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  • MELANOMA  (15)
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  • 1
    Keywords: APOPTOSIS ; CANCER ; CELLS ; EXPRESSION ; INHIBITION ; DISTINCT ; GENE ; PROTEIN ; LINES ; DNA ; CELL-CYCLE ; IDENTIFICATION ; REPAIR ; MELANOMA ; MALIGNANT-MELANOMA ; CISPLATIN ; drug resistance ; ABCC2 ; MRP2 ; ANTICANCER DRUGS ; ACQUIRED DRUG-RESISTANCE ; cMOAT ; ETOPOSIDE ; FOTEMUSTINE ; MeWo
    Abstract: Resistance to various anti-neoplastic agents is a common observation in clinical management of melanoma. The biologic mechanisms conferring these different drug-resistant phenotypes, including resistance against the commonly used anti-cancer drug cisplatin, are unclear. In order to elucidate the role of the membrane adenosine triphosphate binding cassette-transporter cMOAT (canalicular multispecific anion transporter) (MRP2/ABCC2) in cisplatin resistance of melanoma, the expression of this protein was analyzed in the platinum drug-resistant cell line MeWo CIS 1. Cisplatinresistant melanoma cells showed a distinct overexpression of cMOAT on mRNA and protein level. This observation was accompanied by a reduced formation of platinum-induced intrastrand cross-links in the nuclear DNA measured by an immunocytologic assay. This decrease in DNA platination was accompanied by an accelerated re-entry into the cell cycle after the typical cisplatin- induced G(2) arrest, and a resistance to undergo apoptosis. Kinetics of formation and elimination of platinum-DNA adducts suggest that the DNA repair capacity for Pt-d(GpG) adducts was not elevated in platinum drug-resistant melanoma cells. The decrease in platinum-DNA adduct formation in cisplatin- resistant melanoma cells was rather a reflection of the protecting activity of the transporter cMOAT. In conclusion, the functional inhibition of cMOAT might be a promising strategy in the reversal of resistance to platinum-based anti- cancer drugs in human melanoma
    Type of Publication: Journal article published
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  • 2
    Keywords: APOPTOSIS ; CELLS ; EXPRESSION ; Germany ; PROTEIN ; DRUG ; SKIN ; resistance ; inactivation ; MELANOMA ; CISPLATIN ; CUTANEOUS MELANOMA ; drug resistance ; DRUG-RESISTANCE ; ETOPOSIDE ; DEFICIENCY ; DEPENDENT APOPTOSIS ; 12Q22-23
    Type of Publication: Journal article published
    PubMed ID: 16098052
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  • 3
    Keywords: CANCER CELLS ; CELLS ; EXPRESSION ; tumor ; TUMOR-CELLS ; CELL ; CLINICAL-TRIAL ; COMBINATION ; evaluation ; Germany ; human ; IN-VIVO ; MODEL ; THERAPY ; NEW-YORK ; EFFICIENCY ; TRANSDUCTION ; primary ; prognosis ; DOMAIN ; culture ; GLYCOPROTEIN ; virus ; TRIAL ; TRIALS ; VECTORS ; VECTOR ; MEMBRANE ; CLINICAL-TRIALS ; chemotherapy ; EFFICIENT ; MELANOMA ; MALIGNANT-MELANOMA ; malignant melanoma ; CUTANEOUS MELANOMA ; ADENOVIRUS ; DACARBAZINE ; DOMAINS ; THERAPIES ; MELANOMA-CELLS ; VIROTHERAPY ; USA ; EFFICIENT TRANSDUCTION ; SHORT-TERM ; xenograft ; clinical trial ; ONCOLYTIC ADENOVIRUSES ; B ADENOVIRUSES ; CELLULAR RECEPTOR ; FUSOGENIC MEMBRANE-GLYCOPROTEINS ; REPLICATING ADENOVIRUS ; SUICIDE GENE-THERAPY ; ADENOVIRUS VECTORS ; IMMUNE-MEDIATED CONTROL ; oncolytic adenovirus
    Abstract: Advanced melanoma is associated with poor prognosis warranting the development of new therapeutics, such as oncolytic adenoviruses for immunovirotherapy. Since this approach critically depends on efficient transduction of targeted tumor cells, we screened a panel of 22 different adenovirus types for their internalization efficiency in melanoma cells. We demonstrated that the virions of Ad35, Ad38, and Ad3 have significantly higher internalization efficiency in melanoma cells than Ad5, so far the only adenovirus type used in clinical trials for melanoma. Therefore, we developed a conditionally replication-competent Ad5-based vector with the Ad35 fiber shaft and knob domains (Ad5/35) and compared its therapeutic efficacy with the homologous vector carrying the native Ad5 fiber. To further enhance virotherapy, we combined the oncolytic adenovirus vectors with intratumoral expression of measles virus fusogenic membrane glycoproteins H and F (MV-H/F) and dacarbazine chemotherapy. In a human melanoma xenograft model, established from a short-term culture of primary melanoma cells, we demonstrated that the Ad5/35-based therapy had a significantly greater anti-neoplastic effect than the homologous Ad5-based therapy. Furthermore, the combination of virotherapy, intratumoral expression of MV-H/F, and chemotherapy was clearly superior to single- or double-agent therapy. In conclusion, Ad35-based vectors are promising for the treatment of melanoma
