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  • pancreatic cancer  (15)
  • 11
    Keywords: CANCER ; EXPRESSION ; SURVIVAL ; tumor ; BLOOD ; CELL ; neoplasms ; FOLLOW-UP ; DISEASE ; SITE ; SAMPLES ; transcription ; DIFFERENTIATION ; TISSUE ; SURGERY ; TIME ; PATIENT ; BONE-MARROW ; STAGE ; statistics ; COLORECTAL-CANCER ; RESECTION ; CANCER-PATIENTS ; DISSEMINATED TUMOR-CELLS ; POLYMERASE-CHAIN-REACTION ; RT-PCR ; adenocarcinoma ; ADENOCARCINOMAS ; CANCER PATIENTS ; pancreatic cancer ; CELL-DIFFERENTIATION ; PANCREATIC-CANCER ; DUCTAL ADENOCARCINOMA ; GRADE ; polymerase chain reaction ; SWITZERLAND ; methods ; pancreatic ; cell differentiation ; PROGNOSTIC INDICATORS
    Abstract: Background. After complete removal of the neoplasm (RO resection), approximately 80% of pancreatic cancer patients will die of the disease within 5 years. The expression panel of cytokeralins (CK) is linked closely with cell differentiation. The aim of the study was to investigate the expression of CK-20 in pancreatic cancer tissue and to correlate CK-20 expression with survival in R0-resected pancreatic cancer patients. Methods. Tissue samples of 63 patients with pancreatic cancer were subjected to CK-20 reverse transcription polymerase chain reaction. Thirty-four of 63 patients underwent RO resection and were followed-up for survival statistics. From these 34 patients, 26 (76%) neoplasms were CK-20 positive and 8 (24%) samples were CK-20 negative. The mean follow-up period for the entire group was 17 months (range, 4-36 mo), the follow-up period in censored patients was 23 months (range, 10-36 mo). Results. In the R0-resected group, 3 of 8 (38%) patients with CK-20-negative neoplasms, and 16 of 26 (62%) patients with CK-20-positive neoplasms (P = .15) died of recurrent disease. The median survival time of patients with CK-20-positive neoplasms was 13 months (range, 4-36), the median survival in R0-resected patients with CK-20-negative neoplasm was 26 months (range, 13-35; P =. 06). The survival difference observed in patients with CK-20-negative neoplasms could not be attributed to intergroup variations in tumor stage or tumor grade. Conclusions. A majority of primary ductal pancreatic adenocarcinomas express CK-20. This seems to be associated with poorer survival in R0-resecled patients. Our data suggest that ductal pancreatic adenocarcinomas negative for CK-20 constitute a subgroup of patients showing a more favorable disease outcome. The expression of CK-20 in resected pancreatic cancer may be of interest as a prognostic parameter
    Type of Publication: Journal article published
    PubMed ID: 16364723
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  • 12
    Keywords: CANCER ; CANCER CELLS ; CELLS ; EXPRESSION ; GROWTH ; INVASION ; CELL ; Germany ; human ; IN-VIVO ; GENE-EXPRESSION ; transcription ; TISSUE ; RELEASE ; COMPLEX ; COMPLEXES ; TRANSCRIPTION FACTOR ; TISSUES ; tumour ; DOWN-REGULATION ; treatment ; cytokines ; TRANSCRIPTION FACTORS ; LESIONS ; immunohistochemistry ; VECTOR ; PCR ; SIGNALING PATHWAY ; CANCER-CELLS ; EXTRACELLULAR-MATRIX ; MAMMALIAN-CELLS ; adenocarcinoma ; GROWTH-FACTOR-BETA ; OVEREXPRESSION ; real-time PCR ; pancreatic cancer ; microenvironment ; CYTOKINE ; MATRIX ; ONCOLOGY ; PANCREATIC-CANCER ; DUCTAL ADENOCARCINOMA ; INCREASE ; extracellular matrix ; regulation ; ENHANCED EXPRESSION ; REAL-TIME ; TGF-BETA ; TGF-beta 1 ; LEVEL ; analysis ; pancreatic ; pancreatic adenocarcinoma ; coculture ; quantitative ; FULL-LENGTH ; transforming growth factor ; pancreatic ductal adenocarcinoma ; beta-tumour microenvironment ; CHEMICAL-MODIFICATIONS ; INDIAN-HEDGEHOG ; matrix metalloprotease ; osteonectin ; stellate cells ; STELLATE-CELLS
