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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
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  • 3
    Keywords: EXPRESSION ; INHIBITOR ; tumor ; carcinoma ; Germany ; KINASE ; TYROSINE KINASE ; GENE ; HYBRIDIZATION ; microarray ; PROTEIN ; TISSUE ; TUMORS ; TYROSINE KINASE INHIBITOR ; IN-SITU ; immunohistochemistry ; NUMBER ; PATHOGENESIS ; FISH ; MUTATIONS ; SQUAMOUS-CELL CARCINOMA ; HEAD ; NECK ; PREVALENCE ; FLUORESCENCE ; OVEREXPRESSION ; imatinib ; fluorescence in situ hybridization ; GAINS ; C-KIT ; ADENOID CYSTIC CARCINOMA ; GASTROINTESTINAL STROMAL TUMORS ; INHIBITORS ; in situ hybridization ; salivary gland tumor ; AMPLIFICATIONS ; GLAND ; intensity ; SUBTYPE ; TUMOR TISSUE ; KINASE INHIBITORS ; SUBTYPES ; KIT ; tissue microarray ; tissue microarray analysis
    Abstract: Adenoid cystic carcinoma (ACC) of the salivary gland is characterized by a prolonged but inevitably unfavorable clinical course. Recent studies suggested the transmembrane tyrosine kinase KIT to be involved in ACC pathogenesis. To investigate KIT expression in histologically defined subgroups of ACC and to clarify whether KIT gene copy number gain contributes to KIT overexpression, tumor tissue microarray sections including 55 ACC tumors were analyzed by fluorescence in situ hybridization (FISH) and immunohistochemistry (IHC). The prevalence of positive KIT immunostaining was 89% (49/55). Strong immunostaining of KIT was only found in cribriform and tubular but never in solid subtypes (p = 0.02). Average KIT staining intensity was higher in cribriform and tubular (n = 37) compared to solid (n = 18) ACC subtypes (p = 0.005). FISH analysis revealed copy number gains of the KIT gene in 6.1% (3/49) of tumors analyzed. Our results implicate that specific KIT tyrosine kinase inhibitors such as imatinib, might be used in future therapeutic approaches against subgroups of ACC. (c) 2005 Elsevier Ltd. All rights reserved
    Type of Publication: Journal article published
    PubMed ID: 16054424
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  • 4
    Keywords: EXPRESSION ; tumor ; carcinoma ; Germany ; GENE ; GENES ; HYBRIDIZATION ; microarray ; PROTEIN ; TISSUE ; TUMORS ; DNA ; PROGRESSION ; AMPLIFICATION ; COMPARATIVE GENOMIC HYBRIDIZATION ; microarrays ; HEAD ; NECK ; squamous cell carcinoma ; PROGNOSTIC VALUE ; CYCLIN D1 OVEREXPRESSION ; OVEREXPRESSION ; POOR-PROGNOSIS ; CHROMOSOMAL IMBALANCES ; CHRONIC LYMPHOCYTIC-LEUKEMIA ; CANDIDATE GENES ; tissue microarray analysis ; SPECIMENS ; ARRAY CGH
    Abstract: Chromosomal band 11q13 is frequently amplified in oral squamous cell carcinoma (OSCC) and assumed to be critically involved in tumor initiation and progression by proto-oncogene activation. Though cyclin D1 (CCND1) is supposed to be the most relevant oncogene, several additional putative candidate genes are inside this chromosomal region, for which their actual role in tumorigenesis still needs to be elucidated. To characterize the 11q13 amplicon in detail, 40 OSCCs were analyzed by comparative genomic hybridization to DNA microarrays (matrix-CGH) containing BAC clones derived from chromosomal band 11q13. This high-resolution approach revealed a consistent amplicon about 1.7 Mb in size including the CCND1 oncogene. Seven BAC clones covering FGF3, EMS1, and SHANK2 were shown to be frequently coamplified inside the CCND1 amplicon. Subsequent analysis of tissue microarrays; by FISH revealed amplification frequencies of 36.8% (88/239) for CCND1, 34.3% (60/ 175) for FGF3, 37.4% (68/182) for EMS1, and 36.3% (61/168) for SHANK2. Finally, quantitative mRNA expression analysis demonstrated consistent overexpression of CCND1 in all tumors and of EMS1 and SHANK2 in a subset of specimens with 11q13 amplification, but no expression of FGF3 in any of the cases. Our study underlines the critical role of CCND1 in OSCC development and additionally points to the functionally related genes EMS1 and SHANK2, both encoding for cytoskeleton-associated proteins, which are frequently coamplified with CCND1 and therefore could cooperatively contribute to OSCC pathogenesis. (c) 2005 Wiley-Liss, Inc