    Type of Publication: Journal article published
    PubMed ID: 17960177
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  • 4
    Keywords: CELLS ; EXPRESSION ; GROWTH ; IN-VITRO ; proliferation ; SURVIVAL ; CELL ; CELL-PROLIFERATION ; Germany ; IN-VIVO ; VIVO ; microarray ; RNA ; ADHESION MOLECULES ; MOLECULES ; TISSUE ; SUPPRESSION ; BREAST-CANCER ; TARGET ; CELL-SURVIVAL ; PROGRESSION ; METASTASIS ; MELANOMA ; ADHESION ; MIGRATION ; EPITHELIAL-CELLS ; L1 ; MALIGNANT-MELANOMA ; TARGETS ; CELL-ADHESION MOLECULE ; OVEREXPRESSION ; DIFFERENTIAL EXPRESSION ; AMYLOID PRECURSOR PROTEIN ; chemoresistance ; CELL-GROWTH ; E-cadherin ; development ; tissue microarray ; ALPHA-SECRETASE
    Abstract: ADAM10 (a disintegrin and metalloproteinase 10) is involved in the ectodomain shedding of various substrates, including adhesion molecules such as L1 cell adhesion molecule (L1-CAM) and CD44, which are known to have important roles in the development of malignant melanoma. In our Study, we characterized the expression of ADAM10 in melanoma cells in vitro and in vivo Immunohistochemical analysis oil tissue microarrays indicated that ADAM-10 expression was significantly elevated in melanoma metastasis compared with primary melanomas. In vitro downregulation of ADAM10 with specific small interfering RNA (siRNA) resulted in a suppression of the anchorage-independent cell growth and reduced the migration of melanoma cells. In addition, overexpression of ADAM-10 induced the migration of melanoma cells. In cell lines from melanoma patients with metastasis, ADAM10 was significantly overexpressed, and ADAM10 expression correlated with increased cell proliferation. Furthermore, we present evidence that ADAM-10 is involved in the release of L1-CAM from melanoma cells. It is important that knockdown of cellular L1-CAM reduced the migration of melanoma cells and abrogated the chemoresistance against cisplatin. In contrast, soluble L1-CAM had no effect on melanoma cell migration or cell survival. Taken together, Our data demonstrate that ADAM10 and L1-CAM have important roles during melanoma progression and both molecules represent attractive targets for therapeutical intervention of melanomas
    Type of Publication: Journal article published
    PubMed ID: 19865098
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  • 5
    Keywords: ANGIOGENESIS ; CANCER ; EXPRESSION ; INVASION ; proliferation ; SURVIVAL ; tumor ; CELL-PROLIFERATION ; MICROVESSEL DENSITY ; DENSITY ; GENE ; GENES ; TUMORS ; PATIENT ; ACTIVATION ; FAMILY ; prognosis ; PROGRESSION ; MUTATION ; metastases ; MELANOMA ; MUTATIONS ; ONCOGENE ; CHILDREN ; CUTANEOUS MELANOMA ; INITIATION ; BRAF ; N-RAS ; Ras ; neuroblastoma ; RE ; PATIENT SURVIVAL ; cell proliferation ; CODON ; CUTANEOUS MELANOMAS ; Ki-67 ; NEVI ; RAS MUTATIONS ; VERTICAL GROWTH-PHASE
    Abstract: Previous studies have shown frequent mutations in the BRAF (V-raf murine sarcoma viral oncogene homolog B1) or NRAS ( neuroblastoma RAS viral [V-ras] oncogene homolog) genes in cutaneous melanoma, but the relationship between these alterations and tumor cell proliferation has not been examined in human melanoma. In our study of 51 primary nodular melanomas and 18 paired metastases, we found mutations in BRAF ( codon 600, previously denoted 599) in 15 primary tumors (29%) and eight metastases (44%). The figures for NRAS mutations were 27% and 22%, respectively. Mutations in BRAF and NRAS genes were mutually exclusive in all but one case, and were maintained from primary tumors through their metastases. Mutations, however, were not associated with tumor cell proliferation by Ki-67 expression, tumor thickness, microvessel density, or vascular invasion, and there were no differences in patient survival. Although BRAF and NRAS mutations are likely to be important for the initiation and maintenance of some melanomas, other factors might be more significant for proliferation and prognosis in subgroups of aggressive melanoma
