Alves, Frauke

[["dc.bibliographiccitation.journal","Journal of Investigative Dermatology"],["dc.bibliographiccitation.volume","130"],["dc.contributor.author","Hippe, Andreas"],["dc.contributor.author","Schorr, Anne"],["dc.contributor.author","Mueller-Homey, Anja"],["dc.contributor.author","Seeliger, Stefan"],["dc.contributor.author","Jannasch, Katharina"],["dc.contributor.author","Buhren, Bettina Alexandra"],["dc.contributor.author","Sleeman, Jonathan"],["dc.contributor.author","Stoecklein, Nikolas H."],["dc.contributor.author","Alves, Frauke"],["dc.contributor.author","Hoffmann, Thomas"],["dc.contributor.author","Homey, Bernhard"],["dc.date.accessioned","2018-11-07T08:39:51Z"],["dc.date.available","2018-11-07T08:39:51Z"],["dc.date.issued","2010"],["dc.format.extent","S51"],["dc.identifier.isi","000281110100300"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/19099"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.publisher.place","New york"],["dc.relation.eventlocation","Helsinki, FINLAND"],["dc.relation.issn","0022-202X"],["dc.title","Tumor derived CCL20 production critically contributes to angiogenesis and tumor progression"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","942"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","British Journal of Cancer"],["dc.bibliographiccitation.lastpage","954"],["dc.bibliographiccitation.volume","123"],["dc.contributor.author","Hippe, Andreas"],["dc.contributor.author","Braun, Stephan Alexander"],["dc.contributor.author","Oláh, Péter"],["dc.contributor.author","Gerber, Peter Arne"],["dc.contributor.author","Schorr, Anne"],["dc.contributor.author","Seeliger, Stephan"],["dc.contributor.author","Holtz, Stephanie"],["dc.contributor.author","Jannasch, Katharina"],["dc.contributor.author","Pivarcsi, Andor"],["dc.contributor.author","Buhren, Bettina"],["dc.contributor.author","Schrumpf, Holger"],["dc.contributor.author","Kislat, Andreas"],["dc.contributor.author","Bünemann, Erich"],["dc.contributor.author","Steinhoff, Martin"],["dc.contributor.author","Fischer, Jens"],["dc.contributor.author","Lira, Sérgio A."],["dc.contributor.author","Boukamp, Petra"],["dc.contributor.author","Hevezi, Peter"],["dc.contributor.author","Stoecklein, Nikolas Hendrik"],["dc.contributor.author","Hoffmann, Thomas"],["dc.contributor.author","Alves, Frauke"],["dc.contributor.author","Sleeman, Jonathan"],["dc.contributor.author","Bauer, Thomas"],["dc.contributor.author","Klufa, Jörg"],["dc.contributor.author","Amberg, Nicole"],["dc.contributor.author","Sibilia, Maria"],["dc.contributor.author","Zlotnik, Albert"],["dc.contributor.author","Müller-Homey, Anja"],["dc.contributor.author","Homey, Bernhard"],["dc.date.accessioned","2021-04-14T08:25:49Z"],["dc.date.available","2021-04-14T08:25:49Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1038/s41416-020-0943-2"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/81742"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","1532-1827"],["dc.relation.haserratum","/handle/2/103504"],["dc.relation.issn","0007-0920"],["dc.title","EGFR/Ras-induced CCL20 production modulates the tumour microenvironment"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","4275"],["dc.bibliographiccitation.issue","41"],["dc.bibliographiccitation.journal","Oncogene"],["dc.bibliographiccitation.lastpage","4288"],["dc.bibliographiccitation.volume","30"],["dc.contributor.author","Gerstel, Daniela"],["dc.contributor.author","Wegwitz, Florian"],["dc.contributor.author","Jannasch, Katharina"],["dc.contributor.author","Ludewig, P."],["dc.contributor.author","Scheike, K."],["dc.contributor.author","Alves, Frauke"],["dc.contributor.author","Beauchemin, Nicole"],["dc.contributor.author","Deppert, Wolfgang R."],["dc.contributor.author","Wagener, Christoph"],["dc.contributor.author","Horst, Andrea Kristina"],["dc.date.accessioned","2018-11-07T08:51:04Z"],["dc.date.available","2018-11-07T08:51:04Z"],["dc.date.issued","2011"],["dc.description.abstract","We have studied the effects of carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1) on tumor angiogenesis in murine ductal mammary adenocarcinomas. We crossed transgenic mice with whey acidic protein promoter-driven large T-antigen expression (WAP-T mice) with oncogene-induced mammary carcinogenesis with CEA-CAM1null mice, and with Tie2-Ceacam1 transgenics, in which the Tie2 promoter drives endothelial overexpression of CEACAM1 (WAP-T