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  • CANCER  (14)
  • EXPRESSION  (10)
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  • 1
    Keywords: EXPRESSION ; tumor ; carcinoma ; CELL ; Germany ; TYROSINE KINASE ; screening ; SITE ; SITES ; DISTINCT ; microarray ; PROTEIN ; TISSUE ; TUMORS ; primary ; GROWTH-FACTOR RECEPTOR ; FREQUENCY ; FREQUENCIES ; STAGE ; PROGRESSION ; immunohistochemistry ; ABERRATIONS ; HEAD ; ONCOPROTEIN ; CARCINOMAS ; NECK ; squamous cell carcinoma ; GREECE ; gene amplification ; head and neck ; laryngeal carcinoma ; OROPHARYNGEAL ; C-MYC ; CANCER PATIENTS ; CYCLIN D1 OVEREXPRESSION ; cytogenetic aberration ; head and neck squamous cell carcinoma (HNSCC) ; immunohistochemistry (IHC) ; MICROARRAY ANALYSIS ; oncoprotein overexpression ; OVEREXPRESSION ; POOR-PROGNOSIS ; tissue microarray (TMA) ; tumor classification
    Abstract: Background: Tissue microarray (TMA) analysis is a high-throughput approach that allows the screening of large tumor collectives for cytogenetic aberrations. In this study, a TMA of a large collection of clinically well-defined primary squamous cell carcinomas of the head and neck (HNSCC) was used to determine the expression of several oncoproteins. Materials and Methods: A TMA containing 547 primary HNSCC was used for the analysis of cyclinD1, c-myc, erbb1 and erbb2 expression by immunohistochemistry (IHC). Results: CyclinD1 and c-myc were overexpressed at higher frequencies in primary pharyngeal and laryngeal carcinomas compared with primary oral carcinomas (p 〈 0.001 and p 〈 0.001), while erbb1 and erbb2 overexpression was associated with oral site (p 〈 0.001 and p = 0.04, respectively). Furthermore, cyclinD1 overexpression correlated with stage IV primary carcinomas (p = 0.04). Conclusion: HNSCC is a heterogenous group of tumors, which, depending on anatomic sites and clinical stage, shows variable expressions of the oncoproteins described. This indicates a specific pathogenic role of these oncoproteins in different subtypes of HNSCC and may have therapeutic implications
    Type of Publication: Journal article published
    PubMed ID: 14666705
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  • 2
    Keywords: CANCER ; CELLS ; tumor ; carcinoma ; Germany ; THERAPY ; TUMORS ; PATIENT ; treatment ; 5-FLUOROURACIL ; ASSAY ; chemotherapy ; EPITHELIAL-CELLS ; HEAD ; NECK ; squamous cell carcinoma ; PREDICTION ; sensitivity ; head and neck carcinoma ; HNSCC ; INFUSION ; SOLID TUMORS ; COLONY FORMATION ; chemosensitivity testing ; head and neck squamous cell carcinoma ; SPECIMENS ; 5-FU ; drug combinations ; tumor stroma
    Abstract: Previous studies focusing on response prediction to chemotherapy by chemosensitivity testing of tumor explants has focused on the response determination of single cytostatic drugs, in contrast to the common clinical application of cytostatic drug combinations. Therefore, the present study was aimed at determining the quantitative ex vivo chemoreactivity of epithelial cells from head and neck squamous cell carcinoma (HNSCC) specimens to cytostatic drug combinations. Specimens from 12 histologically-confirmed HNSCC were investigated. According to a previously established ex vivo colony formation assay, the individual cellular chemoreactivity was determined quantitatively for combinations of 4 cytostatic drugs: cis-platinum (cis-DDP), carboplatin (CBDCA), 5-Fluorouracil (5-FU) and docetaxel (DTX). The tests were performed using drug combinations according to recent clinical therapy regimens in the treatment of solid tumors: i) cis-DDP + 5FU, ii) CBDCA + 5FU, iii) cis-DDP + DTX and iv) CBDCA + DTX The approach provides individual drug response patterns of epithelial as well as of stromal