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  • 1
    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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  • 2
    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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  • 3
    Keywords: brain ; ANGIOGENESIS ; CELLS ; ENDOTHELIAL-CELLS ; EXPRESSION ; Germany ; MODEL ; THERAPY ; SITE ; SITES ; GENE-EXPRESSION ; transcription ; TUMORS ; MICE ; TIME ; MARKER ; CARCINOGENESIS ; INDUCTION ; DOWN-REGULATION ; MOUSE ; LESIONS ; REGULATOR ; molecular ; RE ; TUMORIGENESIS ; endothelial cells ; BLOOD-VESSELS ; astrocytoma ; ANGIOGENIC SWITCH ; TUMOR VASCULATURE ; PDGF-B ; RGS PROTEIN
    Abstract: We identified regulator of G-protein signaling-5 (RGS-5) as an angiogenic pericyte marker at sites of physiologic and pathologic angiogenesis. In a mouse model of pancreatic islet cell carcinogenesis, RGS-5 is specifically induced in the vasculature of premalignant lesions during the "angiogenic switch" and further elevated in tumor vessels. Similarly, RGS-5 is over-expressed in highly angiogenic astrocytomas but not in hypoxia-inducible factor-1alpha (HIF-1alpha)-deficient tumors, which grow along preexisting brain capillaries without inducing neovessels. Elevated levels of RGS-5 in pericytes are also observed during wound healing and ovulation indicating a strong correlation between RGS-5 expression and active vessel remodeling beyond tumor angiogenesis. Moreover, antitumor therapy, which reverses tumor vasculature to an almost normal morphology, results in down-regulation of RGS-5 transcription. Taken together, these data demonstrate for the first time a factor that is specific for "activated" pericytes. This further supports the notion that pericytes, like endothelial cells, undergo molecular changes during neovascularization that makes them a novel target for antiangiogenic therapy. (C) 2005 by The American Society of Hematology
    Type of Publication: Journal article published
    PubMed ID: 15459006
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  • 4
    Keywords: PEPTIDE ; CANCER ; CELLS ; Germany ; IN-VIVO ; MODEL ; PHASE-I ; VIVO ; SYSTEM ; DISTINCT ; PROTEIN ; PROTEINS ; DNA ; FAMILY ; RAT ; MR ; BINDING ; CELL-LINES ; SEQUENCE ; treatment ; IDENTIFICATION ; METASTASIS ; colorectal cancer ; COLORECTAL-CANCER ; chemotherapy ; CRYSTAL-STRUCTURE ; EXCHANGE ; PEPTIDES ; Jun ; LECTIN ; DE-NOVO ; SEQUENCE-ANALYSIS ; AFFINITY ; ENDOPLASMIC-RETICULUM ; CYTOTOXICITY ; FAMILIES ; SOLID TUMORS ; EXTRACTION ; CANCER-TREATMENT ; in vivo ; FRAGMENT ; AGREEMENT ; PRIMERS ; anticancer agent ; RAT-LIVER METASTASIS ; AVISCUMINE RVISCUMIN ; liver metastasis model ; peroral activity ; plant protein ; RICIN-A-CHAIN
    Abstract: The aim of this study was to identify and characterize the active component(s) of Ximenia americana plant material used to treat cancer in African traditional medicine. By a combination of preextraction, extraction, ion exchange and affinity chromatography, a mixture of two cytotoxic proteins was isolated. Using degenerated primers designed on the de novo sequence of two tryptic peptides from one of these proteins, a DNA fragment was amplified and the sequence obtained was used to determine the complete cDNA sequence by the RACE method. Sequence analysis and molecular modeling showed that the new protein, riproximin, belongs to the family of type II ribosome inactivating proteins. These results are in good agreement with the ability of riproximin to inhibit protein synthesis in a cell-free system, as well as with the cytotoxicity of riproximin, as demonstrated by its IC50 value of 0.5 pM in MCF7, 1.1 pM in HELA and 0.6 pM in CC531-lacZ cells. To assess the antineoplastic efficacy of the purified riproximin in vivo, the CC531-lacZ colorectal cancer rat metastasis model was used. Significant anticancer activity was found after administration of total dosages of 100 (perorally) and 10 (intraperitoneally) pmol riproximin/kg. These results suggest that riproximin has distinct potential for cancer treatment
    Type of Publication: Journal article published
    PubMed ID: 16641197
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  • 5
    Keywords: ONCOLOGY ; pancreatic cancer ; METASTASIS ; RAT ; liver ; MODEL ; MODELS ; CANCER
    Type of Publication: Meeting abstract published
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  • 6
    Keywords: CELL ; MODELS ; MODEL ; CELLS ; CANCER CELLS ; CANCER ; EXPRESSION ; RAT ; GENE-EXPRESSION ; GENE ; liver ; RAT-LIVER ; CANCER-CELLS ; COLORECTAL-CANCER ; colorectal cancer ; gene expression ; ONCOLOGY
    Type of Publication: Meeting abstract published
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