Klemm, Florian

[["dc.bibliographiccitation.firstpage","285"],["dc.bibliographiccitation.journal","Oncology Research and Treatment"],["dc.bibliographiccitation.lastpage","286"],["dc.bibliographiccitation.volume","37"],["dc.contributor.author","Menck, Kerstin"],["dc.contributor.author","Bleckmann, Annalen"],["dc.contributor.author","Scharf, Christian"],["dc.contributor.author","Pukrop, Tobias"],["dc.contributor.author","Dyck, Lydia"],["dc.contributor.author","Klemm, Florian"],["dc.contributor.author","Binder, Claudia"],["dc.date.accessioned","2018-11-07T09:34:18Z"],["dc.date.available","2018-11-07T09:34:18Z"],["dc.date.issued","2014"],["dc.identifier.isi","000343816900702"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/32144"],["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","EMMPRIN/CD147-positive tumor cell microvesicles are pro-invasive and detectable in the blood of cancer patients with metastasis"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Onkologie"],["dc.bibliographiccitation.volume","34"],["dc.contributor.author","Bleckmann, Annalen"],["dc.contributor.author","Siam, Laila"],["dc.contributor.author","Klemm, Florian"],["dc.contributor.author","Rietkoetter, Eva"],["dc.contributor.author","Binder, Claudia"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Pukrop, Tobias"],["dc.date.accessioned","2018-11-07T08:52:16Z"],["dc.date.available","2018-11-07T08:52:16Z"],["dc.date.issued","2011"],["dc.format.extent","151"],["dc.identifier.isi","000295160600393"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/22130"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Karger"],["dc.publisher.place","Basel"],["dc.relation.issn","0378-584X"],["dc.title","LEF1 identifies a prognostically unfavourable subgroup of lung adenocarcinoma brain metastases"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Onkologie"],["dc.bibliographiccitation.volume","35"],["dc.contributor.author","Menck, Kerstin"],["dc.contributor.author","Pukrop, Tobias"],["dc.contributor.author","Schulz, M."],["dc.contributor.author","Dyck, Lydia"],["dc.contributor.author","Binder, Claudia"],["dc.contributor.author","Klemm, Florian"],["dc.date.accessioned","2018-11-07T09:04:54Z"],["dc.date.available","2018-11-07T09:04:54Z"],["dc.date.issued","2012"],["dc.format.extent","195"],["dc.identifier.isi","000310766700508"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/25205"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Karger"],["dc.publisher.place","Basel"],["dc.relation.issn","0378-584X"],["dc.title","Breast cancer invasion mediated by plasma membrane-derived microvesicles is EMMPRIN-dependent"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Onkologie"],["dc.bibliographiccitation.volume","35"],["dc.contributor.author","Bleckmann, Annalen"],["dc.contributor.author","Bayerlova, M."],["dc.contributor.author","Kramer, Franz-Josef"],["dc.contributor.author","Klemm, Florian"],["dc.contributor.author","Binder, Claudia"],["dc.contributor.author","Pukrop, Tobias"],["dc.contributor.author","Beißbarth, Tim"],["dc.date.accessioned","2018-11-07T09:04:54Z"],["dc.date.available","2018-11-07T09:04:54Z"],["dc.date.issued","2012"],["dc.format.extent","65"],["dc.identifier.isi","000310766700159"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/25203"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Karger"],["dc.publisher.place","Basel"],["dc.relation.issn","0378-584X"],["dc.title","Analyzing breast-cancer gene expression data using a newly developed graph-based WNT model in breast cancer"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Onkologie"],["dc.bibliographiccitation.volume","33"],["dc.contributor.author","Klemm, Florian"],["dc.contributor.author","Menck, Kerstin"],["dc.contributor.author","Schulz, M."],["dc.contributor.author","Binder, Claudia"],["dc.date.accessioned","2018-11-07T08:38:50Z"],["dc.date.available","2018-11-07T08:38:50Z"],["dc.date.issued","2010"],["dc.format.extent","199"],["dc.identifier.isi","000282988401115"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/18852"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Karger"],["dc.publisher.place","Basel"],["dc.relation.issn","0378-584X"],["dc.title","Tumor-Microparticles