    Type of Publication: Journal article published
    PubMed ID: 16235239
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  • 5
    Keywords: EXPRESSION ; GROWTH ; proliferation ; carcinoma ; Germany ; INHIBITION ; PATHWAY ; DISTINCT ; GENE ; GENES ; microarray ; PROTEIN ; DIFFERENTIATION ; TISSUE ; TUMORS ; SKIN ; IN-SITU ; AMPLIFICATION ; COPY NUMBER ; immunohistochemistry ; NUMBER ; MUTATIONS ; ONCOGENE ; HUMAN HOMOLOG ; HEAD ; PREVALENCE ; PRECURSORS ; EFFECTOR ; basal cell carcinoma ; N-MYC ; CELL CARCINOMA ; SUBSET ; fluorescence in situ hybridisation ; LOCUS ; tissue microarray ; NMYC ; HUMAN NEUROBLASTOMA ; SPECIMENS
    Abstract: Formation of basal cell carcinoma (BCC) has been linked to deregulation in the sonic hedgehogh (Shh) signalling pathway. Though mutations of the genes, PTCHI and SMO, are known to be involved in aberrant Shh signalling, the distinct downstream effectors of these genes are poorly described. Studies have indicated that the NMYC oncogene is a potential Shh downstream effector. To assess the expression of Nmyc protein and gene copy numbers of the NMYC gene locus in a representative BCC tumour collection, immunohistochemistry (IHC) and fluorescence in situ hybridisation (FISH) were performed on 273 BCC specimens of different growth patterns and anatomic localisations on tissue microarray (TMA) sections. High Nmyc protein expression was detected in 72.7% (160/220) of all BCC specimens. Strong Nmyc immunopositivity was more frequently found in infiltrative BCCs compared to nodular/superficial BCCs (p=0.005), and in BCCs of the head compared to BCCs of other anatomic localisations (p=0.021). The prevalence of NMYC copy number gains was 17.5% (37/211), including three tumours with nodular differentiation that exhibited a distinct high-level amplification of the NMYC locus. These data indicate that high expression of the Shh downstream mediator, Nmyc, is a frequent event in BCC, predominantly in more aggressive subtypes. Although the NMYC copy number gain found in a subset of cases might contribute to this aberrant Nmyc protein expression by a gene dosage effect, our data suggests that Nmyc protein can also be induced by aberrant Shh signalling, acting as an effector molecule of the Shh pathway. Novel systemic anti-sense NMYC inhibition strategies could be a promising option for therapy-refractory BCC
    Type of Publication: Journal article published
    PubMed ID: 16596176
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  • 6
    Keywords: EXPRESSION ; carcinoma ; CELL ; Germany ; human ; THERAPY ; GENE ; HYBRIDIZATION ; microarray ; PROTEIN ; TISSUE ; SURGERY ; ACTIVATION ; CONTRAST ; TARGET ; IN-SITU ; PROGRESSION ; AMPLIFICATION ; COMPARATIVE GENOMIC HYBRIDIZATION ; COPY NUMBER ; immunohistochemistry ; CATALYTIC SUBUNIT ; NUMBER ; metastases ; CANCER-CELLS ; HEAD ; CARCINOMAS ; NECK ; squamous cell carcinoma ; pathology ; FLUORESCENCE ; fluorescence in situ hybridization ; protein expression ; in situ hybridization ; CELL CARCINOMA ; development ; methods ; tissue microarray ; tissue microarray analysis ; CANDIDATE ; SQUAMOUS-CELL ; reverse transcriptase ; human telomerase ; IMMORTALITY ; oral squamous cell carcinoma ; TERT