x CEACAM1(endo+) mice), and analyzed tumor vascularization, angiogenesis and vessel maturation in these mice. Using flat-panel volume computed tomography (fpVCT) and histology, we found that WAP-T x CEACAM1(endo+) mice exhibited enhanced tumoral vascularization owing to CEACAM1(+) vessels in the tumor periphery, and increased intratumoral angiogenesis compared with controls. In contrast, vascularization of CEACAM1null/WAP-T-derived tumors was poor, and tumor vessels were dilated, leaky and showed poor pericyte coverage. Consequently, the tumoral vasculature could not be visualized in CEACAM1null/WAP-T mice by fpVCT, and we observed poor organization of the perivascular extracellular matrix (ECM), accompanied by the accumulation of collagen IV-degrading matrix metalloproteinase 9(+) (MMP9(+)) leukocytes and stromal cells. Vascular instability and alterations in ECM structure were accompanied by a significant increase in pulmonary metastases in CEACAM1null/WAP-T mice, whereas only occasional metastases were observed in CEACAM1(+) hosts. In CEACAM1(+) hosts, intratumoral vessels did not express CEACAM1, but they were intact, extensively covered with pericytes and framed by a well-organized perivascular ECM. MMP9(+) accessory cells were largely absent. Orthotopic transplantation of primary WAP-T- and CEACAM1null/WAP-T tumors into all three mouse lines confirmed that a CEACAM1(+) host environment is a prerequisite for productive angiogenic remodeling of the tumor microenvironment. Hence, CEACAM1 expression in the tumor periphery determines the vascular phenotype in a tumor, whereas systemic absence of CEACAM1 interferes with the formation of an organized tumor matrix and intratumoral vessel maturation. Oncogene (2011) 30, 4275-4288; doi: 10.1038/onc.2011.146; published online 2 May 2011"],["dc.description.sponsorship","German Research Foundation [SPP1190]"],["dc.identifier.doi","10.1038/onc.2011.146"],["dc.identifier.isi","000296356300005"],["dc.identifier.pmid","21532628"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/21845"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","0950-9232"],["dc.title","CEACAM1 creates a pro-angiogenic tumor microenvironment that supports tumor vessel maturation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","25"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","International Journal of Cancer"],["dc.bibliographiccitation.lastpage","36"],["dc.bibliographiccitation.volume","137"],["dc.contributor.author","Jannasch, Katharina"],["dc.contributor.author","Wegwitz, Florian"],["dc.contributor.author","Lenfert, Eva"],["dc.contributor.author","Maenz, Claudia"],["dc.contributor.author","Deppert, Wolfgang R."],["dc.contributor.author","Alves, Frauke"],["dc.date.accessioned","2018-11-07T09:55:37Z"],["dc.date.available","2018-11-07T09:55:37Z"],["dc.date.issued","2015"],["dc.description.abstract","In this study, the effects of the standard chemotherapy, cyclophosphamide/adriamycin/5-fluorouracil (CAF) on tumor growth, dissemination and recurrence after orthotopic implantation of murine G-2 cells were analyzed in the syngeneic immunocompetent whey acidic protein-T mouse model (Wegwitz et al., PLoS One 2010; 5:e12103; Schulze-Garg et al., Oncogene 2000; 19:1028-37). Single-dose CAF treatment reduced tumor size significantly, but was not able to eradicate all tumor cells, as recurrent tumor growth was observed 4 weeks after CAF treatment. Nine days after CAF treatment, residual tumors showed features of regressive alterations and were composed of mesenchymal-like tumor cells, infiltrating immune cells and some tumor-associated fibroblasts with an intense deposition of collagen. Recurrent tumors were characterized by coagulative necrosis and less tumor cell differentiation compared with untreated tumors, suggesting a more aggressive tumor phenotype. In support, tumor cell dissemination was strongly enhanced in mice that had developed recurrent tumors in comparison with untreated controls, although only few disseminated tumor cells could be detected in various organs 9 days after CAF application. In vitro experiments revealed that CAF treatment of G-2 cells eliminates the vast majority of epithelial tumor cells, whereas tumor cells with a mesenchymal phenotype survive. These results together with the in vivo findings suggest that tumor cells that underwent epithelial-mesenchymal transition and/or exhibit