cells. Individual, selective sensitivities were found for each drug combination tested. The stromal and epithelial chemoreactivity profiles differed in most of the specimens. Moreover, stromal cell chemoresistance dominated selective epithelial chemosensitivities in the majority of cases. The determination of the epithelial ex vivo chemoreactivity identified individual chemosensitivities which were verified by the clinical history of the patient. Therefore, the described protocol to determine the ex vivo chemoresponse of HNSCC specimens to cytostatic drug combinations may help to provide clinicaly useful information concerning the individual chemoresponse of HNSCC with regard to individualization of oncological decision making
    Type of Publication: Journal article published
    PubMed ID: 16619587
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  • 3
    Keywords: ANGIOGENESIS ; CANCER ; CELLS ; EXPRESSION ; GROWTH ; INHIBITOR ; INVASION ; tumor ; BLOOD ; CELL ; Germany ; IN-VIVO ; INHIBITION ; MODEL ; THERAPY ; VIVO ; imaging ; TISSUE ; SKIN ; fibroblasts ; PROGRESSION ; REQUIRES ; skin cancer ; EXTRACELLULAR-MATRIX ; INHIBITORS ; CYTOKINE ; ONCOLOGY ; fibroblast ; MATRIX METALLOPROTEINASES ; STROMAL CELLS ; matrix metalloproteinase ; MATRIX-METALLOPROTEINASE INHIBITORS ; EPITHELIAL TUMOR PHENOTYPE ; MMP inhibition
    Abstract: Tumor invasion requires intense interactions with stromal cells and a profound extracellular matrix remodelling by matrix metalloproteinases (MMPs). Here, we assessed the specific contribution of fibroblasts to tumor invasion, MMPs, tissue inhibitors of MMPs and angiogenesis-related cytokine expression in organotypic cultures of highly malignant HaCaT-ras A-5RT3 cells, with and without MMP inhibition. Collagen degradation, the hallmark of tumor invasion, was dependent on fibroblasts and active MMP-2. Additionally, MMP blockade down-regulated VEGF-A and up-regulated PDGF-BB. These results were paralleled in xenotransplants in vivo, demonstrating strong inhibitory effects of MMP blockade on tumor invasion and vascularization, as shown by the almost complete absence of VEGF-A and MMP-14 and by the decrease in relative blood volume. MMP blockade also increased the fraction of mature vessels, as demonstrated by an increased mean tumor vessel diameter and a higher ratio of Ng2-positive vessels. Thus, this study highlights the importance of targeting the tumor stroma to defeat cancer
    Type of Publication: Journal article published
    PubMed ID: 20392987
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  • 4
    Keywords: APOPTOSIS ; CANCER ; GROWTH ; KINASE ; MODELS ; PATHWAY ; DISEASE ; GENE ; LINES ; CYCLE ; ASSAY ; HEAD ; CELL CARCINOMA ; pharmacogenomics ; macrophage ; CYTOTOXIC ACTIVITY ; natural product ; head and neck squamous cell carcinoma HNSCC ; oral cavity squamous cell carcinoma OCSCC ; APIACEAE ; Levisticum officinale lovage ; POLYACETYLENES
    Abstract: Background: Oral squamous cell carcinoma (OSCC) is a challenging disease with a high mortality rate. Natural products represent a valuable source for the development of novel anticancer drugs. We investigated the cytotoxic potential of essential oil from the leaves of a medicinal plant, Levisticum officinale (lovage) on head and neck squamous carcinoma cells (HNSCC). Materials and Methods: Cytotoxicity of lovage essential oil was investigated on the HNSCC cell line, UMSCC1. Additionally, we performed pharmacogenomics analyses. Results: Lovage essential oil extract had an IC50 value of 292.6 mu g/ml. Genes involved in apoptosis, cancer, cellular growth and cell cycle regulation were the most prominently affected in microarray analyses. The three pathways to be most significantly regulated were extracellular signal-regulated kinase 5 (ERK5) signaling, integrin-linked kinase (ILK) signaling, virus entry via endocytic pathways and p53 signaling. Conclusion: Levisticum officinale essential oil inhibits human HNSCC cell growth
