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  • METASTASIS  (38)
  • 1
    Keywords: METASTASIS ; PROTEIN ; CANCER ; EXPRESSION ; cancer research ; BONE ; protein expression
    Type of Publication: Book chapter
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  • 2
    Keywords: CANCER ; CANCER CELLS ; CELLS ; EXPRESSION ; GROWTH ; proliferation ; TUMOR-CELLS ; CELL ; Germany ; human ; MODEL ; PROTEIN ; PROTEINS ; REDUCTION ; MR ; BREAST ; breast cancer ; BREAST-CANCER ; antibodies ; antibody ; GLYCOPROTEIN ; TARGET ; ASSAY ; METASTASIS ; PROSTATE-CANCER ; chemotherapy ; oligonucleotides ; CANCER-CELLS ; MIGRATION ; PROGNOSTIC VALUE ; GREECE ; GREEN FLUORESCENT PROTEIN ; ANTISENSE OLIGONUCLEOTIDES ; HUMAN BREAST ; GFP-MDA-MB-231,migration,metastasis,antisense oligonucleotides,osteopontin,bone sialoprotein ; HUMAN BREAST-CANCER ; SPARC
    Abstract: MDA-MB-231 human breast cancer cells transfected with GFP were used as model to determine the reduction in proliferation, colony formation, and migration in response to agents with anti-metastatic properties. These agents consisted of antisense oligonucleotides (ASOs) directed against osteopontin (OPN), bone sialoprotein II (BSP II), and osteonectin (ON), as well as an antibody directed against BSP II. A bisphosphonate derivative (ibandronate) and an alkylphosphocholine (erucylphospho-NNN-trimethylpropanolamine; ErPC3) were used as positive controls. The ASOs directed against OPN, BSP II and ON suppressed the expression of their respective target proteins by 81%, 74% and 69%, respectively. They were barely but significantly active in inhibiting the proliferation, but intermediately to highly active in inhibiting the colony formation and migration of GFP-MDA-MB-231 breast cancer cells. The antibody against human BSP II was significantly more active than all ASOs used and was equally active or even surpassed the activity of ibandronate and ErPC3 in all three assays. The results obtained suggest a specific anti-metastatic activity of this antibody as well as of the ASOs found effective in decreasing OPN and BSP II expression
    Type of Publication: Journal article published
    PubMed ID: 15067347
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  • 3
    Keywords: RECEPTOR ; CANCER ; CELLS ; EXPRESSION ; GROWTH ; IN-VITRO ; SURVIVAL ; tumor ; TUMOR-CELLS ; carcinoma ; CELL LUNG-CANCER ; Germany ; VITRO ; DISEASE ; LINES ; PATIENT ; ACTIVATION ; RECEPTOR EXPRESSION ; prognosis ; CELL-LINES ; PROGRESSION ; ASSAY ; DESIGN ; NUMBER ; METASTASIS ; colorectal cancer ; COLORECTAL-CANCER ; LINE ; CANCER-CELLS ; MIGRATION ; RECEPTORS ; BEHAVIOR ; POOR-PROGNOSIS ; cell lines ; CELL-MIGRATION ; chemokine ; LOCATION ; ANTAGONIST ; intensity ; LYMPH-NODE METASTASIS ; CHEMOKINE RECEPTORS ; cell migration ; ASSAYS ; DISSEMINATION ; CELL-DERIVED FACTOR ; DISEASE PROGRESSION ; MATURE DENDRITIC CELLS
    Abstract: Purpose: The expression of chemokine receptors CXCR4 and CCR.7 has been associated with tumor dissemination and poor prognosis in a limited number of tumor entities. However, no data are currently available on the impact of chemokine receptor expression on disease progression and prognosis in human colorectal cancer. Experimental Design: The expression of CXCR4 and CCR7 was evaluated in 96 patients with histologically confirmed colorectal cancers and in four colorectal cancer cell lines by immunohistochemical staining. Furthermore, cell migration assays were done with SW480, SW620, and LS174T cancer cells to confirm the effect of the CXCR4 ligand stromal cell-derived factor 1alpha on migration. Results: Human colorectal cancer specimens and cell lines displayed a CXCR4 and CCR7 expression with variable intensities. Interestingly, strong expression of CXCR4, but not of CCR7, was significantly associated with higher Union International Contre Cancer stages 3/4 (P = 0.0017), lymph node metastasis (P = 0.00375), and distant metastasis (P = 0.00003) and further correlated with a reduced 3-year survival rate (P = 0.1). Strong CXCR4 and CCR7 expression positively correlated with the location of the primary tumor in the rectum (P 〈 0.01). Furthermore, activation of CXCR4-expressing cancer cells by stromal cell-derived factor 1alpha resulted in a significant increase of cell migration (P 〈 0.014). Conclusion: Strong expression of CXCR4 by colorectal cancer cells is significantly associated with lymphatic and distant dissemination in patients with colorectal cancer as well as with cancer cell migration in vitro
