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  • 1
    Keywords: tumor ; TUMORS ; MARKER
    Type of Publication: Patent
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  • 2
    Keywords: CANCER ; CELLS ; EXPRESSION ; GROWTH ; carcinoma ; GENE ; GENE-EXPRESSION ; GENES ; microarray ; PROTEIN ; SAMPLE ; SAMPLES ; murine ; AP-1 ; CARCINOGENESIS ; tumour ; SKIN ; MOUSE ; TRANSCRIPTION FACTORS ; IDENTIFICATION ; PROGRESSION ; gene expression ; PROMOTERS ; skin carcinogenesis ; METASTASIS ; SSH ; PCR ; TRANSFORMATION ; EPITHELIAL-CELLS ; squamous cell carcinoma ; FRAGMENTS ; MULTISTAGE CARCINOGENESIS ; real-time PCR ; expression profiling ; PHORBOL ESTER ; CDNA MICROARRAY ; NMRI MOUSE SKIN ; tumour promoter
    Abstract: Malignant transformation of mouse skin by chemical carcinogens and tumour promoters, such as the phorbol ester 12-O- tetradecanoylphorbol-13-acetate (TPA), is a multi-stage process that leads to squamous cell carcinoma (SCC) formation. In an effort to identify turnour-associated genes, we studied the influence of short-term TPA-treatment on the gene expression profile of murine skin. A comprehensive microarray with some 5,000 murine gene specific cDNA fragments was established and hybridised with pooled RNA derived from control and TPA-treated dorsal skin samples. Of these genes, 54 were up- and 35 were down-regulated upon TPA application. Additionally, we performed suppression subtractive hybridisation (SSH) with respective RNA pools to generate and analyse a cDNA library enriched for TPA- inducible genes. Expression data of selected genes were confirmed by quantitative real-time PCR and Northern blot analysis. Comparison of microarray and SSH data revealed that 26% of up-regulated genes identified by expression profiling matched with those present in the SSH library. Besides numerous known genes, we identified a large set of unknown cDNAs that represent previously unrecognised TPA-regulated genes in murine skin with potential function in tumour promotion. Additionally, some TPA-induced genes, such as SprrIA, Saa3, junB, II4ralpha, Gp38, RalGDS and Slpi exhibit high basal level in advanced stages of skin carcinogenesis, suggesting that at least a subgroup of the identified TPA-regulated genes may contribute to tumour progression and metastasis. (C) 2003 Wiley-Liss, Inc
    Type of Publication: Journal article published
    PubMed ID: 12640676
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  • 3
    Keywords: ACTIVATION, ADULT, AP-1, AP-1 SUBUNITS, BENIGN, BREAST-TUMORS, CANCER, CANCERS, CARCINOGENESIS, carc
    Abstract: Homeostasis of stratified epithelia, such as the epidermis of the skin, is a sophisticated process that represents a tightly controlled balance between proliferation and differentiation. Alterations of this balance are associated with common human diseases including cancer. Here, we report the cloning of a novel cDNA sequence, from mouse back skin, that is induced by the phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA) and codes for a hitherto unknown aspartic proteinase-like protein (Taps). Taps represents a potential AP-1 target gene because TPA-induced expression in epidermal keratinocytes critically depends on c-Fos, and co-treatment with dexamethasone, a potent inhibitor of AP-1-mediated gene regulation, resulted in impaired activation of Taps expression. Taps mRNA and protein are restricted to stratified epithelia in mouse embryos and adult tissues, implicating a crucial role for this aspartic proteinase-like gene in differentiation and homeostasis of multilayered epithelia. During chemically induced carcinogenesis, transient elevation of Taps mRNA and protein levels was detected in benign skin tumors. However, its expression is negatively associated with dedifferentiation and malignant progression in squamous cell carcinomas of the skin. Similar expression was observed in squamous skin tumors of patients, suggesting that detection of Taps levels represents a novel strategy to discriminate the progression state of squamous skin cancers
    Type of Publication: Journal article published
    PubMed ID: 16565508
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  • 4
    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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  • 5
    Keywords: RECEPTOR ; EXPRESSION ; GENE ; transcription ; DIFFERENTIATION ; AP-1 ; CALCIUM-BINDING PROTEINS ; MALIGNANT PROGRESSION ; MOUSE KERATINOCYTES ; MRP14
    Abstract: The two calgranulins S100A8 and S100A9 were found to be differentially expressed at sites of acute and chronic inflammation. Here we have employed the phorbol ester-induced multistage skin carcinogenesis protocol in mice to determine the expression of both genes in inflamed skin and in skin tumors. We show that expression is coordinately induced by the phorbol ester TPA in epithelial cells as well as infiltrating leukocytes. By comparing S100A8 and S100A9 mRNA levels in wild type and c-Fos deficient mice (c-fos(-/-)) we found that expression is negatively regulated by c-Fos/AP-1. Glucocorticoids, which exhibit potent anti-inflammatory and anti-tumor promoting activities repressed TPA-mediated S100A8 and S100A9 induction in wild type, but not in c-fos(-/-) mice, thus identifying both genes as the first examples of AP-1 target genes whose repression of TPA-induced transcription by glucocorticoids depends on c-Fos. Finally, we show that enhanced expression is not restricted to the initial TPA-induced inflammatory response but is observed at all stages of skin carcinogenesis. These data identify S100A8 and S100A9 as novel, tumor-associated genes and may point to an as yet unrecognized function of both genes in the development of epithelial skin tumors.
    Type of Publication: Journal article published
    PubMed ID: 12082614
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  • 6
    Electronic Resource
    Electronic Resource
    Weinheim : Wiley-Blackwell
    Chemie Ingenieur Technik - CIT 67 (1995), S. 1168-1169 
    ISSN: 0009-286X
    Keywords: Chemistry ; Polymer and Materials Science
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Chemistry and Pharmacology , Process Engineering, Biotechnology, Nutrition Technology
    Type of Medium: Electronic Resource
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