    Type of Publication: Journal article published
    PubMed ID: 21273597
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  • 5
    Keywords: CANCER ; GROWTH ; IN-VITRO ; KINASE ; PATHWAY ; TOXICITY ; DEATH ; GENE ; COMPONENTS ; LINES ; CYCLE ; ASSAY ; HEAD ; CELL CARCINOMA ; pharmacogenomics ; natural product ; ESSENTIAL PLANT OILS ; head and neck squamous cell carcinoma HNSCC ; oral cavity squamous cell carcinoma OCSCC ; Thymus vulgaris L.(thyme)
    Abstract: Background: Oral cavity squamous cell carcinoma (OCSCC) accounts for 2% to 3% of all malignancies and has a high mortality rate. The majority of anticancer drugs are of natural origin. However, it is unknown whether the medicinal plant Thymus vulgaris L. (thyme) is cytotoxic towards head and neck squamous cell carcinoma (HNSCC). Materials and Methods: Cytotoxicity of thyme essential oil was investigated on the HNSCC cell line, UMSCC1. The IC50 of thyme essential oil extract was 369 mu g/ml. Moreover, we performed pharmacogenomics analyses. Results: Genes involved in the cell cycle, cell death and cancer were involved in the cytotoxic activity of thyme essential oil at the transcriptional level. The three most significantly regulated pathways by thyme essential oil were interferon signaling, N-glycan biosynthesis and extracellular signal-regulated kinase 5 (ERK5) signaling. Conclusion: Thyme essential oil inhibits human HNSCC cell growth. Based on pharmacogenomic approaches, novel insights into the molecular mode of anticancer activity of thyme are presented
    Type of Publication: Journal article published
    PubMed ID: 21273584
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  • 6
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    Anticancer Research 23 (2C), 1769-1772 
    Keywords: CANCER ; CANCER CELLS ; CELLS ; EXPRESSION ; tumor ; SITES ; microarray ; DRUG ; TUMORS ; PATIENT ; DNA ; mechanisms ; GLYCOPROTEIN ; DNA microarray ; DNA microarray technology ; c-Fos ; CROSS-RESISTANCE ; drug resistance ; MULTIDRUG-RESISTANCE ; protooncogenes ; CELL LUNG CARCINOMAS ; DEFICIENT ACTIVATION ; DETOXIFYING ENZYMES ; O-6-ALKYLGUANINE-DNA ALKYLTRANSFERASE ; resistance-related proteins ; S-TRANSFERASE-PI
    Abstract: Drug resistance is an important problem in the treatment of patients with cancer. Tumors become resistant not only to the drugs used initially, but also to those to which they have not yet been exposed. Multiple mechanisms contribute to drug resistance. Many of them are inter-related or independent Of each other, but may exist simultaneously in cancer cells or subpopulations of cells, producing an overall drug-resistant phenotype. Consequently, clinical reversal of drug resistance may ultimately require intervention at several different sites in the tumor cell. In the future, the use of DNA microarray technology in drug resistance in cancer will yield insight into the mechanisms of drug resistance and the rational design of more effective strategies to circumvent resistance
    Type of Publication: Journal article published
    PubMed ID: 12820456
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  • 7
    Keywords: CANCER ; CANCER CELLS ; CELLS ; IN-VITRO ; SURVIVAL ; Germany ; human ; LUNG ; THERAPY ; PROTEIN ; PROTEINS ; PATIENT ; tumour ; BINDING ; CANCER-CELLS ; MAMMALIAN-CELLS ; PROGNOSTIC FACTORS ; adenocarcinoma ; glycosylation ; PROGNOSTIC FACTOR ; BINDS ; HUMAN BREAST ; non-small cell lung cancer ; CANCER CELL-LINES ; MALIGNANT-CELLS ; RECOMBINANT ; RESIDUES ; BINDING-ACTIVITY ; overall survival ; PROGNOSTIC-FACTOR ; GALACTOSIDE-SPECIFIC LECTIN ; adenocarcinoma of the lung ; aviscumine ; EXTRACT ; recombinant mistletoe lectin