mediate invasiveness and elicit a M2-response in macrophages"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e51554"],["dc.bibliographiccitation.issue","91"],["dc.bibliographiccitation.journal","Journal of Visualized Experiments"],["dc.contributor.author","Menck, Kerstin"],["dc.contributor.author","Behme, Daniel"],["dc.contributor.author","Pantke, Mathias"],["dc.contributor.author","Reiling, Norbert"],["dc.contributor.author","Binder, Claudia"],["dc.contributor.author","Pukrop, Tobias"],["dc.contributor.author","Klemm, Florian"],["dc.date.accessioned","2018-11-07T09:35:29Z"],["dc.date.available","2018-11-07T09:35:29Z"],["dc.date.issued","2014"],["dc.description.abstract","Human macrophages are involved in a plethora of pathologic processes ranging from infectious diseases to cancer. Thus they pose a valuable tool to understand the underlying mechanisms of these diseases. We therefore present a straightforward protocol for the isolation of human monocytes from buffy coats, followed by a differentiation procedure which results in high macrophage yields. The technique relies mostly on commonly available lab equipment and thus provides a cost and time effective way to obtain large quantities of human macrophages. Briefly, buffy coats from healthy blood donors are subjected to a double density gradient centrifugation to harvest monocytes from the peripheral blood. These monocytes are then cultured in fluorinated ethylene propylene (FEP) Teflon-coated cell culture bags in the presence of macrophage colony-stimulating factor (M-CSF). The differentiated macrophages can be easily harvested and used for subsequent studies and functional assays. Important methods for quality control and validation of the isolation and differentiation steps will be highlighted within the protocol. In summary, the protocol described here enables scientists to routinely and reproducibly isolate human macrophages without the need for cost intensive tools. Furthermore, disease models can be studied in a syngeneic human system circumventing the use of murine macrophages."],["dc.identifier.doi","10.3791/51554"],["dc.identifier.isi","000349301100015"],["dc.identifier.pmid","25226391"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/32396"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Journal Of Visualized Experiments"],["dc.relation.issn","1940-087X"],["dc.title","Isolation of Human Monocytes by Double Gradient Centrifugation and Their Differentiation to Macrophages in Teflon-coated Cell Culture Bags"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","434"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Carcinogenesis"],["dc.bibliographiccitation.lastpage","442"],["dc.bibliographiccitation.volume","32"],["dc.contributor.author","Klemm, Florian"],["dc.contributor.author","Bleckmann, Annalen"],["dc.contributor.author","Siam, Laila"],["dc.contributor.author","Chuang, Han-Ning"],["dc.contributor.author","Rietkoetter, Eva"],["dc.contributor.author","Behme, Daniel"],["dc.contributor.author","Schulz, M."],["dc.contributor.author","Schaffrinski, Meike"],["dc.contributor.author","Schindler, Stefanie"],["dc.contributor.author","Trümper, Lorenz H."],["dc.contributor.author","Kramer, Franz-Josef"],["dc.contributor.author","Beißbarth, Tim"],["dc.contributor.author","Stadelmann, C."],["dc.contributor.author","Binder, Claudia"],["dc.contributor.author","Pukrop, Tobias"],["dc.date.accessioned","2018-11-07T08:59:01Z"],["dc.date.available","2018-11-07T08:59:01Z"],["dc.date.issued","2011"],["dc.description.abstract","A role of WNT signaling for primary breast cancers of the basal-like subtype and as a predictor of brain metastasis has been described. However, a responsible WNT ligand has not been identified. To further clarify this question, we comparatively investigated 22 human breast cancer brain metastases as well as the highly invasive human breast cancer cell line MDA-MB-231 and the weakly motile MCF-7 as models for the basal-like and the luminal A subtype. WNT5A and B were found overexpressed in MDA-MB-231 cells as compared with MCF-7. This corresponded to reduction of MDA-MB-231 invasiveness by WNT inhibitors, whereas