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  • ddc: 610  (23)
  • MICE  (9)
  • tumor  (8)
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  • 11
    Keywords: CANCER ; EXPRESSION ; carcinoma ; PROTEINS ; MICE ; ACTIVATION ; murine ; RAGE ; ROLES ; PROMOTES
    Abstract: The S100A8/A9 heterodimer (calprotectin) acts as a danger signal when secreted into the extracellular space during inflammation and tissue damage. It promotes proinflammatory responses and drives tumor development in different models of inflammation-driven carcinogenesis. S100A8/A9 is strongly expressed in several human tumors, including hepatocellular carcinoma (HCC). Apart from this evidence, the role of calprotectin in hepatocyte transformation and tumor microenvironment is still unknown. The aim of this study was to define the function of S100A8/A9 in inflammation-driven HCC. Mice lacking S100a9 were crossed with the Mdr2(-/-) model, a prototype of inflammation-induced HCC formation. S100a9(-/-) Mdr2(-/-) (dKO) mice displayed no significant differences in tumor incidence or multiplicity compared to Mdr2(-/-) animals. Chronic liver inflammation, fibrosis and oval cell activation were not affected upon S100a9 deletion. Our data demonstrate that, although highly upregulated, calprotectin is dispensable in the onset and development of HCC, and in the maintenance of liver inflammation. What's new? Liver cancers often overexpress a protein, S100A9, which functions as a danger signal during inflammation. It promotes inflammation and can drive the development of some tumors. In this paper, the authors sought to define the role of S100A9 in liver cancer. When they eliminated the protein from mice prone to inflammation-driven hepatocellular cancer, the liver tumors continued to develop unabated. Although it's highly upregulated in liver cancers, S100A9 isn't required for liver tumors to form, and wouldn't be useful as a therapeutic target.
    Type of Publication: Journal article published
    PubMed ID: 25331529
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  • 12
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    German Medical Science GMS Publishing House; Düsseldorf
    In:  GMS Current Posters in Otorhinolaryngology - Head and Neck Surgery; VOL: 12; DOC202 /20160411/
    Publication Date: 2016-04-12
    Description: Einleitung: Trotz moderner radioonkologischer Therapieansätze stellt die Entwicklung von Radioresistenz in durch Heterogenität charakterisierten Kopf-Hals-Plattenepithelkarzinomen (HNSCC) ein erhebliches Problem dar. Die Etablierung innovativer präklinischer Modellsysteme für die systematische Charakterisierung von Resistenzmechanismen und Testung neuer gezielter Pharmakotherapeutika ist daher unbedingt erforderlich.Methoden: Das Zusammenspiel zwischen Bestrahlung und Aktivierung der MAP-Kinasen ERK, p38 und JNK wurde in vitro sowie im humanen ex vivo-Kopf-Hals-Karzinommodell untersucht. Nach MAPK-Inhibition erfolgte die Bestrahlung von HNSCC-Zelllinien (p53WT/mut). Das Bestrahlungsansprechen wurde funktionell analysiert und im ex vivo-Modell bestätigt. Ergebnisse: Zwei HNSCC-Linien zeigten eine deutliche strahlungsinduzierte ERK-Phosphorylierung, welche mit Radiosensibilisierung nach MEK-Hemmung im Colony Forming Assay (CFA) assoziiert war, während sich eine Linie mit geringer postradiogener ERK-Phosphorylierung im CFA als weniger sensibel auf MEK-Inhibition erwies. Das heterogene Ansprechen spiegelte sich auch im ex vivo-Modell wider. JNK und p38 zeigten keine relevante bestrahlungsinduzierte Aktivierung. Schlussfolgerungen: Die heterogene strahlungsinduzierte ERK-Phosphorylierung in der Zellkultur und im ex vivo-Modell weist auf einen kontextabhängigen Regulationsmodus hin. Aufgrund der geringen Fallzahl war eine Korrelation mit klinischen Parametern nur begrenzt möglich, jedoch kam es interessanterweise bei Patienten mit geringer basaler ERK-Phosphorylierung und postradiogener Induktion im Verlauf zu einem Rezidiv. In geplanten Studien an großen Kohorten sollte daher diese Subgruppe genauer analysiert werden.Der Erstautor gibt keinen Interessenkonflikt an.
