐Rubio, Paula"],["dc.contributor.author","Engelmann, Julia C."],["dc.contributor.author","Limm, Katharina"],["dc.contributor.author","Reinke, Sarah"],["dc.contributor.author","Dullin, Christian"],["dc.contributor.author","Sun, Xueni"],["dc.contributor.author","Specht, Rieke"],["dc.contributor.author","Maulhardt, Markus"],["dc.contributor.author","Linke, Franziska"],["dc.contributor.author","Bunt, Gertrude"],["dc.contributor.author","Klapper, Wolfram"],["dc.contributor.author","Vockerodt, Martina"],["dc.contributor.author","Wilting, Jörg"],["dc.contributor.author","Pukrop, Tobias"],["dc.contributor.author","Dettmer, Katja"],["dc.contributor.author","Gronwald, Wolfram"],["dc.contributor.author","Oefner, Peter J."],["dc.contributor.author","Spang, Rainer"],["dc.contributor.author","Kube, Dieter"],["dc.date.accessioned","2021-04-14T08:27:44Z"],["dc.date.available","2021-04-14T08:27:44Z"],["dc.date.issued","2020"],["dc.description.abstract","Macrophages (Mφ) are abundantly present in the tumor microenvironment and may predict outcome in solid tumors and defined lymphoma subtypes. Mφ heterogeneity, the mechanisms of their recruitment, and their differentiation into lymphoma‐promoting, alternatively activated M2‐like phenotypes are still not fully understood. Therefore, further functional studies are required to understand biological mechanisms associated with human tumor‐associated Mφ (TAM). Here, we show that the global mRNA expression and protein abundance of human Mφ differentiated in Hodgkin lymphoma (HL)‐conditioned medium (CM) differ from those of Mφ educated by conditioned media from diffuse large B‐cell lymphoma (DLBCL) cells or, classically, by macrophage colony‐stimulating factor (M‐CSF). Conditioned media from HL cells support TAM differentiation through upregulation of surface antigens such as CD40, CD163, CD206, and PD‐L1. In particular, RNA and cell surface protein expression of mannose receptor 1 (MRC1)/CD206 significantly exceed the levels induced by classical M‐CSF stimulation in M2‐like Mφ; this is regulated by interleukin 13 to a large extent. Functionally, high CD206 enhances mannose‐dependent endocytosis and uptake of type I collagen. Together with high matrix metalloprotease9 secretion, HL‐TAMs appear to be active modulators of the tumor matrix. Preclinical in ovo models show that co‐cultures of HL cells with monocytes or Mφ support dissemination of lymphoma cells via lymphatic vessels, while tumor size and vessel destruction are decreased in comparison with lymphoma‐only tumors. Immunohistology of human HL tissues reveals a fraction of cases feature large numbers of CD206‐positive cells, with high MRC1 expression being characteristic of HL‐stage IV. In summary, the lymphoma‐TAM interaction contributes to matrix‐remodeling and lymphoma cell dissemination."],["dc.description.abstract","The study highlights the ability of Hodgkin lymphoma cells to attract and to differentiate monocytes into M2‐like Mφ and the role of IL13 in regulating CD206 but also that CD206 contributes to the remodeling of the tumor microenvironment via take up glycoconjugates as well as type‐I collagen and immunosuppression by PD‐L1 upregulation. image"],["dc.description.sponsorship","Stiftung der Georg‐August‐Universität"],["dc.description.sponsorship","Wilhelm‐Sander‐Stiftung"],["dc.description.sponsorship","Deutsche Krebshilfe http://dx.doi.org/10.13039/501100005972"],["dc.description.sponsorship","Bundesministerium für Bildung und Forschung http://dx.doi.org/10.13039/501100002347"],["dc.description.sponsorship","Interreg"],["dc.identifier.doi","10.1002/1878-0261.12616"],["dc.identifier.eissn","1878-0261"],["dc.identifier.issn","1574-7891"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17183"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/82387"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.notes.intern","Merged from goescholar"],["dc.relation.eissn","1878-0261"],["dc.relation.issn","1574-7891"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","High CD206 levels in Hodgkin lymphoma‐educated macrophages are linked to matrix‐remodeling and lymphoma