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  • 1
    Keywords: CANCER ; EXPRESSION ; INVASION ; carcinoma ; CELL ; Germany ; CLASSIFICATION ; DIAGNOSIS ; SYSTEM ; SYSTEMS ; TOOL ; SITE ; GENE ; GENE-EXPRESSION ; MOLECULES ; MARKER ; prognosis ; BIOMARKERS ; SKIN ; MOLECULE ; immunohistochemistry ; LYMPHOMA ; MALIGNANCIES ; gene expression ; skin cancer ; MELANOMA ; METASTATIC MELANOMA ; PATHOGENESIS ; SQUAMOUS-CELL CARCINOMA ; squamous cell carcinoma ; MALIGNANT-MELANOMA ; SKIN-CANCER ; SERUM ; CELL CARCINOMA ; MALIGNANCY ; RE ; biomarker ; INTERCELLULAR-ADHESION MOLECULE-1 ; SERUM-LEVELS ; UNIT ; TOOLS ; SQUAMOUS-CELL ; LACTATE-DEHYDROGENASE ; SOLUBLE INTERLEUKIN-2-RECEPTOR ; AMERICAN-JOINT-COMMITTEE ; CANCER STAGE-IV ; MELANOMA-INHIBITING ACTIVITY ; RELIABLE TUMOR-MARKER
    Abstract: Biomarkers are important tools in clinical diagnosis and prognostic classification of various cutaneous malignancies. Besides clinical and histopathological aspects (e.g. anatomic site and type of the primary tumour, tumour size and invasion depth, ulceration, vascular invasion), an increasing variety of molecular markers have been identified, providing the possibility of a more detailed diagnostic and prognostic subgrouping of tumour entities, up to even changing existing classification systems. Recently published gene expression or proteomic profiling data relate to new marker molecules involved in skin cancer pathogenesis, which may, after validation by suitable studies, represent future prognostic or predictive biomarkers in cutaneous malignancies. We, here, give an overview on currently known serologic and newer immunohistochemical biomarker molecules in the most common cutaneous malignancies, malignant melanoma, squamous cell carcinoma and cutaneous lymphoma, particularly emphasizing their prognostic and predictive significance
    Type of Publication: Journal article published
    PubMed ID: 17221215
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  • 2
    Abstract: In primary melanoma, ETV1 transcription factor was suggested to be activated mainly by gene amplification and to promote tumor growth in cooperation with BRAF (V600E) . Aim of this study was to investigate ETV1 expression in human melanoma with a focus on brain metastases. We investigated ETV1 in 68 human melanoma brain metastases using FISH for ETV1 gene (located at chromosome 7p21) and centromere chromosome 7 and immunohistochemistry for ETV1, BRAF (V600E) , and ETV1/BRAF associated proteins pMSK1, pRSK1, pp38, pMEK1/2, MAPKAP kinase 2, CIC, HIF-1alpha and Ki-67. We further studied ETV1 copy number variations in 32 melanoma cell lines from primary and metastatic lesions using array CGH. The influence of the MAP kinase pathway activity on ETV1 mRNA and protein expression under BRAF wild-type and BRAF (V600E) conditions were determined in melanoma cell lines using qRT-PCR and Western Blot. No ETV1 high grade amplifications were observed in tissue samples, but low grade ETV1 gene amplifications were found in 7 (10.3 %) melanoma brain metastases. ETV1 protein expression in tissue samples (15 %) correlated with BRAF (V600E) status (p = 0.007) and HIF-1alpha expression (p = 0.049), but not with ETV1 gene dose. Application of the BRAF(V600E)-specific inhibitor vemurafenib and the BRAF(V6ooE/V600K)-inhibitor dabrafenib revealed predominant regulation of ETV-1 mRNA and protein via MAPK-pathway. ETV1 expression is a rare event in human melanoma and seems to be rather based on hyperactivation of MAPK signals, by BRAF (V600E) mutation, than on ETV1 gene amplification. Consequently, therapeutic inhibition of BRAF and the downstream MAPK pathway also down-regulates oncogenic ETV1 expression.