    Type of Publication: Journal article published
    PubMed ID: 15755995
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  • 4
    Keywords: CANCER ; CELLS ; GROWTH ; IN-VITRO ; proliferation ; tumor ; TUMOR-CELLS ; AGENTS ; CELL LUNG-CANCER ; COMBINATION ; Germany ; IN-VIVO ; INHIBITION ; MODEL ; VITRO ; EXPOSURE ; liver ; PATIENT ; RAT ; RATS ; SEQUENCE ; RAT-LIVER ; ASSAY ; METASTASIS ; colorectal cancer ; COLORECTAL-CANCER ; EFFICACY ; metastases ; chemotherapy ; arteries ; CANCER-CELLS ; COLON-CANCER ; LIVER METASTASES ; BOLUS ; AGENT ; GEMCITABINE ; colon cancer ; TUMOR-GROWTH ; END ; COLON ADENOCARCINOMA ; HEPATIC METASTASES ; PHASE-II TRIAL ; STARCH MICROSPHERES ; ANIMAL-MODEL ; liver metastasis ; PEMETREXED DISODIUM ; CC531-lac-Z ; chemoembolization ; chemoluminescence ; INTRAARTERIAL CHEMOTHERAPY ; MULTITARGETED ANTIFOLATE LY231514 ; SELECTIVE CHEMOEMBOLIZATION
    Abstract: Purpose: The aim of this study was to evaluate the combination effect of pemetrexed disodium (MTA; Alimta; LY 231514) and gemcitabine ( GEM) administered by hepatic artery and portal vein chemoembolization (HACE and PVCE) in a colorectal cancer rat liver metastasis model. Materials and methods: Proliferation studies on CC531-lac-Z rat colon cancer cells were performed using the MTT assay to obtain the optimal combination schedule of the two antineoplastic agents. To generate diffuse liver metastasis, 4 x 10(6) tumor cells were implanted into the portal vein of male WAG/Rij rats. MTA ( 30 mg/kg, 60 mg/kg, and 90 mg/kg) was administered locoregionally by portal vein chemoembolization ( PVCE) and compared with repeated systemic intravenous injection. GEM ( 50 mg/kg) was also given locoregionally by hepatic artery chemoembolization ( HACE) as well as systemically. All routes of administration were examined alone as well as in combination. Efficacy of treatment in terms of liver metastases burden was determined at the end of the experiment by measuring the beta-galactosidase activity of CC531-lac-Z cells with a chemoluminescence assay. Results: Combination experiments in vitro showed a more than additive tumor cell reduction after sequential exposure to MTA preceding GEM (observed/expected ratio [O/ E] = 0.73). Experiments with the reverse sequence ( GEM. MTA) resulted only in additive combination effects ( O/ E ratio = 1.08). Simultaneous drug exposure showed less than additive combination effects (O/ E ratios 〉= 1.25). In vivo, locoregional administration by HACE with GEM was significantly more effective than systemic intravenous bolus treatment (P = 0.03). Portal vein chemoembolization with MTA performed immediately after tumor cell inoculation was ineffective. Repeated systemic treatment with MTA yielded a slight reduction in tumor cell load that was significant versus control at the medium and high doses ( 60 mg/kg, P = 0.009; 90 mg/kg, P = 0.046) but not versus intraportal chemoembolization. The combination treatment of systemic ( 60 and 90 mg/kg) or locoregional ( 60 mg/kg) MTA with HACE using GEM ( 50 mg/kg) resulted in more than 80 % tumor growth inhibition; this antineoplastic combination effect was maximally additive. Conclusion: A regimen-dependent synergistic combination effect of both drugs was found in vitro. In animals, hepatic artery chemoembolization with GEM was superior to systemic intravenous bolus treatment. Portal vein chemoembolization with MTA was ineffective. The optimal in vitro regimen of MTA ( intravenous or PVCE) preceding GEM ( HACE) resulted in a maximally additive tumor growth inhibition. The results indicate that MTA and GEM can successfully be combined and favor further evaluation in patients