    Type of Publication: Journal article published
    PubMed ID: 16098042
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  • 6
    Keywords: RECEPTOR ; CELLS ; EXPRESSION ; GROWTH ; GROWTH-FACTOR ; IN-VITRO ; INVASION ; tumor ; TUMOR-CELLS ; Germany ; VITRO ; SYSTEM ; SYSTEMS ; ENZYMES ; TISSUE ; MECHANISM ; FAMILY ; INDUCTION ; mechanisms ; fibroblasts ; ALPHA ; antibodies ; antibody ; PROGRESSION ; METASTASIS ; NUDE-MICE ; MELANOMA ; DEGRADATION ; ANTAGONIST ; HUMAN DERMAL FIBROBLASTS ; MATRIX ; TUMOR INVASION ; collagen ; MATRIX METALLOPROTEINASES ; MELANOMA-CELLS ; TUMORIGENICITY ; regulation ; interaction ; basic fibroblast growth factor ; bFGF ; dermal fibroblasts ; IL-1 alpha ; MALIGNANT MELANOMAS ; TIMP-1 ; TISSUE INHIBITOR
    Abstract: Tumor invasion and metastasis of melanoma have been shown to require proteolytic degradation of the extracellular environment, achieved primarily by enzymes of the matrix metalloproteinases (MMP) family. Increased enzyme activity is localized at the border of tumor cells and the adjacent peritumoral connective tissue, emphasizing the crucial role of tumor-stroma interactions in the regulation of MMP activity. To analyze whether direct cell-cell contacts of melanoma cells and stromal fibroblasts or whether soluble factors, secreted by melanoma cells are involved in the regulation of MMP, we used different in vitro co-culture systems. Both direct and indirect co-cultures of high invasive BLM melanoma cells and human dermal fibroblasts resulted in an induction of pro-MMP-1 synthesis. Medium conditioned by BLM cells strongly induced pro-MMP-1 synthesis in fibroblasts, indicating the importance of diffusible factors for this induction. Competition by recombinant human interleukin (IL)-1 receptor antagonist, neutralizing IL-1alpha and basic fibroblast growth factor (bFGF) antibodies, resulted in a concentration-dependent reduction of pro-MMP-1 synthesis. Taken together, our results indicate an essential role for soluble factors, mainly IL-1alpha and bFGF, in the stimulation of dermal fibroblasts by human melanoma cells to secrete MMP-1
    Type of Publication: Journal article published
    PubMed ID: 15737206
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  • 7
    Keywords: RECEPTOR ; CANCER ; EXPRESSION ; tumor ; carcinoma ; GENE ; PROTEIN ; transcription ; LINES ; PATIENT ; DNA ; SERA ; colon ; DENDRITIC CELLS ; BREAST ; IDENTIFICATION ; AMPLIFICATION ; MELANOMA ; POLYMERASE-CHAIN-REACTION ; IMMUNE-RESPONSE ; IMMUNOTHERAPY ; vaccination ; CTCL ; sero-reactivity ; head and neck ; cancer-testis antigens ; MYCOSIS-FUNGOIDES ; PSEUDOGENES ; tumor immunology
    Abstract: cTAGE-1 is a cutaneous-T-cell-lymphoma-specific tumor antigen recently identified by serologic identification of antigens by recombinant expression cloning. This study was aimed at identifying and characterizing related genes. Rapid amplification of cDNA ends and DNA screening led to five new members of the cTAGE gene family belonging to four different genes, two of which were differentially spliced (cTAGE-1/2 and cTAGE-5). Expression analysis using reverse transcription polymerase chain reaction revealed that cTAGE-1, cTAGE-1B, and cTAGE-5A expression was restricted to testis and tumor tissues, whereas the other cTAGE members were found in two to eight other normal tissues (of 27 tissues tested). Tumor-specific protein expression of cTAGE-5 was confirmed by Western blotting. Sero-reactivity against cTAGE-1, cTAGE-4, cTAGE-5A, and cTAGE-5B was found only in tumor patients (cutaneous T cell lymphoma and melanoma). The immunogenic epitope of cTAGE-1 was determined by using epitope mapping and sera of two cutaneous T cell lymphoma patients. Moreover, cTAGE-1, cTAGE-4, cTAGE-5A, and cTAGE-5B could be detected in most types of tumor tissues and cell lines at variable frequencies, including those of cutaneous T cell lymphoma, melanoma, head and neck squamous cell carcinoma, breast carcinoma, and colon carcinoma. We conclude that cTAGE-1 and cTAGE-5 are new cancer germline antigens and that tumor-specific splicing of cTAGE genes may lead to further candidate proteins for specific immunotherapy of cutaneous T cell lymphoma and other malignancies