MCF-7 invasion was enhanced by recombinant WNT5B and abolished by WNT and Jun-N-terminal kinase antagonists. Expression and subcellular distribution of beta-catenin remained uninfluenced. Consistently, beta-catenin was not localized in the nuclei of brain metastases while there was strong nuclear c-Jun staining. Similar to MDA-MB-231, metastases showed expression of WNT5A/B and the alternative WNT receptors ROR1 and 2. These findings were validated using external gene expression datasets (Gene Expression Omnibus) of different breast cancer subtypes and brain metastases. Hierarchical cluster analysis yielded a close relation between basal-like cancers and brain metastases. Gene set enrichment analyses confirmed WNT pathway enrichment not only in basal-like primaries but also in cerebral metastases of all subtypes. In conclusion, WNT signaling seems highly relevant for basal-like and other subtypes of breast cancers metastasizing into the brain. beta-catenin-independent WNT signaling, presumably via ROR1-2, plays a major role in this context."],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft [FOR 942]"],["dc.identifier.doi","10.1093/carcin/bgq269"],["dc.identifier.isi","000288027800025"],["dc.identifier.pmid","21173432"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/23785"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","0143-3334"],["dc.title","beta-catenin-independent WNT signaling in basal-like breast cancer and brain metastasis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","193"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Surgical Research"],["dc.bibliographiccitation.lastpage","205"],["dc.bibliographiccitation.volume","203"],["dc.contributor.author","Monin, Malte B."],["dc.contributor.author","Krause, Petra"],["dc.contributor.author","Stelling, Robin"],["dc.contributor.author","Bocuk, Derya"],["dc.contributor.author","Niebert, Sabine"],["dc.contributor.author","Klemm, Florian"],["dc.contributor.author","Pukrop, Tobias"],["dc.contributor.author","Koenig, Sarah"],["dc.date.accessioned","2018-11-07T10:13:22Z"],["dc.date.available","2018-11-07T10:13:22Z"],["dc.date.issued","2016"],["dc.description.abstract","Background: Wnt/beta-catenin signaling is known to play an important role in colorectal cancer (CRC). Niclosamide, a salicylamide derivative used in the treatment of tapeworm infections, targets the Wnt/beta-catenin pathway. The objective of this study was to investigate niclosamide as a therapeutic agent against CRC. Methods: The antiproliferative effects of 1, 3, 10, and 50 mu M concentrations of niclosamide on human (SW480 and SW620) and rodent (CC531) CRC cell lines were determined by MTS assay and direct cell count. The lymphoid enhancer-binding factor 1/transcription factor (LEF/TCF) reporter assay monitored the activity of Wnt signaling. Immunofluorescence staining demonstrated the expression pattern of active beta-catenin. Gene expression of canonical and noncanonical Wnt signaling components was analyzed using qRT-PCR. Western blot analysis was performed with antibodies detecting nuclear localization of beta-catenin and c-jun. Results: Cell proliferation in CRC cell lines was blocked dose dependently after 12 and 24 h of incubation. The Wnt promoter activity of LEF/TCF significantly decreased with niclosamide concentrations of 10 and 50 mM after 12 h of incubation. Active beta-catenin did not shift from the nuclear to the cytosolic pool. However, canonical target genes (met, MMP7, and cyclin D1) as well as the coactivating factor Bcl9 were downregulated, whereas the noncanonical key player c-jun was clearly activated. Conclusions: Niclosamide treatment is associated with an inhibitory effect on CRC development and reduced Wnt activity. It may exert its effect by interfering with the nuclear beta-catenin-Bcl9-LEF/TCF triple-complex and by upregulation of c-jun representing noncanonical Wnt/JNK signaling. Thus, our findings warrant further research into this substance as a treatment option for patients with advanced CRC. (C) 2016 Elsevier Inc. All rights reserved."],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft [KO 