dissemination"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","361"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Leukemia"],["dc.bibliographiccitation.lastpage","372"],["dc.bibliographiccitation.volume","31"],["dc.contributor.author","Linke, F."],["dc.contributor.author","Harenberg, M."],["dc.contributor.author","Nietert, M. M."],["dc.contributor.author","Zaunig, S."],["dc.contributor.author","Bonin, F. von"],["dc.contributor.author","Arlt, A."],["dc.contributor.author","Szczepanowski, M."],["dc.contributor.author","Weich, H. A."],["dc.contributor.author","Lutz, S."],["dc.contributor.author","Dullin, C."],["dc.contributor.author","Janovská, P."],["dc.contributor.author","Krafčíková, M."],["dc.contributor.author","Trantírek, L."],["dc.contributor.author","Ovesná, P."],["dc.contributor.author","Klapper, W."],["dc.contributor.author","Beißbarth, T."],["dc.contributor.author","Alves, Frauke"],["dc.contributor.author","Bryja, V."],["dc.contributor.author","Trümper, L."],["dc.contributor.author","Wilting, J."],["dc.contributor.author","Kube, D."],["dc.date.accessioned","2018-11-07T10:28:03Z"],["dc.date.available","2018-11-07T10:28:03Z"],["dc.date.issued","2017"],["dc.description.abstract","The interaction between vascular endothelial cells (ECs) and cancer cells is of vital importance to understand tumor dissemination. A paradigmatic cancer to study cell-cell interactions is classical Hodgkin Lymphoma (cHL) owing to its complex microenvironment. The role of the interplay between cHL and ECs remains poorly understood. Here we identify canonical WNT pathway activity as important for the mutual interactions between cHL cells and ECs. We demonstrate that local canonical WNT signaling activates cHL cell chemotaxis toward ECs, adhesion to EC layers and cell invasion using not only the Wnt-inhibitor Dickkopf, tankyrases and casein kinase 1 inhibitors but also knockdown of the lymphocyte enhancer binding-factor 1 (LEF-1) and beta-catenin in cHL cells. Furthermore, LEF-1- and beta-catenin-regulated cHL secretome promoted EC migration, sprouting and vascular tube formation involving vascular endothelial growth factor A (VEGF-A). Importantly, high VEGFA expression is associated with a worse overall survival of cHL patients. These findings strongly support the concept that WNTs might function as a regulator of lymphoma dissemination by affecting cHL cell chemotaxis and promoting EC behavior and thus angiogenesis through paracrine interactions."],["dc.identifier.doi","10.1038/leu.2016.232"],["dc.identifier.isi","000394058800012"],["dc.identifier.pmid","27535218"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/43339"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","1476-5551"],["dc.relation.issn","0887-6924"],["dc.title","Microenvironmental interactions between endothelial and lymphoma cells: a role for the canonical WNT pathway in Hodgkin lymphoma"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","289"],["dc.bibliographiccitation.journal","Biochemical Journal"],["dc.bibliographiccitation.lastpage","295"],["dc.bibliographiccitation.volume","389"],["dc.contributor.author","Link, T."],["dc.contributor.author","Lohaus, Gertrud"],["dc.contributor.author","Heiser, I."],["dc.contributor.author","Mendgen, K."],["dc.contributor.author","Hahn, M."],["dc.contributor.author","Voegele, R. T."],["dc.date.accessioned","2018-11-07T08:38:43Z"],["dc.date.available","2018-11-07T08:38:43Z"],["dc.date.issued","2005"],["dc.description.abstract","We have identified and characterized a novel NADP+-dependent D-arabitol dehydrogenase and the corresponding gene from the rust fungus Uromyces fabae, a biotrophic plant pathogen on broad bean (Vicia faba). The new enzyme was termed ARD1p (D-arabitol dehydrogenase 1). It recognizes D-arabitol and mannitol as substrates in the forward reaction, and D-xylulose, D-ribulose and D-fructose as substrates in the reverse reaction. Co-factor specificity was restricted to NADP(H). Kinetic data for the major substrates and co-factors are presented. A detailed analysis of the organization and expression pattern of the ARD1 gene are