    Type of Publication: Journal article published
    PubMed ID: 25073704
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  • 3
    Keywords: CELLS ; GROWTH-FACTOR ; IN-VITRO ; CELL ; Germany ; human ; VITRO ; SYSTEM ; NEW-YORK ; PROTEIN ; ACTIVATION ; MECHANISM ; KERATINOCYTES ; mechanisms ; PHOSPHORYLATION ; ASSAY ; MEMBRANE ; CELL-LINE ; DELIVERY ; PROTEIN-KINASE-C ; ARACHIDONIC-ACID ; TYROSINE-PHOSPHORYLATION ; C-GAMMA-1 ; EGF-RECEPTOR ; HaCaT cells,arachidonic acid,DAG,IP,calcium,sorbitol ; OSMOTIC-STRESS ; PHOSPHATIDIC-ACID
    Abstract: Human keratinocytes are exposed to strong physical changes, and have the potentiality to react to external stimuli by switching on adaptation mechanisms. In hyperosmotically shocked keratinocytes a rapid and strong increase in calcium has been observed. We showed that this increase could not be prevented by growing the cells in medium devoid of calcium and in the presence of EGTA, indicating that the intracellular calcium increase was due to delivery from internal stores. Further, we observed an increased synthesis of dyacylglycerol and inositol trisphosphates after shock, suggesting that phospholipase C mediates both events. Our experiments demonstrated that osmotic shock in human keratinocytes leads to activation of phospholipase C-gamma1, as measured using an in vitro assay system. This activation is independent of protein tyrosine phosphorylation and corresponded to a relocation of the enzyme to perinuclear membranes as shown by immunofluorescence
    Type of Publication: Journal article published
    PubMed ID: 15014953
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  • 4
    Keywords: CELLS ; EXPRESSION ; Germany ; human ; GENE ; GENES ; PROTEIN ; DIFFERENTIATION ; TISSUE ; COMPLEXES ; DOMAIN ; SKIN ; BINDING ; MEMBERS ; DNA-BINDING ; epidermis ; human hair follicle ; FOLLICLE ; INNER-ROOT-SHEATH ; MATRIX ; RE ; hair keratins ; HOMEODOMAIN PROTEINS ; gene regulation ; EPITHELIAL KERATINS ; HOX PROTEINS ; TALE proteins
    Abstract: We previously showed that the homeodomain protein HOXC13 is involved in the expression control of the early human hair keratin genes hHa5 and hHa2, which contain specific HOXC13 binding sites in their proximal promoters. Hox specificity is generally thought to be enhanced by the interaction with members of the TALE superclass of homeodomain proteins Pbx, Meis, and Prep. Using reverse transcription PCR with total human hair follicle RNA, we demonstrated transcripts of the major TALE proteins PBX1-4, MEIS1, 2 and PREP1, 2 in the human hair follicle. In view of the presence of MEIS/PREP responsive elements in close vicinity to the HOXC13 binding sites of the hHa5 and hHa2 promoters, we determined the expression sites of these TALE proteins in the human hair follicle. We found that MEIS1, MEIS2, PREP1 and PREP2 were differentially expressed in the three layers of the inner root sheath. In addition, MEIS2 and PREP1 exhibited expression in the mid-to upper hair cortex, with PREP1 being also expressed in the dermal papilla and the connective tissue sheath of the hair follicle. In virtually all cases, the expression of these TALE proteins was exclusively cytoplasmic. Considering that in contrast, HOXC13 is expressed in the nuclei of matrix, precortex and lower cuticle cells of the hair follicle, our data suggest that despite the presence of MEIS/PREP binding sites in the hHa5 and hHa2 promoters, the HOXC13-controlled activation of these genes in the hair follicle does not seem to involve these TALE proteins as cofactors
    Type of Publication: Journal article published
    PubMed ID: 16292560
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  • 5
    Abstract: The keratin filament cytoskeleton is vital to the normal function of epithelial cells. It provides structural support and regulates different aspects of cell metabolism. Mutations in keratins 5 and 14 cause a skin fragility disorder, epidermolysis bullosa simplex (EBS). Patients with severe EBS have an increased cumulative risk for basal cell carcinoma. In this study, we tested how keratin 5 and 14 mutant EBS patient-derived keratinocytes behave in the face of two different types of stressors that are able to induce cell death: ionizing radiation and cytokines TNF-alpha and TRAIL. The data point out to a substantial difference between how normal and keratin mutant keratinocytes deal with such stresses. When case of DNA damage, the ATM/Chk2-pathway is one of the two main tracks that can prevent the progression of mitosis and so allow repair. This was altered in all investigated keratin mutants with a particular down-regulation of the activated form of checkpoint kinase 2 (pChk2). Keratin mutants also appear less sensitive than normal cells to treatment with TNF-alpha or TRAIL, and this may be linked to the up-regulation of two pro-survival proteins, Bcl-2 and FLIP. Such changes are likely to have a profound effect on mutant keratinocytes ability to survive and withstand stress, and in theory this may be also a contributing factor to cell transformation.