    Keywords: ddc: 610
    Language: German
    Type: article
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  • 13
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    German Medical Science GMS Publishing House; Düsseldorf
    In:  87. Jahresversammlung der Deutschen Gesellschaft für Hals-Nasen-Ohren-Heilkunde, Kopf- und Hals-Chirurgie; 20160504-20160507; Düsseldorf; DOC16hnod251 /20160330/
    Publication Date: 2016-03-31
    Keywords: ddc: 610
    Language: German
    Type: conferenceObject
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  • 14
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    German Medical Science GMS Publishing House; Düsseldorf
    In:  87. Jahresversammlung der Deutschen Gesellschaft für Hals-Nasen-Ohren-Heilkunde, Kopf- und Hals-Chirurgie; 20160504-20160507; Düsseldorf; DOC16hnod200 /20160330/
    Publication Date: 2016-03-31
    Keywords: ddc: 610
    Language: German
    Type: conferenceObject
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  • 15
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    German Medical Science GMS Publishing House; Düsseldorf
    In:  85. Jahresversammlung der Deutschen Gesellschaft für Hals-Nasen-Ohren-Heilkunde, Kopf- und Hals-Chirurgie; 20140528-20140601; Dortmund; DOC14hnod300 /20140414/
    Publication Date: 2014-04-15
    Keywords: ddc: 610
    Language: German
    Type: conferenceObject
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  • 16
    Keywords: CANCER ; CELLS ; EXPRESSION ; GROWTH ; IN-VITRO ; INHIBITOR ; tumor ; carcinoma ; Germany ; IN-VIVO ; VITRO ; GENE ; PROTEIN ; TUMORS ; MICE ; PATIENT ; FAMILY ; AP-1 ; CARCINOGENESIS ; INDUCTION ; KERATINOCYTES ; SKIN ; BINDING ; fibroblasts ; MOUSE ; c-Fos ; PROMOTER ; MOUSE SKIN ; TRANSFORMATION ; BENIGN ; CARCINOMAS ; squamous cell carcinoma ; GLUCOCORTICOID-RECEPTOR ; SKIN-CANCER ; BINDING PROTEIN ; keratinocyte ; TRANSITION ; MALIGNANT PROGRESSION ; INTERSTITIAL COLLAGENASE ; CELL-CARCINOMA ; dexamethasone ; MOUSE KERATINOCYTES ; RECYCLING ENDOSOMES
    Abstract: Malignant transformation of mouse skin by tumor promoters and chemical carcinogens, such as the phorhol ester 12-O-tetradecanoylphorbol-13-acetate (TPA), is a multistage process leading to the formation of squamous cell carcinomas. it has been shown that mice lacking the AP-1 family member c-Fos exhibit an impaired transition from benign to malignant skin tumors. Here, we demonstrate enhanced expression of the small Ras-related GTPase Rab11a after short-term TPA treatment of mouse back skin. Expression of Rab11a in vivo and in vitro critically depended on c-Fos, because TPA application to the back skin of c-Fos-deficient mice and to mouse embryonic fibroblasts did not induce Rab11a mRNA or protein expression. Moreover, dexamethasone, which is a potent inhibitor of AP-1-mediated transactivation that exhibits anti-inflammatory and antitumor promoting activities, inhibited TPA-induced expression of Rab11a. Within the Rab11a gene promoter, we identified a functional AP-1 binding element that exhibited elevated c-Fos binding activity after TPA treatment of keratinocytes. Enhanced expression was not restricted to chemically induced mouse skin tumors but was also found in tumor specimens derived from patients with epithelial skin tumors. These data identify Rab11a as a novel, tumor-associated c-Fos/AP-1 target and may point to an as yet unrecognized function of Rab11a in the development of skin cancer
    Type of Publication: Journal article published
    PubMed ID: 15972968
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  • 17
    Keywords: APOPTOSIS ; CANCER ; EXPRESSION ; CELL ; Germany ; human ; IN-VIVO ; KINASE ; MODEL ; VIVO ; GENE ; GENE-EXPRESSION ; GENES ; HYBRIDIZATION ; PROTEIN ; RNA ; METABOLISM ; cell line ; LINES ; MICE ; DNA ; CARCINOGENESIS ; animals ; KERATINOCYTES ; SKIN ; BIOLOGY ; cell cycle ; CELL-CYCLE ; CELL-LINES ; CYCLE ; DOWN-REGULATION ; MOUSE ; IDENTIFICATION ; IN-SITU ; PROGRESSION ; MALIGNANCIES ; gene expression ; EXPRESSION ANALYSIS ; HUMANS ; DESIGN ; UP-REGULATION ; MOUSE SKIN ; skin carcinogenesis ; genetics ; statistics ; CELL-LINE ; LINE ; ADHESION ; CELL-ADHESION ; ONCOGENE ; INVOLVEMENT ; RT-PCR ; KINETICS ; cell lines ; heredity ; SKIN-CANCER ; HUMAN SKIN ; in situ hybridization ; MALIGNANCY ; ONCOLOGY ; ANNOTATION ; ENHANCED EXPRESSION ; cell adhesion ; LEVEL ; analysis ; CANCER DEVELOPMENT ; cluster analysis ; S100A8 ; MAP ; in vivo ; RELEVANCE ; Oligonucleotide Array Sequence Analysis ; SPECIMENS ; animal ; Carcinoma,Squamous Cell ; SQUAMOUS-CELL ; SET ; animal model ; molecular genetics ; Reverse Transcriptase Polymerase Chain Reaction ; Skin Neoplasms ; Cell Line,Tumor ; cytology ; DNA,Complementary ; epithelial skin cancer ; Gene Expression Regulation,Neoplastic ; HUMAN-SKIN ; Microscopy,Fluorescence ; Protein-Serine-Threonine Kinases ; RNA,Messenger ; tumour specimen
