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  • 1
    Keywords: CANCER ; EXPRESSION ; SURVIVAL ; tumor ; carcinoma ; Germany ; FOLLOW-UP ; GENE-EXPRESSION ; PROTEIN ; DIFFERENTIATION ; TUMORS ; LINES ; TIME ; PATIENT ; primary ; ANTIGEN ; BIOLOGY ; ASSOCIATION ; MOLECULE ; BREAST ; breast cancer ; BREAST-CANCER ; antibodies ; antibody ; IDENTIFICATION ; PROGRESSION ; immunohistochemistry ; MALIGNANCIES ; DESIGN ; OVARIAN-CANCER ; CARCINOMA-CELLS ; BREAST-CARCINOMA ; PARAMETERS ; MULTIVARIATE ; CARCINOMAS ; FOLLOW-UP TIME ; P-SELECTIN ; CD24 ; CELL MONOCLONAL-ANTIBODIES ; protein expression
    Abstract: Purpose: CD24 is expressed in hematological malignancies as well as in a large variety of solid tumors including breast cancer. We aimed to evaluate CD24 protein expression in breast cancer and to correlate to clinicopatbological data including patient survival.Experimental Design: Primary breast carcinomas (201) with a mean clinical follow-up time of 53 months were immunostained using a monoclonal CD24 antibody (Ab-2, clone 24C02). The staining was evaluated as negative versus positive for statistical analysis.Results: In invasive breast carcinomas, CD24 expression was observed in 84.6% of cases. In univariate survival analyses, a significant association of CD24 expression with shortened patient overall survival (5-year survival rate 91.9% versus 83.8%; P = 0.031; log rank test) and disease-free survival (5-year progression rate 88.3% versus 57.0%; P = 0.0008) was demonstrated. In multivariate analyses CD24, tumor grading and nodal status were significant prognostic parameters for shortened disease-free survival.Conclusions: Our data suggest that CD24 expression in primary breast cancer as detected by immunohistochemistry might be a new marker for a more aggressive breast cancer biology
    Type of Publication: Journal article published
    PubMed ID: 14581365
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  • 2
    Keywords: CANCER ; CELLS ; EXPRESSION ; IN-VITRO ; INVASION ; carcinoma ; CELL ; Germany ; PATHWAY ; PATHWAYS ; VITRO ; GENE ; GENE-EXPRESSION ; GENES ; microarray ; RNA ; SAMPLE ; SAMPLES ; transcription ; COMPONENTS ; TISSUE ; LINES ; TRANSDUCTION ; ACTIVATION ; TISSUES ; BIOLOGY ; CELL-LINES ; fibroblasts ; MOLECULAR-BIOLOGY ; signal transduction ; SIGNAL ; BREAST-CANCER ; PROGRESSION ; immunohistochemistry ; gene expression ; DIFFERENCE ; NUMBER ; METASTASIS ; SIGNAL-TRANSDUCTION ; CELL-LINE ; LINE ; adenocarcinoma ; TARGETS ; MICROARRAY ANALYSIS ; OVEREXPRESSION ; DIFFERENTIAL EXPRESSION ; gene expression profiling ; expression profiling ; microdissection ; pancreatic cancer ; pancreatic carcinoma ; chronic pancreatitis ; WNT ; molecular biology ; molecular ; PANCREATIC-CANCER ; fibroblast ; DUCTAL ADENOCARCINOMA ; PANCREATITIS ; PROTOCOL ; quantitative RT-PCR ; interaction ; analysis ; DIFFERENTIALLY EXPRESSED GENES ; signalling ; WNT pathway ; tumor microenvironment ; ENGLAND ; SET ; MEDICINE ; quantitative ; PROFILE ; pancreatic ductal adenocarcinoma ; response ; interactions ; SFRP1 ; expression profile ; stroma ; in vitro ; ABERRANT METHYLATION ; WNT5a
    Abstract: Pancreatic ductal adenocarcinoma (PDAC) is characterized by an abundant desmoplastic stroma. Interactions between cancer and stromal cells play a critical role in tumour invasion, metastasis and chemoresistance. Therefore, we hypothesized that gene expression profile of the stromal components of pancreatic carcinoma is different from chronic pancreatitis and reflects the interaction with the tumour. We investigated the gene expression of eleven stromal tissues from PDAC, nine from chronic pancreatitis and cell lines of stromal origin using the Affymetrix