stem-cell-like properties are difficult to eliminate using one round of CAF chemotherapy. The model system described here provides a valuable tool for the characterization of the effects of chemotherapeutic regimens on recurrent tumor growth and on tumor cell dissemination, thereby enabling the development and preclinical evaluation of novel therapeutic strategies to target mammary carcinomas."],["dc.identifier.doi","10.1002/ijc.29369"],["dc.identifier.isi","000353297600003"],["dc.identifier.pmid","25449528"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/36792"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","1097-0215"],["dc.relation.issn","0020-7136"],["dc.title","Chemotherapy of WAP-T mouse mammary carcinomas aggravates tumor phenotype and enhances tumor cell dissemination"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Experimental Dermatology"],["dc.bibliographiccitation.volume","18"],["dc.contributor.author","Hippe, Andreas"],["dc.contributor.author","Schorr, Anne"],["dc.contributor.author","Mueller-Horney, A."],["dc.contributor.author","Lierop, A. van"],["dc.contributor.author","Steinhoff, Martin"],["dc.contributor.author","Seeliger, Stefan"],["dc.contributor.author","Kubitza, R."],["dc.contributor.author","Buenemann, E."],["dc.contributor.author","Liersch, Ruediger"],["dc.contributor.author","Heroult, M."],["dc.contributor.author","Hoffmann, T. K."],["dc.contributor.author","Jannasch, Katharina"],["dc.contributor.author","Brema, S."],["dc.contributor.author","Boukamp, P."],["dc.contributor.author","Mueller, M."],["dc.contributor.author","Alves, Frauke"],["dc.contributor.author","Sleeman, J. P."],["dc.contributor.author","Augustin, H."],["dc.contributor.author","Zlotnik, A."],["dc.contributor.author","Horney, B."],["dc.date.accessioned","2018-11-07T08:32:02Z"],["dc.date.available","2018-11-07T08:32:02Z"],["dc.date.issued","2009"],["dc.identifier.isi","000263520200222"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/17255"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell Publishing, Inc"],["dc.publisher.place","Malden"],["dc.relation.eventlocation","Heidelberg, GERMANY"],["dc.title","The role of the chemokine CCL20 in tumor-associated angiogenesis"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","513"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Gastroenterology"],["dc.bibliographiccitation.lastpage","+"],["dc.bibliographiccitation.volume","150"],["dc.contributor.author","Matzke-Ogi, Alexandra"],["dc.contributor.author","Jannasch, Katharina"],["dc.contributor.author","Shatirishvili, Marine"],["dc.contributor.author","Fuchs, Beatrix"],["dc.contributor.author","Chiblak, Sara"],["dc.contributor.author","Morton, Jennifer"],["dc.contributor.author","Tawk, Bouchra"],["dc.contributor.author","Lindner, Thomas"],["dc.contributor.author","Sansom, Owen"],["dc.contributor.author","Alves, Frauke"],["dc.contributor.author","Warth, Arne"],["dc.contributor.author","Schwager, Christian"],["dc.contributor.author","Mier, Walter"],["dc.contributor.author","Kleeff, Joerg"],["dc.contributor.author","Ponta, Helmut"],["dc.contributor.author","Abdollahi, Amir"],["dc.contributor.author","Orian-Rousseau, Veronique"],["dc.date.accessioned","2018-11-07T10:18:53Z"],["dc.date.available","2018-11-07T10:18:53Z"],["dc.date.issued","2016"],["dc.description.abstract","BACKGROUND & AIMS: Cancer cells with high metastatic potential and stem cell-like characteristics express the cell surface marker CD44. CD44 isoforms that include the v6 exon are co-receptors for the receptor tyrosine kinases MET and Vascular Endothelial Growth factor Receptor-2 (VEGFR2). We studied CD44v6 signaling in several pancreatic cancer cell lines, and its role in tumor growth and metastasis in several models of pancreatic cancer. METHODS: We analyzed the effects of v6 peptides that interfere with the co-receptor functions of CD44v6 for MET and VEGFR-2 in tumors and metastases grown from cells that express different CD44 isoforms, including CD44v6. The peptides were injected into rats with syngeneic tumors and mice with orthotopic or xenograft tumors. We also tested the effects of the peptides in mice with xenograft tumors grown from patient tumor samples and mice that express an oncogenic form of RAS and develop spontaneous pancreatic cancer (KPC mice). We measured levels of CD44v6 messenger RNA (mRNA) in pancreatic cancer tissues from 136 patients. RESULTS: