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  • 1
    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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  • 2
    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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  • 3
    Keywords: RECEPTOR ; CANCER ; EXPRESSION ; GROWTH ; IN-VITRO ; INVASION ; SURVIVAL ; tumor ; TUMOR-CELLS ; carcinoma ; Germany ; human ; DISEASE ; PATIENT ; STAGE ; PROGRESSION ; immunohistochemistry ; TUMOR PROGRESSION ; METASTASIS ; metastases ; ADHESION ; MIGRATION ; INTEGRIN ; pancreatic cancer ; ANTAGONIST ; IMMUNE ESCAPE ; CHEMOKINE RECEPTOR ; pancreas ; PANCREATIC-CANCER ; TUMOR-GROWTH ; chemokines ; ESCAPE ; pancreatic ; CXCR4 ; METASTATIC BEHAVIOR
    Abstract: Certain chemokines have been proposed to distinctly contribute to tumor growth, dissemination and local immune escape. Expression of the chemokine receptor CXCR4 has been linked to tumor progression in diverse tumor entities. The aim of this study was to evaluate if the expression of CXCR4 influences progression of human pancreatic cancer. CXCR4 expression of pancreatic cancer was retrospectively assessed by immunohistochemistry in 103 patients with pancreatic cancer. Intensity of CXCR4 expression was correlated with both tumor and patient characteristics. Human pancreatic cancer revealed variable intensities of CXCR4 expression. Strong CXCR4 expression was significantly associated with advanced UICC stages (P = 0.03) and revealed a trend for hematogenous metastasis (P = 0.09) and progressed local tumor stages (P = 0.15). In summary, strong expression of CXCR4 was significantly associated with advanced pancreatic cancer
    Type of Publication: Journal article published
    PubMed ID: 17089032
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  • 4
    Keywords: CANCER ; CANCER CELLS ; CELLS ; IN-VITRO ; tumor ; AGENTS ; Germany ; IN-VIVO ; VITRO ; GENE ; PROTEIN ; PROTEINS ; LINES ; DNA ; MECHANISM ; RAT ; MR ; BREAST ; breast cancer ; BREAST-CANCER ; ACIDS ; IDENTIFICATION ; COLORECTAL-CANCER ; mass spectrometry ; CELL-LINE ; chemotherapy ; leukemia ; LINE ; CANCER-CELLS ; MASS-SPECTROMETRY ; AMINO-ACIDS ; sensitivity ; AFFINITY ; CYTOTOXICITY ; antitumor agents ; Chinese herbal medicines ; LEUKEMIA-CELLS ; GEMCITABINE ; in vivo ; ANTITUMOR ; Miltefosine ; CC531 isogenic rat model ; MOLECULAR COMPOUNDS ; new antineoplastic agent ; plant origin ; RAT-LIVER METASTASIS ; RIBOSOME-INACTIVATING PROTEINS ; selective cytotoxicity
    Abstract: The antineoplastic activity of a plant powder used in African traditional medicine for treating cancer was investigated by analyzing the activity of various extracts in vitro. The most active, aqueous extract was subsequently subjected to a detailed investigation in a panel of 17 tumor cell lines, showing an average IC50 of 49 mg raw powder/ml medium. The sensitivity of the cell lines varied by two orders of magnitude, from 1.7 mg/ml in MCF7 breast cancer cells to 170 mg/ml in AR230 chronic-myeloid leukemia cells. Immortalized, non-tumorigenic cell lines showed a marginal sensitivity. In addition, kinetic and recovery experiments performed in MCF7 and U87-MG cells and a comparison with the antineoplastic activity of miltefosine, gemcitabine, and cisplatinum in MCF7, U87-MG, HEp2, and SAOS2 cells revealed no obvious similarity between the sensitivity profiles of the extract and the three standard agents, suggesting a different mechanism of cytotoxicity. The in vivo antitumor activity was determined in the CC531 colorectal cancer rat model. Significant anticancer activity was found following administration of equitoxic doses of 100 (perorally) and 5 (intraperitoneally) mg raw powder/kg, indicating a 95% reduced activity following intestinal absorption. By sequencing the mitochondrial gene for the large Subunit of the ribulose bis-phosphate carboxylase (rbcL) in DNA from the plant material, the source plant was identified as Ximenia americana. A physicochemical characterization showed that the active antineoplastic component(s) of the plant material are proteins with galactose affinity. Moreover, by mass spectrometry, one of these proteins was shown to contain a stretch of 11 amino acids identical to a tryptic peptide from the ribosome-inactivating protein ricin. (c) 2005 Elsevier Inc. All rights reserved
    Type of Publication: Journal article published
    PubMed ID: 16005923
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  • 5
    Keywords: PROTEINS ; PROTEIN ; transcription ; TRANSCRIPTION FACTOR ; VITRO ; CELL ; IN-VITRO ; CANCER ; CELLS ; CANCER CELLS ; MIGRATION ; CANCER-CELLS ; DOWN-REGULATION ; BREAST-CANCER ; BREAST ; breast cancer ; ONCOLOGY
    Type of Publication: Meeting abstract published
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  • 6
    Keywords: CELL ; IN-VITRO ; IN-VIVO ; VITRO ; VIVO ; ONCOLOGY ; EFFICACY
    Type of Publication: Meeting abstract published
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