U133 GeneChip set. The tissue samples were microdissected, the RNA was extracted, amplified and labelled using a repetitive in vitro transcription protocol. Differentially expressed genes were identified and validated using quantitative RT-PCR and immuno-histochemistry. We found 255 genes to be overexpressed and 61 genes to be underexpressed within the stroma of pancreatic carcinoma compared to the stroma of chronic pancreatitis. Analysis of the involved signal transduction pathways revealed a number of genes associated with the Wnt pathway of which the differential expression of SFRP1 and WNT5a was confirmed using immunohistochemistry. Moreover, we could demonstrate that WNT5a expression was induced in fibroblasts during cocultivation with a pancreatic carcinoma cell line. The identified differences in the expression profile of stroma cells derived from tumour compared to cells of inflammatory origin suggest a specific response of the tissue surrounding malignant cells. The overexpression of WNT5a, a gene involved in the non canonical Wnt signalling and chondrocyte development might contribute to the strong desmoplastic reaction seen in pancreatic cancer
    Type of Publication: Journal article published
    PubMed ID: 18298655
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  • 3
    Keywords: APOPTOSIS ; CANCER ; CELLS ; EXPRESSION ; IN-VITRO ; INVASION ; tumor ; carcinoma ; CELL ; Germany ; human ; DEATH ; GENE ; GENE-EXPRESSION ; GENES ; microarray ; cell line ; TISSUE ; LINES ; DNA ; CARCINOGENESIS ; CELL-LINES ; IDENTIFICATION ; immunohistochemistry ; gene expression ; EXPRESSION ANALYSIS ; CELL-LINE ; LINE ; MUTATIONS ; BENIGN ; adenocarcinoma ; REVEALS ; gene expression profiling ; cell lines ; expression profiling ; pancreatic cancer ; pancreatic carcinoma ; CDNA MICROARRAY ; E-cadherin ; pancreas ; PANCREATIC-CANCER ; DUCTAL ADENOCARCINOMA ; ARRAY ; development ; SWITZERLAND ; analysis ; CANCER DEVELOPMENT ; carcinoma cell ; DUCT CELLS ; methods ; pancreatic ; pancreatic adenocarcinoma ; primary isolates ; REGULATED GENE ; thymosin ; THYMOSIN BETA-10 GENE ; TUMOR-CELL
    Abstract: Background: Pancreatic cancer is one of the leading causes of cancer-related death. Using DNA gene expression analysis based on a custom made Affymetrix cancer array, we investigated the expression pattern of both primary and established pancreatic carcinoma cell lines. Methods: We analyzed the gene expression of 5 established pancreatic cancer cell lines (AsPC-1, BxPC-3, Capan-1, Capan-2 and HPAF II) and 5 primary isolates, 1 of them derived from benign pancreatic duct cells. Results: Out of 1,540 genes which were expressed in at least 3 experiments, we found 122 genes upregulated and 18 downregulated in tumor cell lines compared to benign cells with a fold change 〉3. Several of the upregulated genes (like Prefoldin 5, ADAM9 and E-cadherin) have been associated with pancreatic cancer before. The other differentially regulated genes, however, play a so far unknown role in the course of human pancreatic carcinoma. By means of immunohistochemistry we could show that thymosin beta-10 (TMSB10), upregulated in tumor cell lines, is expressed in human pancreatic carcinoma, but not in non-neoplastic pancreatic tissue, suggesting a role for TMSB10 in the carcinogenesis of pancreatic carcinoma. Conclusion: Using gene expression profiling of pancreatic cell lines we were able to identify genes differentially expressed in pancreatic adenocarcinoma, which might contribute to pancreatic cancer development. Copyright (C) 2005 S. Karger AG, Basel and IAP
    Type of Publication: Journal article published
    PubMed ID: 15983444
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