    Abstract: Recent evidence suggests that Runt-related transcription factors play a role in different human tumours. In the present study, the localisation of the Runt-related transcription factor-2 (Runx2), its transcriptional activity, as well as its regulation of expression was analysed in human pancreatic ductal adenocarcinoma (PDAC). Quantitative real-time PCR and immunohistochemistry were used for Runx2 expression and localisation analysis. Runt-related transcription factor-2 expression was silenced using specific siRNA oligonucleotides in pancreatic cancer cells (Panc-1) and immortalised pancreatic stellate cells (IPSCs). Overexpression of Runx2 was achieved using a full-length expression vector. TGF-beta 1, BMP2, and other cytokines were assessed for their potential to regulate Runx2 expression. There was a 6.1-fold increase in median Runx2 mRNA levels in PDAC tissues compared to normal pancreatic tissues (P〈0.0001). Runt-related transcription factor-2 was localised in pancreatic cancer cells, tubular complexes, and PanIN lesions of PDAC tissues as well as in tumour-associated fibroblasts/stellate cells. Coculture of IPSCs and Panc-1 cells, as well as treatment with TGF-beta 1 and BMP2, led to increased Runx2 expression in Panc-1 cells. Runt-related transcription factor-2 overexpression was associated with decreased MMPI release as well as decreased growth and invasion of Panc-1 cells. These effects were reversed by Runx2 silencing. In conclusion, Runx2 is overexpressed in PDAC, where it is regulated by certain cytokines such as TGF-beta 1 and BMP2 in an auto- and paracrine manner. In addition, Runx2 has the potential to regulate the transcription of extracellular matrix modulators such as SPARC and MMPI, thereby influencing the tumour microenvironment
    Type of Publication: Journal article published
    PubMed ID: 17876328
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  • 13
    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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  • 14
    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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  • 15
    Keywords: CANCER ; CANCER CELLS ; CELLS ; GROWTH ; GROWTH-FACTOR ; proliferation ; tumor ; CELL ; Germany ; PATHWAY ; TYROSINE KINASE ; TISSUES ; MICROARRAY DATA ; METASTASIS ; PATHOGENESIS ; RESECTION ; CANCER-CELLS ; MIGRATION ; adenocarcinoma ; CENTRAL-NERVOUS-SYSTEM ; pancreatic cancer ; SMOOTH-MUSCLE ; SERUM ; PANCREATIC-CANCER ; cell proliferation ; cell migration ; pancreatic ductal adenocarcinoma ; C-MET ; WELL ; EXPERIMENT ANNOTATIONS ; CONSCIOUS RATS ; DEVELOPMENTAL PATTERN ; HUMAN GASTROINTESTINAL-TRACT ; Neuromedin U ; Neuromedin U receptor ; PORCINE SPINAL-CORD ; SCATTER FACTOR
    Abstract: Neuromedin U (NmU) is a bioactive peptide, ubiquitously expressed in the gastrointestinal tract. Here, we analyzed the role of NmU in pancreatic ductal adenocarcinoma (PDAC) pathogenesis. NmU and NmU receptor-2 mRNA were significantly overexpressed in PDAC and in metastatic tissues. NmU and NmU receptor-2 were localized predominantly in cancer cells. NmU serum levels decreased after tumor resection. Although NmU exerted no effects on cancer cell proliferation, it induced c-Met and a trend towards increased invasiveness as well as an increased hepatocyte growth factor (HGF)-mediated scattering. Thus, NmU may be involved in the HGF-c-Met paracrine loop regulating cell migration, invasiveness and dissemination of PDAC. (C) 2008 Elsevier Ireland Ltd. All rights reserved
    Type of Publication: Journal article published
    PubMed ID: 19118941
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