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  • DKFZ Publication Database  (13)
  • immunohistochemistry  (13)
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  • DKFZ Publication Database  (13)
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  • 11
    Keywords: CANCER ; CANCER CELLS ; CELLS ; EXPRESSION ; GROWTH ; IN-VITRO ; INVASION ; proliferation ; carcinoma ; CELL ; Germany ; GENE ; microarray ; SAMPLES ; cell line ; TISSUE ; LINES ; COMPLEX ; COMPLEXES ; DNA ; TISSUES ; CELL-LINES ; GLYCOPROTEIN ; immunohistochemistry ; ASSAY ; ELEMENTS ; METASTASIS ; PROSTATE-CANCER ; CELL-LINE ; LINE ; CANCER-CELLS ; LOCALIZATION ; ADHESION ; MIGRATION ; adenocarcinoma ; cell lines ; pancreatic cancer ; chronic pancreatitis ; HUMAN BREAST-CANCER ; RECOMBINANT ; PANCREATIC-CANCER ; DUCTAL ADENOCARCINOMA ; MATRIX PROTEINS ; LEVEL ; analysis ; pancreatic ; ASSAYS ; DNA-MICROARRAY ; function ; MIDDLE-EAR ; OSTEOPONTIN EXPRESSION ; VASCULAR CALCIFICATION
    Abstract: Bone sialoprotein (BSP) is an acidic glycoprotein that plays an important role in cancer cell growth, migration and invasion. The expression, localization and possible function of BSP in chronic pancreatitis (CP) and pancreatic ductal adenocarcinoma (PDAC) were analyzed by QRT-PCR, laser capture microdissection, DNA microarray analysis, immunoblotting, radioimmunoassays and immunohistochemistry as well as cell growth, invasion, scattering, and adhesion assays. BSP mRNA was detected in 40.7% of normal, in 80% of CP and in 86.4% of PDAC samples. The median BSP mRNA levels were 6.1 and 0.9 copies/mu l cDNA in PDAC and CP tissues, respectively, and zero copies/mu l cDNA in normal pancreatic tissues. BSP was weakly present in the cytoplasm of islet cells and ductal cells in 20% of normal pancreatic tissues. BSP was localized in the tubular complexes of both CP and PDAC, as well as in pancreatic cancer cells. Five out of 8 pancreatic cancer cell lines expressed BSP mRNA. Recombinant BSP (rBSP) inhibited Capan-1 and SU8686 pancreatic cancer cell growth, with a maximal effect of -46.4 +/- 12.0% in Capan-1 cells and -45.7 +/- 14.5% in SU8686 cells. rBSP decreased the invasion of SU8686 cells by -59.1 +/- 11.2% and of Capan-1 cells by -13.3 +/- 3.8% (P 〈 0.05), whereas it did not affect scattering or adhesion of both cell lines. In conclusion, endogenous BSP expression levels in pancreatic cancer cells and low to absent BSP expression in the surrounding stromal tissue elements may indirectly act to enhance the proliferation and invasion of pancreatic cancer cells. (c) 2006 Elsevier Ireland Ltd. All rights reserved
    Type of Publication: Journal article published
    PubMed ID: 16488077
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  • 12
    Keywords: APOPTOSIS ; CANCER ; CANCER CELLS ; CELLS ; EXPRESSION ; GROWTH ; radiotherapy ; carcinoma ; CELL ; Germany ; GENE ; GENES ; microarray ; PROTEIN ; transcription ; cell line ; MOLECULES ; TISSUE ; LINES ; COMPLEX ; COMPLEXES ; DNA ; TRANSCRIPTION FACTOR ; TISSUES ; CONTRAST ; CELL-LINES ; DOWN-REGULATION ; GROWTH-FACTOR RECEPTOR ; MOLECULE ; NUCLEI ; immunohistochemistry ; MICROARRAY DATA ; ASSAY ; UP-REGULATION ; METASTASIS ; colorectal cancer ; COLORECTAL-CANCER ; CELL-LINE ; chemotherapy ; LINE ; CANCER-CELLS ; LOCALIZATION ; adenocarcinoma ; KAPPA-B ; cell lines ; pancreatic cancer ; REGULATOR ; CELL-GROWTH ; ONCOLOGY ; PANCREATIC-CANCER ; DUCTAL ADENOCARCINOMA ; HUMAN-MELANOMA ; ARRAY ; GENE-TRANSCRIPTION ; LEVEL ; analysis ; pancreatic ; ASSAYS ; ATM ; USA ; colorectal ; GENOMIC STRUCTURE ; pancreatic ductal adenocarcinoma ; CYTOPLASM ; ARRAY HYBRIDIZATION ; BTF3 ; EPHB2 ; HEPARANASE EXPRESSION