also given. Immunocytological data indicate a localization of the gene product predominantly in haustoria, the feeding structures of these fungi. Analyses of metabolite levels during pathogenesis indicate that the D-arabitol concentration rises dramatically as infection progresses, and D-arabitol was shown in an in vitro system to be capable of quenching reactive oxygen species involved in host plant defence reactions. ARD1p may therefore play an important role in carbohydrate metabolism and in establishing and/or maintaining the biotrophic interaction in U. fabae."],["dc.identifier.doi","10.1042/BJ20050301"],["dc.identifier.isi","000230779000005"],["dc.identifier.pmid","15796718"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/18824"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Portland Press Ltd"],["dc.relation.issn","1470-8728"],["dc.relation.issn","0264-6021"],["dc.title","Characterization of a novel NADP(+)-dependent D-arabitol dehydrogenase from the plant pathogen Uromyces fabae"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Oncology Research and Treatment"],["dc.bibliographiccitation.volume","38"],["dc.contributor.author","Harenberg, M."],["dc.contributor.author","Linke, F."],["dc.contributor.author","Wilting, J."],["dc.contributor.author","Szczepanowski, Monika"],["dc.contributor.author","Klapper, Wolfram"],["dc.contributor.author","Truemper, Lorenz H."],["dc.contributor.author","Kube, Dieter"],["dc.date.accessioned","2018-11-07T09:50:38Z"],["dc.date.available","2018-11-07T09:50:38Z"],["dc.date.issued","2015"],["dc.format.extent","144"],["dc.identifier.isi","000364268800341"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/35742"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Karger"],["dc.publisher.place","Basel"],["dc.relation.issn","2296-5262"],["dc.relation.issn","2296-5270"],["dc.title","Lymphocyte enhancer binding factor 1 (LEF-1) affects the interaction of Hodgkin lymphoma with endothelial cells"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","190"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","PLANT PHYSIOLOGY"],["dc.bibliographiccitation.lastpage","198"],["dc.bibliographiccitation.volume","137"],["dc.contributor.author","Voegele, R. T."],["dc.contributor.author","Hahn, M."],["dc.contributor.author","Lohaus, Gertrud"],["dc.contributor.author","Link, T."],["dc.contributor.author","Heiser, I."],["dc.contributor.author","Mendgen, K."],["dc.date.accessioned","2018-11-07T08:46:47Z"],["dc.date.available","2018-11-07T08:46:47Z"],["dc.date.issued","2005"],["dc.description.abstract","Levels of the C6-polyol mannitol were observed to rise dramatically in the biotrophic interaction of the rust fungus Uromyces fabae and its host plant Vicia faba. Mannitol was found in millimolar concentrations in extracts and apoplastic fluids of infected leaves and also in extracts of spores. We suggest that this polyol might have at least a dual function: first, as a carbohydrate storage compound, and second, as a scavenger of reactive oxygen species. Mannitol accumulation is accompanied by high expression of a mannitol dehydrogenase (MAD1) in haustoria. While MAD1 transcripts were detected in haustoria only, immunolocalization studies show that the gene product is also present in spores. Kinetic and thermodynamic analyses of the MAD1p catalyzed reactions indicate that the enzyme might be responsible for the production of mannitol in haustoria and for the utilization of mannitol in spores. Since V. faba is normally unable to synthesize or utilize polyols, the multipurpose usage of mannitol seems an ideal strategy for the fungal pathogen."],["dc.identifier.doi","10.1104/pp.104.051839"],["dc.identifier.isi","000226613100017"],["dc.identifier.pmid","15618426"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/20780"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Soc Plant Biologists"],["dc.relation.issn","1532-2548"],["dc.relation.issn","0032-0889"],["dc.title","Possible roles for mannitol and mannitol dehydrogenase in the biotrophic plant pathogen Uromyces fabae"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]