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  • Cell Line, Tumor  (20)
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  • 1
    Language: English
    In: BMC Research Notes, June 23, 2014, Vol.7(1)
    Description: Background Different flavonoids are known to interfere with influenza A virus replication. Recently, we showed that the structurally similar flavonoids baicalein and biochanin A inhibit highly pathogenic avian H5N1 influenza A virus replication by different mechanisms in A549 lung cells. Here, we investigated the effects of both compounds on H5N1-induced reactive oxygen species (ROS) formation and the role of ROS formation during H5N1 replication. Findings Baicalein and biochanin A enhanced H5N1-induced ROS formation in A549 cells and primary human monocyte-derived macrophages. Suppression of ROS formation induced by baicalein and biochanin A using the antioxidant N-acetyl-L-cysteine strongly increased the anti-H5N1 activity of both compounds in A549 cells but not in macrophages. Conclusions These findings emphasise that flavonoids induce complex pharmacological actions some of which may interfere with H5N1 replication while others may support H5N1 replication. A more detailed understanding of these actions and the underlying structure-activity relationships is needed to design agents with optimised anti-H5N1 activity. Keywords: H5N1, Biochanin A, Baicalein, Antiviral, Reactive oxygen species, N-acetyl-L-cysteine
    Keywords: Antiviral Agents -- Research ; Antioxidants (Nutrients) -- Research ; Avian Influenza -- Research ; Cystine ; Avian Influenza Viruses ; Macrophages
    ISSN: 1756-0500
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  • 2
    Language: English
    In: Biomaterials, 03/2010, Vol.31(8), pp.2388-2398
    Description: To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.biomaterials.2009.11.093 Byline: Sylvia Wagner (a), Florian Rothweiler (b), Marion G. Anhorn (c), Daniel Sauer (a), Iris Riemann (a), Eike C. Weiss (a), Alisa Katsen-Globa (a), Martin Michaelis (b), Jindrich Cinatl (b), Daniel Schwartz (d), Jorg Kreuter (c), Hagen von Briesen (a), Klaus Langer (e) Abstract: Specific transport of anti-cancer drugs into tumor cells may result in increased therapeutic efficacy and decreased adverse events. Expression of [alpha]v[beta]3 integrin is enhanced in various types of cancer and monoclonal antibodies (mAbs) directed against [alpha]v[beta]3 integrins hold promise for anti-cancer therapy. DI17E6 is a monoclonal antibody directed against [alpha]v integrins that inhibits growth of melanomas in vitro and in vivo and inhibits angiogenesis due to interference with [alpha]v[beta]3 integrins. Here, DI17E6 was covalently coupled to human serum albumin nanoparticles. Resulting nanoparticles specifically targeted [alpha]v[beta]3 integrin positive melanoma cells. Moreover, doxorubicin loaded DI17E6 nanoparticles showed increased cytotoxic activity in [alpha]v[beta]3-positive melanoma cells than the free drug. Therefore, DI17E6-coupled human serum albumin nanoparticles represent a potential delivery system for targeted drug transport into [alpha]v[beta]3-positive cells. Author Affiliation: (a) Fraunhofer Institute for Biomedical Engineering, D-66386 St.Ingbert, Germany (b) Institut fur Medizinische Virologie, Universitatsklinikum, Goethe-University, D-60590 Frankfurt, Germany (c) Institute of Pharmaceutical Technology, Biocenter of Goethe-University, D-60438 Frankfurt, Germany (d) Merck Serono, Biotech Products Development, D-64293 Darmstadt, Germany (e) Institute of Pharmaceutical Technology and Biopharmacy, Westfalische Wilhelms Universitat, Corrensstrasse 1, D-48149 Munster, Germany Article History: Received 4 November 2009; Accepted 26 November 2009
    Keywords: Drugs ; Monoclonal Antibodies ; Serum Albumin ; Anthracyclines ; Biological Products ; Integrins ; Melanoma ; Nanoparticles;
    ISSN: 01429612
    E-ISSN: 18785905
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  • 3
    In: Molecular BioSystems, 2011, Vol.7(1), pp.200-214