    Type of Publication: Journal article published
    PubMed ID: 15657768
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  • 5
    Keywords: CANCER ; CANCER CELLS ; CELLS ; EXPRESSION ; IN-VITRO ; proliferation ; carcinoma ; Germany ; VITRO ; LUNG-CANCER ; PROTEIN ; PATIENT ; RATS ; treatment ; BREAST ; breast cancer ; BREAST-CANCER ; antibodies ; LESIONS ; METASTASIS ; NUDE-MICE ; chemotherapy ; CANCER-CELLS ; MIGRATION ; INTEGRIN ALPHA(V)BETA(3) ; SERUM ; MATRIX ; MATRIX METALLOPROTEINASES ; anti-BSP antibody ; bone metastasis ; COLONY FORMATION ; MDA-MB-231 human breast cancer cell line ; nude rat model ; OSTEOPONTIN ; bone sialoprotein
    Abstract: The extracellular bone matrix protein bone sialoprotein (BSP) is considered to play an important role in the pathogenesis of lytic skeletal lesions which are associated with severe morbidity in breast, prostate or lung cancer patients. In addition to in vitro Studies, nude rats were implanted with 105 MDA-MB-231 cells transfected with GFP into a small branch of the femoral artery. Osteolytic lesions of the respective hind leg were detected by X-ray and CT analysis as well as by inimunohistochemistry. Exposure of MDA-MB-231(GFP) cells in vitro to an antibody against BSP (0-400 mu g/ml) decreased proliferation, colony formation and migration of these cells by up to 95, 83 and 89 T/C%, respectively. In nude rats, preincubation of MDA-MB-231GFP cells prior to inoculation (25-100 mu g/ml) reduced the mean osteolytic lesion size to 22 T/C% after 90 days of observation (p 〈 0.05). Treatment of overt lytic metastasis with the anti-BSP antibody (10 mg/kg) resulted in a significantly smaller mean lesion size of 57 T/C% at the end of the observation period (p 〈 0.05) as well as in new bone formation. Immunohistochemical analysis revealed the presence of BSP in MDA-MB-231(GFP) cells and in vessel endothelium cells during processes such as migration and invasion. In conclusion, an anti-BSP antibody decreased proliferation, colony formation and migration of MDA-MB-231(GFP) cells in vitro and reduced osteolysis besides inducing bone formation in a nude rat model
    Type of Publication: Journal article published
    PubMed ID: 16465361
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  • 6
    Keywords: APOPTOSIS ; CANCER ; CANCER CELLS ; CELLS ; EXPRESSION ; IN-VITRO ; INVASION ; proliferation ; CELL ; Germany ; IN-VIVO ; LUNG ; MODEL ; PATHWAY ; VITRO ; VIVO ; SAMPLE ; SAMPLES ; transcription ; DIFFERENTIATION ; LINES ; MICE ; IMPACT ; prognosis ; CELL-LINES ; PHOSPHORYLATION ; TARGET ; ASSAY ; METASTASIS ; colorectal cancer ; COLORECTAL-CANCER ; metastases ; SIGNALING PATHWAY ; CANCER-CELLS ; MIGRATION ; POLYMERASE-CHAIN-REACTION ; adenocarcinoma ; TARGETS ; cell lines ; AKT ; HOMEOBOX GENE ; signaling ; HUMAN PROSTATE ; development ; ASSAYS ; PROGENITORS ; colorectal ; TAIL ; MicroRNAs ; POLYMERASE ; CANCER-CELL-LINES ; RESTRICTION ; Homeobox ; HOXB8 ; HUMAN LUNG CANCERS ; Micro-RNA ; miR-196a
    Abstract: AIM: To analyze the relevance of the microRNA miR-196a for colorectal oncogenesis. METHODS: The impact of miR-196a on the restriction targets HoxA7, HoxB8, HoxC8 and HoxD8 was analyzed by reverse transcription polymerase chain reaction (RT-PCR) after transient transfection of SW480 cancer cells. The miR-196a transcription profile in colorectal cancer samples, mucosa samples and diverse cancer cell lines was quantified by RT-PCR. Transiently miR-196a-transfected colorectal cancer cells were used for diverse functional assays in vitro and for a xenograft lung metastasis model in vivo. RESULTS: HoxA7, HoxB8, HoxC8 and HoxD8 were restricted by miR-196a in a dose-dependent and gene-specific manner. High levels of miR-196a activated the AKT signaling pathway as indicated by increased phosphorylation of AKT. In addition, high levels of miR-196a promoted cancer cell detachment, migration, invasion and chemosensitivity towards platin derivatives but did not impact on proliferation or apoptosis. Furthermore, miR-196a increased the development of lung metastases in mice after tail vein injection. CONCLUSION: miR-196a exerts a pro-oncogenic influence in colorectal cancer.(C) 2009 The WIG Press and Baishideng. All rights reserved