    Abstract: Background: Lectins, carbohydrate proteins, bind to glycoconjugates of all mammalian cells, including cancer cells. Aberrant glycosylation, detected by lectin histochemistry, can predict outcome in some tumour entities. One such lectin is aviscumine (recombinant mistletoe lectin). Aviscumine has cytotoxic effects and can therefore be used as anti-tumour therapy. Materials and Methods: Lectin histochemistry with aviscumine was performed on primary tumour sections from resected adenocarcinoma of the lung. Staining results were then correlated with the clinical course of the patients. Results: Most of the adenocarcinomas (92.5%) bound aviscumine. Kaplan-Meier analysis revealed no correlation between aviscumine binding and progression-free survival or overall survival. Conclusion: These results suggest that for the selected group of patients with adenocarcinoma of the lung aviscumine binding activity can not serve as a prognostic factor. More strikingly, however, aviscumine binds to malignant cells in 92.5% of the patients. This is an indicator for the use of aviscumine as a possible target for tumour therapy
    Type of Publication: Journal article published
    PubMed ID: 16101142
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  • 8
    Keywords: CELLS ; EXPRESSION ; INHIBITOR ; proliferation ; tumor ; TUMOR-CELLS ; Germany ; IN-VIVO ; KINASE ; MODEL ; THERAPY ; TYROSINE KINASE ; SYSTEM ; CDNA ; GENE ; PROTEIN ; DIFFERENTIATION ; MICE ; T-CELL ; T-CELLS ; TYROSINE KINASE INHIBITOR ; MOUSE ; TRANSGENIC MICE ; LYMPHOMA ; PROMOTER ; LINE ; ONCOGENE ; PHENOTYPE ; FUSION PROTEIN ; thymus ; INFILTRATION ; LYMPHOMAS ; EVENTS ; anaplastic ; ALCL ; ANAPLASTIC LYMPHOMA ; LARGE-CELL LYMPHOMA ; NPM-ALK
    Abstract: Background: The t(2;5)(p23;q35) translocation is associated with a high percentage of anaplastic large-cell lymphomas (ALCL) of T- or null-cell phenotype. The translocation produces an 80 kDa hyperphosphorylated chimeric protein (p80) derived from the fusion of the anaplastic lymphoma kinase (ALK) with nucleophosmin (NPM). The NPM-ALK chimeric protein is an activated tyrosine kinase that has been shown to be a potent oncogene and presumably plays a causative role in lymphomagenesis. Materials and Methods: A transgenic mouse line was generated, where the human NPM-ALK cDNA is driven by the lck promoter conferring transgene expression to early T-cells. Results: Mice rapidly developed large cell lymphoblastic lymphomas with a median latency of 8 weeks, primarily involving the thymus, with lymph node as well as histologically evident extranodal organ infiltration by large tumor cells. Conclusion: The transgenic approach described provides direct evidence for the strong transforming potential of NPM-ALK in T-cells and furthermore represents a system for the analysis of the oncogenic events mediated by NPM-ALK in vivo, which might be instrumental in the development of tyrosine kinase inhibitor therapies of potential clinical use
    Type of Publication: Journal article published
    PubMed ID: 16101126
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  • 9
    Keywords: CANCER ; CELLS ; EXPRESSION ; carcinoma ; Germany ; human ; PATIENT ; DNA ; INFECTION ; papillomavirus ; ASSOCIATION ; PROGRESSION ; CERVICAL-CANCER ; human papillomavirus ; HUMAN-PAPILLOMAVIRUS ; SQUAMOUS-CELL CARCINOMA ; HEAD ; INVOLVEMENT ; MICROMETASTASES ; NECK ; squamous cell carcinoma ; PREVALENCE ; CYCLE CONTROL ; head and neck squamous cell carcinoma ; LYMPH-NODE ; SPECIMENS ; histologically confirmed tumour-free neck lymph nodes ; neck metastasis