    Type of Publication: Journal article published
    PubMed ID: 12839582
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  • 8
    Keywords: IRRADIATION ; Germany ; COMMON ; GENE ; GENES ; TISSUE ; RISK-FACTORS ; TISSUES ; SKIN ; IN-SITU ; NUMBER ; MUTATION ; CDKN2A ; MELANOMA ; SPORADIC PRIMARY MELANOMAS ; MUTATIONS ; MALIGNANT-MELANOMA ; CUTANEOUS MELANOMA ; RED HAIR ; MELANOCORTIN-1 RECEPTOR ; N-RAS MUTATIONS ; N-ras,melanoma,SSCP
    Abstract: We determined mutations in the BRAF, N-ras, and CDKN2A genes in 27 histologically diverse melanocytic nevi and corresponding surrounding tissues from 17 individuals. Mutations in the BRAF and N-ras gene were found in 22 nevi (81%) from 16 individuals (94%). The predominant BRAF mutation T1799A (V600E) was detected in 18 nevi; 1 nevus had a novel A1781G (D594V) mutation in the same gene and 3 nevi had mutations in codon 61 of the N-ras gene. In 4 individuals both nevi carried a BRAF mutation, whereas in 2 other individuals 1 nevus showed a BRAF mutation and the second nevus had an N-ras mutation. In 2 individuals normal skin distant from nevi showed a BRAF mutation. No mutations were detected in the CDKN2A gene. The mutations in the BRAF and N-ras genes, in this study, were not associated with histologic type, location, skin type, size, or numbers of nevi. Our results suggest that mutations in the BRAF gene and to some extent in the N-ras gene represent early somatic events that occur in melanocytic nevi. We hypothesize the dual effect of solar ultraviolet irradiation on melanoma, through mutagenesis and by increasing the number of melanocytic nevi, many of which carry a BRAF or N-ras mutation
    Type of Publication: Journal article published
    PubMed ID: 15009715
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  • 9
    Keywords: RECEPTOR ; CANCER ; CELLS ; EXPRESSION ; carcinoma ; CELL ; Germany ; LUNG ; lung cancer ; LUNG-CANCER ; SITE ; SITES ; cell line ; DIFFERENTIATION ; LINES ; LIGAND ; CELL-LINES ; BREAST ; METASTASIS ; metastases ; CELL-LINE ; LINE ; MELANOMA ; SURFACE ; adenocarcinoma ; GASTROINTESTINAL-TRACT ; chemokine ; THYMOCYTES ; CHEMOKINE RECEPTOR ; thymus ; homing ; MELANOMA-CELLS ; LYMPH-NODE METASTASIS ; SDF-1 ; small bowel ; small intestine ; SMALL-BOWEL ; TECK
    Abstract: In general, metastases to the small intestine are rare, and mostly occur in melanoma. CCR9 has been shown to be the principal chemokine receptor for the thymus expressed chemokine (TECK), a chemokine selectively expressed in the small intestine and thymus. Here we show that CCR9 is highly expressed on melanoma cells and all melanoma cell lines isolated from small intestinal metastases, and on a proportion of cell lines from other sites. Only melanoma cells and cell lines from small intestinal metastases, however, were responsive to the CCR9 ligand TECK, as assessed by receptor downregulation and by actin polymerization. CCR9 expression was also found on the adenocarcinoma cell line CaCo-2 expressing characteristics of enterocytic differentiation, but not on any other cell line isolated from colorectal, breast, and lung cancer. Our data provide evidence that the aberrant functional cell surface expression of an organ-specific chemokine receptor is associated with metastasis to this site. The regulation of receptor function seems to be a critical step in the metastatic process
    Type of Publication: Journal article published
    PubMed ID: 15086554
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  • 10
    Keywords: USA ; NEW-YORK ; INVASION ; METASTASIS ; MELANOMA
    Type of Publication: Meeting abstract published
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