    Type of Publication: Journal article published
    PubMed ID: 28647894
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  • 6
    Keywords: CELLS ; IN-VITRO ; CELL ; MODEL ; DISEASE ; PATIENT ; CUTTING EDGE ; MECHANISM ; mechanisms ; SKIN ; T cells ; IDENTIFICATION ; PERIPHERAL-BLOOD ; MULTIPLE-SCLEROSIS ; AUTOIMMUNITY ; review ; RHEUMATOID-ARTHRITIS ; AUTOIMMUNE-DISEASES ; FOXP3 ; FUNCTIONAL-CHARACTERIZATION ; IMPAIRMENT ; IMMUNOLOGICAL SELF-TOLERANCE ; regulatory T cells ; Lupus erythematosus ; CD4(+)CD25(+) cells ; DEFECTIVE SUPPRESSOR FUNCTION ; SLE PATIENTS
    Abstract: Natural CD4(+)CD25(+) regulatory T cells (T-reg) show a potent immunosuppressive function and contribute to immunologic self-tolerance by suppressing potentially auto-reactive T cells. Depletion of these cells leads to the induction of severe autoimmune diseases in animal models; more recently, several studies have also reported an impairment of T-reg number and/or function in various human autoimmune diseases. For example, aberrant numbers of circulating CD4(+)CD25(+) T-reg have been seen in patients with type I diabetes, mycosis fungoides, graft-versus-host-reaction, and rheumatoid arthritis. Moreover, increased numbers of functionally active CD4(+)CD25(+) T-reg have been detected in the synovial fluid of patients with rheumatoid arthritis. In systemic lupus erythematosus (SLE), conflicting data on the role of CD4(+)CD25(+) T-reg in human autoimmune diseases have been presented in the literature. Decreased numbers of peripheral blood T-reg have been reported by most studies on SLE patients with active disease, but non-impaired or even increased CD4(+)CD25(+) T-reg numbers have also been described. In addition, both deficient and normal suppressive capacity of isolated T-reg have been observed in SLE. Analysis of CD4(+)FoxP3(+) T-reg in skin lesions of patients with a primarily cutaneous manifestation of the disease showed a significant reduction in cell numbers as compared to other inflammatory skin diseases, suggesting the importance of analyzing T-reg numbers in the affected tissue. In this review, we discuss the role of CD4(+)CD25(+) T-reg in autoimmunity and recent published data on SLE. Furthermore, we highlight the need for additional studies that address specific gaps of knowledge regarding the pathophysiological mechanisms as well as the identification of future therapeutic strategies for autoimmune diseases
    Type of Publication: Journal article published
    PubMed ID: 18985367
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  • 7
    Electronic Resource
    Electronic Resource
    Springer
    Archives of dermatological research 107 (1911), S. 109-122 
    ISSN: 1432-069X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 8
    ISSN: 1432-069X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1432-069X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    Springer
    Archives of dermatological research 107 (1911), S. 305-328 
    ISSN: 1432-069X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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