    Abstract: Background: Human papillomavirus (HPV) has been demonstrated in lymph node neck metastases (NM) of HPV-positive squamous cell carcinomas of the head and neck (HNSCC), underscoring the possible role of HPV for HNSCC progression. Reports on HPV infections in histopathologically tumour-free lymph-nodes of the SCC of the uterine cervix developing higher rates of lymph-node metastases and recurrences later in the survey of the patients was the starting point of the present study. Materials and Methods: The presence of HPV-DNA in primary tumours (PT, n = 45), NM (n =45) and histologically confirmed tumour-free neck lymph-nodes (LN, n = 102) of HNSCC from 60 patients was analysed by PCR and Southern blot hybridisation. Results: A highly positive correlation of simultaneous HPV-DNA detection in PT and NM was demonstrated. In the case of HPV-positivity of PT and/or NM [24/60 cases (40%)], 11/24 (45.8%) LN contained HPV-DNA, as well. Accepting HPV demonstration as a marker for the presence of micro-metastasis, HPV analysis would result in an upstaging of the N category in 4 out of these 11 patients. Conclusion: Considering the high agreement of HPV-DNA detection in PT and simultaneous HPV-DNA demonstration in the draining NM corroborating the monoclonal character of the tumour cells, the HPV-DNA presence in LN seems to be indicative of micro-metastasis in these lymph nodes. Thus, HPV analysis might be another powerful tool for the definition of the N-status of HPV-positive HNSCC
    Type of Publication: Journal article published
    PubMed ID: 16739336
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  • 10
    Keywords: APOPTOSIS ; CANCER ; CELLS ; EXPRESSION ; carcinoma ; CELL ; Germany ; incidence ; PROTEIN ; MICE ; FAMILY ; CARCINOGENESIS ; INDUCTION ; SKIN ; SUSCEPTIBILITY ; MOUSE ; TRANSGENIC MICE ; PROGRESSION ; CELL-DEATH ; MOUSE SKIN ; skin carcinogenesis ; skin cancer ; TRANSFORMATION ; STEM-CELLS ; CARCINOMAS ; CARCINOGENS ; squamous cell carcinoma ; C-MYC ; OVEREXPRESSION ; epidermis ; INITIATION ; LAYER ; SKIN-CANCER ; Bcl-2 ; CELL CARCINOMA ; ONCOLOGY ; RE ; INCREASE ; HAIR FOLLICLE ; PROTOCOL ; MALIGNANT PROGRESSION ; hair ; stem cells ; methods ; NORMAL SKIN ; INDUCED TUMORIGENESIS ; NOR ; SQUAMOUS-CELL ; STEM ; BASAL-CELL ; PAPILLOMAS ; sensitize
    Abstract: Background: BCL-2 overexpression is firequently detected in nonmelanoma skin cancer. In normal skin, BCL-2 expression is restricted to the basal cell layer and the hair follicle bulge. Both contain stem cells targeted by carcinogens upon initiation of mouse skin carcinogenesis. It is unknown whether the anti-apoptotic activity, of BCL-2 is involved in the susceptibility of this cell type to malignant transformation. If so, extending the pool of BCL-2-expressing cells to suprabasal skin layers should increase the likelihood of skin tumour formation. Materials and Methods: To resolve this issue, we generated a novel transgenic mouse line overexpressing BCL-2 in suprabasal layers of the epidermis. The influence of suprabasal BCL-2 on tumour formation was then tested by chemically inducing skin cancer using the two-stage initiation-promotion protocol. Results: Bcl-2 expression neither influenced the incidence nor the multiplicity of papillomas upon chemical tumour induction with 7,12-dimethylbenz[a]anthracene (DMBA) and 12-O-tetradecanoylphorbol-13-acetate (TPA), nor their progression to carcinomas. Conclusion: Suprobasal expression of BCL-2 in skin does not increase the formation of papillomas or their malignant progression to squamous cell carcinomas in two-stage mouse skin carcinogenesis
    Type of Publication: Journal article published
    PubMed ID: 19035317
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