Xenograft tumors grown from human cancer cells injected with v6 peptides were smaller and formed fewer metastases in mice. The v6 peptide was more efficient than the MET inhibitor crizotinib and/or the VEGFR-2 inhibitor pazopanib in reducing xenograft tumor growth and metastasis. Injection of KPC mice with the v6 peptide increased their survival time. Injection of mice and rats bearing metastases with the v6 peptide induced regression of metastases. Higher levels of CD44v6 mRNA in human pancreatic tumor tissues were associated with increased expression of MET, tumor metastasis, and shorter patient survival times. CONCLUSIONS: Peptide inhibitors of CD44v6 isoforms block tumor growth and metastasis in several independent models of pancreatic cancer. The v6 peptides induced regression of metastases. Levels of CD44v6 mRNA are increased, along with those of MET mRNA, in patients with metastatic pancreatic tumors, compared with nonmetastatic tumors; the increased levels correlated with shorter patient survival time."],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft [OR 124/4-1, OR 124/4-2]"],["dc.identifier.doi","10.1053/j.gastro.2015.10.020"],["dc.identifier.isi","000368629900037"],["dc.identifier.pmid","26597578"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/41544"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","W B Saunders Co-elsevier Inc"],["dc.relation.issn","1528-0012"],["dc.relation.issn","0016-5085"],["dc.title","Inhibition of Tumor Growth and Metastasis in Pancreatic Cancer Models by Interference With CD44v6 Signaling"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","286"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","European Journal of Radiology"],["dc.bibliographiccitation.lastpage","293"],["dc.bibliographiccitation.volume","70"],["dc.contributor.author","Alves, Frauke"],["dc.contributor.author","Dullin, Christian"],["dc.contributor.author","Napp, Joanna"],["dc.contributor.author","Missbach-Guentner, Jeannine"],["dc.contributor.author","Jannasch, Katharina"],["dc.contributor.author","Mathejczyk, Julia"],["dc.contributor.author","Pardo, Luis A."],["dc.contributor.author","Stühmer, Walter"],["dc.contributor.author","Tietze, Lutz Friedjan"],["dc.date.accessioned","2018-11-07T08:30:16Z"],["dc.date.available","2018-11-07T08:30:16Z"],["dc.date.issued","2009"],["dc.description.abstract","Conventional chemotherapy of cancer has its limitations, especially in advanced and disseminated disease and suffers from lack of specificity. This results in a poor therapeutic index and considerable toxicity to normal organs. Therefore, many efforts are made to develop novel therapeutic tools against cancer with the aim of selectively targeting the drug to the turnout site. Drug delivery strategies fundamentally rely on the identification of good-quality biomarkers, allowing unequivocal discrimination between cancer and healthy tissue. At present, antibodies or antibody fragments have clearly proven their value as carrier molecules specific for a tumour-associated molecular marker. This present review draws attention to the use of near-infrared fluorescence (NIRF) imaging to investigate binding specificity and kinetics of carrier molecules such as monoclonal antibodies. In addition, flat-panel volume computed tomography (fpVCT) will be presented to monitor anatomical structures in turnout mouse models over time in a non-invasive manner. Each imaging device sheds light on a different aspect; functional imaging is applied to optimise the dose schedule and the concept of selective tumour therapies, whereas anatomical imaging assesses preclinically the efficacy of novel turnout therapies. Both imaging techniques in combination allow the visualisation of functional information obtained by NIRF imaging within an adequate anatomic framework. (C) 2009 Elsevier Ireland Ltd. All rights reserved."],["dc.description.sponsorship","DFG [SFB 416, AL336/5-1]"],["dc.identifier.doi","10.1016/j.ejrad.2009.01.048"],["dc.identifier.isi","000266868900012"],["dc.identifier.pmid","19285818"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/16849"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation.issn","0720-048X"],["dc.title","Concept of a selective tumour therapy and its evaluation by near-infrared fluorescence imaging and flat-panel volume computed tomography in mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]