    Abstract: Chemically induced mouse skin carcinogenesis represents the most extensively utilized animal model to unravel the multistage nature of tumour development and to design novel therapeutic concepts of human epithelial neoplasia. We combined this tumour model with comprehensive gene expression analysis and could identify a large set of novel tumour-associated genes that have not been associated with epithelial skin cancer development yet. Expression data of selected genes were confirmed by semiquantitative and quantitative RT-PCR as well as in situ hybridization and immunofluorescence analysis on mouse tumour sections. Enhanced expression of genes identified in our screen was also demonstrated in mouse keratinocyte cell lines that form tumours in vivo. Self-organizing map clustering was performed to identify different kinetics of gene expression and coregulation during skin cancer progression. Detailed analysis of differential expressed genes according to their functional annotation confirmed the involvement of several biological processes, such as regulation of cell cycle, apoptosis, extracellular proteolysis and cell adhesion, during skin malignancy. Finally, we detected high transcript levels of ANXA1, LCN2 and S100A8 as well as reduced levels for NDR2 protein in human skin tumour specimens demonstrating that tumour-associated genes identified in the chemically induced tumour model might be of great relevance for the understanding of human epithelial malignancies as well
    Type of Publication: Journal article published
    PubMed ID: 16247483
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  • 18
    Keywords: brain ; CANCER ; CANCER CELLS ; CELLS ; EXPRESSION ; GROWTH ; IN-VITRO ; INHIBITOR ; INVASION ; proliferation ; tumor ; CELL ; CELL-PROLIFERATION ; Germany ; human ; IN-VIVO ; MODEL ; VITRO ; VIVO ; GENE-EXPRESSION ; PROTEIN ; transcription ; cell line ; TISSUE ; TUMORS ; LINES ; MICE ; PATIENT ; TISSUES ; KERATINOCYTES ; SKIN ; T cell ; T-CELL ; CELL-LINES ; SIGNAL ; MOUSE ; STAGE ; UP-REGULATION ; MEMBRANE ; skin carcinogenesis ; CELL-LINE ; LINE ; ADHESION ; MIGRATION ; MORPHOLOGY ; INVOLVEMENT ; MOUSE MODEL ; TRANSLOCATION ; beta-catenin ; ECTODOMAIN ; cell lines ; SUBSTRATE-SPECIFICITY ; MATRIX ; E-cadherin ; ONCOLOGY ; RE ; CAPACITY ; keratinocyte ; cell proliferation ; LEVEL ; NUCLEAR ; USA ; TISSUE INHIBITOR ; cancer research ; in vivo ; PLASMID ; DEFECT ; PROMOTES ; matrix metalloproteinase ; METALLOPROTEINASE ; ectodomain shedding ; MATRIX-METALLOPROTEINASE ; OVARIAN-CARCINOMA ; GROWTH-CONTROL ; EXTRACELLULAR CLEAVAGE ; HUMAN TISSUE KALLIKREINS ; PROTEINASE-ACTIVATED RECEPTORS ; SERINE PROTEINASE ; SERUM BIOMARKER
    Abstract: Recently, we described phorbol ester-induced expression of the brain and skin serine proteinase Bssp/kallikrein 6 (Klk6), the mouse orthologue of human KLK6, in mouse back skin and in advanced tumor stages of a well-established multistage tumor model. Here, we show KLK6 up-regulation in squamous skin tumors of human patients and in tumors of other epithelial tissues. Ectopic Klk6 expression in mouse keratinocyte cell lines induces a spindle-like morphology associated with accelerated proliferation, migration, and invasion capacity. We found reduced E-cadherin protein levels in the cell membrane and nuclear translocation of beta-catenin in Klk6-expressing mouse keratinocytes and human HEK293 cells transfected with a KLK6 expression plasmid. Additionally, HEK293 cells exhibited induced T-cell factor-dependent transcription and impaired cell-cell adhesion in the presence of KLK6, which was accompanied by induced E-cadherin ectodomain shedding. Interestingly, tissue inhibitor of metalloproteinase (TIMP)-l and TIMP-3 interfere with KLK6-induced F-cadherin ectodomain shedding and rescue the cell-cell adhesion defect in vitro, suggesting the involvement of matrix metalloproteinase and/or a disintegrin and metalloproteinase (ADAM) proteolytic activity. In line with this assumption, we found increased levels of the mature 62-kDa ADAM10 proteinase in cells expressing ectopic KLK6 compared with mock controls. Finally, enhanced epidermal keratinocyte proliferation and migration in concert with decreased E-cadherin protein levels are confirmed in an in vivo Klk6 transgenic mouse model
    Type of Publication: Journal article published
    PubMed ID: 17804733
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  • 19
  • 20
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    German Medical Science GMS Publishing House; Düsseldorf
    In:  63. Kongress der Nordrhein-Westfälischen Gesellschaft für Urologie; 20170608-20170609; Essen; DOCV 2.10 /20170419/
    Publication Date: 2017-04-19
    Keywords: ddc: 610
    Language: German
    Type: conferenceObject
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