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  • EXPRESSION  (10)
  • DISEASE  (5)
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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: 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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  • 3
    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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  • 4
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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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  • 5
    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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  • 6
    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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  • 7
    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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  • 8
    Keywords: CELLS ; AGENTS ; CELL ; CELL-PROLIFERATION ; Germany ; human ; IN-VIVO ; MODEL ; MODELS ; VIVO ; imaging ; VISUALIZATION ; DISEASE ; DRUG ; MICE ; prognosis ; MR ; MRI ; MAGNETIC-RESONANCE ; magnetic resonance imaging ; BREAST-CANCER ; MOUSE ; NO ; STAGE ; SCID MOUSE ; POSITRON-EMISSION-TOMOGRAPHY ; tomography ; MOUSE MODEL ; CHILDREN ; TRACER ; ANTICANCER DRUGS ; neuroblastoma ; AGENT ; ONCOLOGY ; RE ; monitoring ; WEIGHT ; MOUSE MODELS ; methods ; DRUGS ; NEUROENDOCRINE TUMORS ; SCANS ; animal ; FDG ; anticancer drug ; xenograft ; small animal imaging ; FLT ; SCAN ; FDG UPTAKE ; MRT ; F-18-FLT PET ; GRANULATION TISSUES ; PET-CT ; THORACIC TUMORS ; [F-18]FLT
    Abstract: Background: Finding new therapeutic agents is of great clinical interest in neuroblastoma research because prognosis of children with disseminated stages of disease is still poor. As xenograft mouse models are frequently used for studying anticancer drugs in vivo, small animal imaging is an important method of monitoring in anticancer research. Materials and Methods: SCID mice inoculated with human neuroblastoma SK-N-SH cells were examined with positron-emission tomography-computed tomography (PET-CT) using [F-18]fluorodeoxyglucose (FDG) or [F-18]fluoro-L-thymidine (FLT) and with magnetic resonance imaging (MRI). Results: All neuroblastomas were detected by MRI. In PET-CT imaging, no tumour was visualized with [F-18]FDG, but 13 out of 14 (93%) were found with [F-18]FLT. Uptake of [F-18]FLT was significantly associated with tumour weight. Necrotic areas could not be identified either by MR imaging or on PET-CT scans. Conclusion: Both MR and PET-CT imaging with [F-18]FLT are highly qualified for the detection of neuroblastomas grown in SCID mice. However, [F-18]FDG, which is the standard tracer in clinical PET-CT imaging, is not suited for PET-CT imaging in the neuroblastoma model
    Type of Publication: Journal article published
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  • 9
    Keywords: CELLS ; EXPRESSION ; BREAST-CANCER ; SIGNAL TRANSDUCER ; ESOPHAGEAL CANCER ; Stat3 ; BEVACIZUMAB ; ADVANCED GASTRIC-CANCER ; TRANSCRIPTION 3 ; HER-2 STATUS
    Abstract: BACKGROUND: Brain metastases (BM) of gastro-oesophageal cancer are exceedingly rare and only limited data exist on their pathobiology. MATERIALS AND METHODS: We identified tissue samples of BM of gastro-oesophageal cancer and analyzed the expression of human epidermal growth factor receptor-2 (HER2), phosphorylated signal transducer and activator of transcription-3 (pSTAT3), epithelial growth factor receptor (EGFR), V600E point mutation of the v-raf murine sarcoma viral oncogene homolog-B1 (BRAF V600E), cluster of differentiation molecule-34 (CD34), hypoxia inducible factor-1alpha (HIF 1-alpha) and Ki-67 by immunohistochemical methods. RESULTS: Our series comprised of twenty adenocarcinomas and one oesophageal squamous cell carcinoma. Three (14%), 7 (33%), 9 (43%), 18 (86%) and 0 BM specimens were scored positively for HER2, EGFR, pSTAT3, HIF1-alpha and BRAF V600E expression. The median Ki-67 index was 59%. The microvascular density was moderate-to-high and active intratumoral microvascular sprouting was evident in 20/21 (95%) of BMs. The HER2 and EGFR expression status were consistent between primary tumors and BM in all three assessable cases. HIF1-alpha and pSTAT3 expression were significantly higher in HER2-positive cases. CONCLUSION: Therapeutic use of agents targeting HER2, pSTAT3, EGFR and angiogenesis may be feasible for selected BM of gastro-esophageal cancer. HER2 positivity does not seem to predispose to brain colonization in gastro-esophageal cancer.
    Type of Publication: Journal article published
    PubMed ID: 23482783
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  • 10
    Keywords: APOPTOSIS ; CANCER ; proliferation ; SURVIVAL ; tumor ; carcinoma ; CELL ; CELL-PROLIFERATION ; Germany ; LUNG ; MODEL ; lung cancer ; VOLUME ; DEATH ; DISEASE ; HEPATOCELLULAR-CARCINOMA ; TUMORS ; ANTIGEN ; NO ; IN-SITU ; PROGRESSION ; immunohistochemistry ; CARCINOMAS ; BODY ; LUNG-CARCINOMA ; SECTIONS ; VOLUMES ; BODIES ; END ; TUMOR VOLUME ; lung tumors ; cell proliferation ; BALANCE ; SUBTYPE
    Abstract: To evaluate the relationship between cell proliferation and apoptosis during progression of lung carcinomas, immunohistochemistry for proliferating cell nuclear antigen (PCNA) and the in situ end labelling (TUNEL) method for identifying apoptotic bodies were performed on paraffin sections front 135 lung carcinomas. These results were correlated with the corresponding tumor volumes as a model of disease progression in lung tumors. We found that, with increasing tumor volume, the proliferation rate decreased significantly, whereas the apoptotic rate increased. There was no relationship between apoptotic and proliferative indices except in carcinomas with a tumor volume between 51 and 100 cm(3). These data suggest that progression of lung carcinomas, i.e. the increase in tumor volume, is accompanied by an increase in apoptosis rather than an increase in cell proliferation
    Type of Publication: Journal article published
    PubMed ID: 15736479
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