    Type of Publication: Journal article published
    PubMed ID: 19418581
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  • 7
    Keywords: ANGIOGENESIS ; CANCER ; CELLS ; CELL ; Germany ; MODEL ; THERAPY ; CLASSIFICATION ; SYSTEM ; SYSTEMS ; computed tomography ; MARKER ; RAT ; BIOMARKERS ; BREAST ; breast cancer ; BREAST-CANCER ; antibodies ; antibody ; METASTASIS ; PROSTATE-CANCER ; MARKERS ; CANCER-CELLS ; COMPUTED-TOMOGRAPHY ; MULTIPLE-MYELOMA ; dynamic contrast enhanced MRI ; ENHANCEMENT ; biomarker ; bone metastasis ; DCE-MRI ; BEVACIZUMAB ; Diffusion weighted imaging ; Dynamic contrast enhanced volumetric CT
    Abstract: As current classification systems for the assessment of treatment response in bone metastasis do not meet the needs of oncologists, new imaging biomarkers are desirable. Therefore, the diagnostic impact of dynamic contrast enhanced (DCE)-volumetric computed tomography (VCT) (descriptive analysis), DCE-MRI (two-compartment model) and diffusion weighted imaging (DWI) for monitoring anti-angiogenic therapy effects of the VEGF antibody bevacizumab in breast cancer bone metastases in rats was studied. Nude rats (n = 8 animals treated with bevacizumab and n = 9 untreated control rats) with site-specific osteolytic bone metastasis of the hind leg were imaged with a 1.5 T clinical MRI-scanner in an animal coil as well as in a volumetric CT-scanner at days 30, 40, 50 and 60 after inoculation of MDA-MB-231 human breast cancer cells. From these data, osteolytic lesion size (OLS), peak enhancement (PE), area under the curve (AUC), amplitude (A), exchange rate constant (k(ep)) and apparent diffusion coefficient (ADC) were determined in bone metastases. Prior to changes in OLS (p 〈= 0.05 at days 50 and 60) there was already a significant decrease in PE, AUC and A (p 〈= 0.05 at days 40-60) in treated animals compared to controls. However, for k(ep) and ADC there were no significant differences between the groups at any time point (p 〉 0.05 at days 40-60). In conclusion, anti-angiogenic treatment response in osteolytic breast cancer bone metastases can be assessed early with surrogate markers of vascularization, while DWI appears to be insensitive. (C) 2008 Elsevier Ireland Ltd. All rights reserved
    Type of Publication: Journal article published
    PubMed ID: 19070445
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  • 8
    Keywords: RECEPTOR ; CANCER ; CELLS ; EXPRESSION ; GROWTH ; tumor ; carcinoma ; CELL ; Germany ; CLASSIFICATION ; SURGERY ; T-CELL ; T-CELLS ; BREAST-CANCER ; PROGRESSION ; immunohistochemistry ; METASTASIS ; colorectal cancer ; COLORECTAL-CANCER ; LYMPHOCYTES ; CANCER-PATIENTS ; IMMUNITY ; GASTRIC-CANCER ; inflammation ; CHEMOKINE RECEPTOR ; CCR5 ; PROGNOSTIC-FACTOR ; IMMUNE ; CCL5/RANTES ; T-cell infiltration
    Abstract: Chemokines and their receptors have been proposed to distinctly contribute to tumor growth, dissemination, and local immune escape. The aim of this study was to evaluate the relevance of the chemokine receptor CCR5 expression for the progression of human colorectal cancer. CCR5 expression was assessed by RT-PCR analysis in 103 colorectal cancer patients. Intensity of CCR5 expression was correlated with both tumor and patient characteristics. Infiltration of tumor margins with CD8(+) T cells in the context of CCR5 expression was analyzed by immunohistochemistry in additional 18 colorectal cancer specimens. Human colorectal cancer revealed variable intensities of CCR5 expression ranging from absent (48/103: 47%), weak (30/103: 29%), intermediate (13/103: 13%), to strong (12/103: 12%). Absent or weak CCR5 expression was significantly associated with advanced UICC stages (P = 0.02) and lymphatic metastasis (P = 0.05). In addition, CCR5 expression positively correlated with CD8(+) T-cell infiltration in tumor margins (P = 0.001). In summary, intermediate and strong CCR5 expression was significantly associated with nonmetastatic colorectal cancer and increased CD8(+) T-cell infiltration