    Abstract: BACKGROUND: Gene copy number gain of chromosomal arm 5p is frequently found in oral squamous cell carcinoma (OSCC) suggesting the activation of proto-oncogenes. TERT is a candidate gene encoding for human telomerase reverse transcriptase (hTERT). The aim of the present study was to elucidate the relevance of TERT copy number gain and high hTERT expression in OSCC. METHODS: Fluorescence in situ hybridization (FISH) for TERT and immunohistochemistry (IHC) for hTERT were performed to analyze TERT copy numbers and hTERT expression, respectively, on tissue microarray (TMA) sections including n = 247 OSCC and n = 105 pharyngeal and laryngeal squamous cell carcinomas (PSCC/LSCC). RESULTS: Increased hTERT protein expression was more frequently found in OSCC (71.1 %, 155/218) than in PSCC/LSCC (36.0%, 35/89) (13 〈 0.001). By contrast, specific TERT amplifications were less common in OSCC (2.1%, 4/191) compared with PSCC/LSCC (9.9%, 8/81) (P = 0.047). CONCLUSIONS: High hTERT expression is a frequent finding in OSCC. It might be a promising target for the development of specific anti-neoplastic therapy approaches
    Type of Publication: Journal article published
    PubMed ID: 17448136
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  • 7
    Keywords: APOPTOSIS ; EXPRESSION ; GROWTH ; proliferation ; tumor ; carcinoma ; CELL ; FACTOR RECEPTOR ; Germany ; human ; KINASE ; PATHWAY ; PATHWAYS ; DISTINCT ; GENE ; GENE-EXPRESSION ; GENES ; microarray ; PROTEIN ; PROTEINS ; SAMPLE ; SAMPLES ; TISSUE ; ACTIVATION ; primary ; PROTEIN-KINASE ; ASSOCIATION ; MAP KINASE ; score ; STAGE ; NEOPLASIA ; immunohistochemistry ; gene expression ; metastases ; ABERRATIONS ; SIGNALING PATHWAY ; RELIABILITY ; HEAD ; squamous cell carcinoma ; GROWTH-FACTOR-BETA ; MICROARRAY ANALYSIS ; gene expression profiling ; CHRONIC LYMPHOCYTIC-LEUKEMIA ; protein expression ; EPIDERMAL-GROWTH-FACTOR ; NECK-CANCER ; signaling ; molecular ; CELL CARCINOMA ; ONCOLOGY ; INCREASE ; analysis ; CHIP ; USA ; lymph node metastases ; SQUAMOUS-CELL ; HUMAN HEPATOCELLULAR-CARCINOMA ; SET ; COLLECTION ; DETECT ; MAP-KINASE ; GENE-ONTOLOGY
    Abstract: In an attempt to further elucidate the pathomechanisms in oral squamous cell carcinoma (OSCC), gene expression profiling was performed using a whole-transcriptome chip that contains 35,035 gene-specific 70mere oligonucleotides (Human OligoSet 4.0; Operon, Cologne, Germany) to a set of 35 primary OSCCs. Altogether, 7390 genes were found differentially expressed between OSCC tumor samples and oral mucosa. To characterize the major biologic processes in this tumor collection, MAPPFinder, a component of GenMAPP version 2.1, was applied to this data set to generate a statistically ranked list of molecular signaling pathways. Among others, cancer-related pathways, such as mitogen-activated protein (MAP) kinase signaling (z score = 4.6, P 〈 .001), transforming growth factor-beta signaling (z score = 3.0, P = .015), and signaling pathways involved in apoptosis (z score = 2.1, P = .037), were found deregulated in the OSCC collection analyzed. Focusing on the MAP kinase signaling pathway, subsequent tissue microarray analyses by immunohistochemistry revealed an increase in protein expression of MAP kinase-related proteins ERK1 in 22.8% (48 of 209) and ERK5 in 27.4% (76 of 277), respectively. An association of high ERK5 but not of high ERK1 expression with advanced tumor stage and the presence of lymph node metastases was found (P = .008 and P = .016, respectively). Our analysis demonstrates the reliability of the combined approach of gene expression profiling, signaling pathway analyses, and tissue microarray analysis to detect novel distinct molecular aberrations in OSCC