    Abstract: Basic transcription factor 3 (BTF3) acts as a transcription factor and modulator of apoptosis, and is differentially expressed in colorectal cancer and glioblastomas. In the present study, the expression of BTF3, as well as its role in apoptosis and gene transcription, was analyzed in pancreatic ductal adenocarcinoma (PDAC). QRT-PCR, immunohistochemistry, immunoblotting, and immunofluorescence analyses were carried out to investigate BTF3 mRNA/protein expression and localization. BTF3 silencing in pancreatic cancer cells was performed using specific siRNA molecules. Functional analyses were carried out using cell growth assays, apoptosis assays, and DNA array analysis. BTF3 and BTF3a exhibited 1.3-fold and 4.6-fold increased median mRNA levels in PDAC tissues, compared to normal pancreatic tissues. BTF3 localized mainly in the cytoplasm and nuclei of tubular complexes and pancreatic cancer cells. Pancreatic cancer cell lines expressed the mRNA and protein of BTF3a (27 kDa) and BTF3b (22 kDa) isoforms. BTF3 silencing using specific siRNA molecules did not influence apoptosis induced by chemotherapy or radiotherapy. In contrast, BTF3 silencing resulted in down-regulation of several cancer-associated genes, including EPHB2, ABL2, HPSE2 and ATM, and up-regulation of KRAG, RRAS2, NFk-B, MRVI1, MADCAM1 and others. In conclusion, BTF3 is overexpressed in PDAC, where it acts as a transcriptional regulator rather than a direct modulator of apoptosis
    Type of Publication: Journal article published
    PubMed ID: 17312387
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  • 13
    Keywords: CANCER ; CELLS ; EXPRESSION ; SURVIVAL ; CELL ; Germany ; DISEASE ; liver ; PATIENT ; NF-KAPPA-B ; MACROPHAGES ; prognosis ; BODY-WEIGHT ; immunohistochemistry ; pancreatic cancer ; development ; INTERLEUKIN-6 ; KUPFFER CELLS ; ACUTE-PHASE RESPONSE ; cachexia ; macrophage ; MONOCYTES ; GROWTH-FACTORS ; grading ; NEUROPEPTIDES
    Abstract: Cachexia is a devastating process especially in pancreatic cancer patients and contributes to their poor survival. We attempted to clarify the pathological and molecular changes that occur in the liver during the development of cachexia. Using immunohistochemistry we investigated the infiltration of inflammatory mononuclear cells in liver biopsies of pancreatic cancer patients with or without cachexia, and the potential relevance of the cells for the nutritional and inflammatory status. Additionally, these findings were compared with the patients' clinical parameters. We found a significantly higher amount of CD68 immunoreactive macrophages in liver cross sections of patients with pancreatic cancer and cachexia. The number of CD68-positive macrophages was significantly inversely correlated with the nutritional status. Additionally, in these CD68-positive areas a significant increase in IL-6 and IL-1 immunoreactive cells was localized. Moreover, we found significantly increased areas of CD68-positive macrophages in liver biopsies of patients with a more dedifferentiated (aggressive) grading of the tumor. In conclusion, these results suggest that a crucial interaction between the tumor, PBMCs, and the liver may play a central role in the development and regulation of cachexia. Furthermore, pancreatic cancer may be able to alter systemic organ function even without obvious metastatic disease
    Type of Publication: Journal article published
    PubMed ID: 19148509
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