2218/5-1]"],["dc.identifier.doi","10.1016/j.jss.2016.03.051"],["dc.identifier.isi","000378170200024"],["dc.identifier.pmid","27338550"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40422"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Academic Press Inc Elsevier Science"],["dc.relation.issn","1095-8673"],["dc.relation.issn","0022-4804"],["dc.title","The anthelmintic niclosamide inhibits colorectal cancer cell lines via modulation of the canonical and noncanonical Wnt signaling pathway"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1197"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","The Journal of Immunology"],["dc.bibliographiccitation.lastpage","1205"],["dc.bibliographiccitation.volume","175"],["dc.contributor.author","Hagemann, T."],["dc.contributor.author","Wilson, Julianna K."],["dc.contributor.author","Kulbe, H."],["dc.contributor.author","Li, NFF"],["dc.contributor.author","Leinster, D. A."],["dc.contributor.author","Charles, K."],["dc.contributor.author","Klemm, Florian"],["dc.contributor.author","Pukrop, Tobias"],["dc.contributor.author","Binder, Claudia"],["dc.contributor.author","Balkwill, F. R."],["dc.date.accessioned","2018-11-07T08:40:35Z"],["dc.date.available","2018-11-07T08:40:35Z"],["dc.date.issued","2005"],["dc.description.abstract","Tumor-associated macrophages may influence tumor progression, angiogenesis and invasion. To investigate mechanisms by which macrophages interact with tumor cells, we developed an in vitro coculture model. Previously we reported that coculture enhanced invasiveness of the tumor cells in a TNF-alpha- and matrix metalloprotease-dependent manner. In this report, we studied intracellular signaling pathways and induction of inflammatory genes in malignant cells under the influence of macrophage coculture. We report that coculture of macrophages with ovarian or breast cancer cell lines led to TNF-alpha-dependent activation of JNK and NF-kappa B pathways in tumor cells, but not in benign immortalized epithelial cells. Tumor cells with increased JNK and NF-kappa B activity exhibited enhanced invasiveness. Inhibition of the NF-kappa B pathway by TNF-alpha neutralizing Abs, an NF-kappa B inhibitor, RNAi to Re1A, or overexpression of I kappa B inhibited tumor cell invasiveness. Blockade of JNK also significantly reduced invasiveness, but blockade of p38 MAPK or p42 MAPK had no effect. Cocultured tumor cells were screened for the expression of 22 genes associated with inflammation and invasion that also contained an AP-1 and NF-kappa B binding site. EMMPRIN and MIF were up-regulated in cocultured tumor cells in a JNK- and NF-kappa B-dependent manner. Knocking down either MIF or EMMPRIN by RNAi in the tumor cells significantly reduced tumor cell invasiveness and matrix metalloprotease activity in the coculture supernatant. We conclude that TNF-alpha, via NF-kappa B, and JNK induces MIF and EMMPRIN in macrophage to tumor cell cocultures and this leads to increased invasive capacity of the tumor cells."],["dc.identifier.isi","000233647600067"],["dc.identifier.pmid","16002723"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/19268"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Assoc Immunologists"],["dc.relation.issn","0022-1767"],["dc.title","Macrophages induce invasiveness of epithelial cancer cells via NF-kappa B and JNK"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Onkologie"],["dc.bibliographiccitation.volume","34"],["dc.contributor.author","Menck, Kerstin"],["dc.contributor.author","Klemm, Florian"],["dc.contributor.author","Schulz, M."],["dc.contributor.author","Pukrop, Tobias"],["dc.contributor.author","Binder, Claudia"],["dc.date.accessioned","2018-11-07T08:52:16Z"],["dc.date.available","2018-11-07T08:52:16Z"],["dc.date.issued","2011"],["dc.format.extent","60"],["dc.identifier.isi","000295160600152"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/22127"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Karger"],["dc.publisher.place","Basel"],["dc.relation.issn","0378-584X"],["dc.title","Identification and further characterization of microparticle populations in microparticle-induced breast cancer invasion"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]