    Type of Publication: Journal article published
    PubMed ID: 18472963
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  • 8
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    Abstract: BACKGROUND: Cetuximab and docetaxel have single-agent activity in squamous cell carcinoma of the head and neck (SCCHN). The efficacy of their combination was evaluated in platinum-pretreated patients with recurrent and/or metastatic SCCHN. PATIENTS AND METHODS: A total of 84 patients were treated with docetaxel 35 mg/m(2) weekly for a maximum of 6 cycles and concomitant cetuximab 250 mg/m(2) weekly until disease progression or unacceptable toxicity. The primary endpoint was the objective response rate and secondary endpoints included the response rate in relation to platinum sensitivity, progression-free survival (PFS), overall survival (OS) and toxicity. RESULTS: Nine (11%) patients achieved a partial response and 34 (40%) stable disease, resulting in a disease control rate of 51%. Response to treatment was 49% in previously platinum-sensitive and 50% in previously platinum-resistant disease. The median PFS was 3.1 months and the median OS 6.7 months. The most common grade 3 or 4 adverse events were mucositis (8%), pneumonia (8%), fatigue (8%) and skin reactions (14%). Sepsis occurred in 3 patients. CONCLUSION: Cetuximab plus docetaxel is an active treatment regimen with moderate toxicity in SCCHN patients. However, no superiority in comparison with monotherapy could be shown. Responsiveness and survival were independent of previous platinum sensitivity.
    Type of Publication: Journal article published
    PubMed ID: 23445718
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  • 10
    Keywords: CANCER ; EXPRESSION ; radiotherapy ; SURVIVAL ; tumor ; carcinoma ; THERAPY ; GENE ; PROTEIN ; TISSUE ; radiation ; PATIENT ; MARKER ; AGE ; FLUORESCENCE ; analysis ; SQUAMOUS-CELL ; PREDICT
    Abstract: Oral squamous cell carcinoma (OSCC) is a solid neoplasm exhibiting aggressive tumor phenotypes with unpredictable biological behavior. Recent studies suggested that high expression of the antiapoptotic protein survivin might be associated with adverse outcome in oral cancer patients. To investigate, whether increased copy numbers of the survivin-encoding gene BIRC5 results in elevated survivin levels and whether BIRC5 and survivin could serve as progression markers in the clinical course of OSCC, tumor tissue microarray analysis was performed applying fluorescence in situ hybridization and immunohistochemistry to 296 OSCC specimens. Gene copy number gain of BIRC5 was detected in 33.9% (150/227) of cases, which correlated significantly with high UICC stage and the presence of lymph node metastases (p = 0.003 and p = 0.001, respectively), but not with unfavorable patients' outcome (p 〉 0.05) in multivariate analysis. High survivin expression was found in 67.3% (169/251) of cases to predict increased 5- and 10-year overall survival of patients in a multivariate model including UICC stage and age as covariables (p = 0.035 and p = 0.026, respectively). Within a subgroup of patients, who received radiation therapy (n = 121), high survivin expression was found to be the only predictor of favorable 3-, 5- and 10-year overall survival in a multivariate cox regression analysis including UICC stage and age as covariables (p = 0.001, p = 0.004 and p = 0.006, respectively). In conclusion, high survivin expression might be useful to identify OSCC patients, who would benefit from radiotherapy. (c) 2006 Wiley-Liss, Inc
    Type of Publication: Journal article published
    PubMed ID: 17187360
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