    Type of Publication: Journal article published
    PubMed ID: 20054600
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  • 9
    Keywords: RECEPTOR ; CANCER ; EXPRESSION ; SURVIVAL ; ENDOTHELIAL GROWTH-FACTOR ; Germany ; KINASE ; TYROSINE KINASE ; GENES ; SURGERY ; IMPACT ; ALPHA ; TARGET ; PROGRESSION ; PATTERNS ; METASTASIS ; STOMACH ; adenocarcinoma ; RECEPTORS ; CELL CARCINOMA ; PATTERN ; overall survival ; UPDATE ; LYMPH-NODE ; receptor tyrosine kinase ; RECEPTOR TYROSINE KINASES ; gastric ; ESOPHAGEAL ; PDGFR ; gastric adenocarcinoma ; RATIONALE ; COEXPRESSION ; MOLECULAR TARGETING STRATEGY ; RECEPTOR-TYROSINE-KINASE
    Abstract: Background/Aims: This study was initiated in order to define the (co-)expression patterns of target receptor tyrosine kinases (RTKs) in human gastric adenocarcinoma and to correlate them with clinicopathological parameters. Methodology: The (co-)expression pattern of VEGFR1, VEGFR2,VEGFR3, PDGFR alpha, PDGFR beta and EGFR1 was analyzed in 56 samples of human gastric adenocarcinoma and correlated with staging and survival. Results: VEGFR1,VEGFR2, VEGFR3, PDGFRa, PDGFR beta and EGFR1 were expressed at relevant levels in 79%, 50%, 50%, 63%, 55% and 30%, respectively. VEGFR2,VEGFR3, and PDGFR beta were significantly co-expressed. Thirty-four percent of gastric adenocarcinoma samples revealed a co-expression of 6 receptors, 27% expressed 5 receptors and only 23% showed expression of 3 receptors or less. Expression of VEGFR1, VEGFR2, VEGFR3, PDGFR alpha, PDGFR beta and EGFR1 in gastric adenocarcinoma did not significantly correlate with a higher pT-category, the presence of lymph node metastasis (pN+) or overall survival. However, a trend towards a higher pT-category was seen for expression of VEGFR1 without reaching statistical significance. Conclusions: The data obtained reveal that specific RTKs are significantly co-expressed. However, co-expression of RTKs did not impact on staging or survival. It has to be further analyzed, if the expression of the respective ligands is of higher relevance than the expression of the receptor itself
    Type of Publication: Journal article published
    PubMed ID: 20583450
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  • 10
    Keywords: LUNG ; BREAST-CANCER ; PROGRESSION ; METASTASIS ; PROGNOSTIC VALUE ; RECONSTRUCTION ; COLORECTAL-CARCINOMA ; EPITHELIAL-MESENCHYMAL TRANSITION ; CIRCULATING TUMOR-CELLS ; SERIAL SECTIONS
    Abstract: Cancer cell invasion takes place at the cancer-host interface and is a prerequisite for distant metastasis. The relationships between current biological and clinical concepts such as cell migration modes, tumour budding and epithelial-mesenchymal transition (EMT) remains unclear in several aspects, especially for the 'real' situation in human cancer. We developed a novel method that provides exact three-dimensional (3D) information on both microscopic morphology and gene expression, over a virtually unlimited spatial range, by reconstruction from serial immunostained tissue slices. Quantitative 3D assessment of tumour budding at the cancer-host interface in human pancreatic, colorectal, lung and breast adenocarcinoma suggests collective cell migration as the mechanism of cancer cell invasion, while single cancer cell migration seems to be virtually absent. Budding tumour cells display a shift towards spindle-like as well as a rounded morphology. This is associated with decreased E-cadherin staining intensity and a shift from membranous to cytoplasmic staining, as well as increased nuclear ZEB1 expression.
    Type of Publication: Journal article published
    PubMed ID: 25081610
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