    Description: Chemotherapy of cancer experiences a number of shortcomings including development of drug resistance. This fact also holds true for neuroblastoma utilizing chemotherapeutics as vincristine. We performed a comparative analysis of molecular and cellular mechanisms associated with vincristine resistance utilizing cell line as well as human tissue data. Differential gene expression analysis revealed molecular features, processes and pathways afflicted with drug resistance mechanisms in general, and specifically with vincristine significantly involving actin associated features. However, specific mode of resistance as well as underlying genotype of parental, vincristine sensitive cells apparently exhibited significant heterogeneity. No consensus profile for vincristine resistance could be derived, but resistance-associated changes on the level of individual neuroblastoma cell lines as well as individual patient profiles became clearly evident. Based on these prerequisites we utilized the concept of synthetic lethality aimed at identifying hub proteins which when inhibited promise to induce cell death due to a synthetic lethal interaction with down-regulated, chemoresistance associated features. Our screening procedure identified synthetic lethal hub proteins afflicted with actin associated processes holding synthetic lethal interactions to down-regulated features individually found in all chemoresistant cell lines tested, therefore promising an improved therapeutic window. Verification of such synthetic lethal hub candidates in human neuroblastoma tissue expression profiles indicated the feasibility of this screening approach for addressing vincristine resistance in neuroblastoma.
    Keywords: Antineoplastic Agents -- Pharmacology ; Drug Resistance, Neoplasm -- Physiology ; Neoplasm Proteins -- Metabolism ; Neuroblastoma -- Metabolism ; Vincristine -- Pharmacology;
    ISSN: 1742-206X
    E-ISSN: 1742-2051
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  • 4
    Language: English
    In: Int. Journal of Clinical Pharmacology and Therapeutics, 2017, Vol.55(08), pp.686-689
    Keywords: A549 Cells–Therapeutic Use ; Antineoplastic Agents–Drug Therapy ; Carcinoma, Non-Small-Cell Lung–Therapeutic Use ; Cell Line, Tumor–Drug Effects ; Cisplatin–Genetics ; Humans–Drug Effects ; Signal Transduction–Genetics ; Transcriptome–Genetics ; Antineoplastic Agents ; Cisplatin;
    ISSN: 0946-1965
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  • 5
    Language: English
    In: International journal of pharmaceutics, 2011, Vol.415(1), pp.244-251
    Description: Glioblastomas belong to the most devastating cancer diseases. For this reason, polysorbate 80 (Tween 80®)-coated poly(isohexyl cyanoacrylate) (PIHCA) (Monorex®) nanoparticles loaded with doxorubicin were developed and tested for their use for the treatment of glioblastomas. The preparation of the nanoparticles resulted in spherical particles with high doxorubicin loading. The physico-chemical properties and the release of doxorubicin from the PIHCA-nanoparticles were analysed, and the influence on cell viability of the rat glioblastoma 101/8-cell line was investigated. In vitro, the empty nanoparticles did not show any toxicity, and the anti-cancer effects of the drug-loaded nanoparticles were increased in comparison to doxorubicin solution, represented by IC₅₀ values. The in vivo efficacy was then tested in intracranially glioblastoma 101/8-bearing rats. Rats were treated with 3×1.5mg/kg doxorubicin and were sacrificed 18 days after tumour transplantation. Histological and immunohistochemical analyses were carried out to assess the efficacy of the nanoparticles. Tumour size, proliferation activity, vessel density, necrotic areas, and expression of glial fibrillary acidic protein demonstrated that doxorubicin-loaded PIHCA-nanoparticles were much more efficient than the free drug. The results suggest that poly(isohexyl cyanoacrylate) nanoparticles hold great promise for the non-invasive therapy of human glioblastomas. ; p. 244-251.
    Keywords: Therapeutics ; Doxorubicin ; Toxicity ; Cell Viability ; Immunohistochemistry ; Polysorbates ; Physicochemical Properties ; Neoplasms ; Inhibitory Concentration 50 ; Humans ; Rats ; Nanoparticles
    ISSN: 0378-5173
    E-ISSN: 18733476
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  • 6
    Language: English
    In: Molecular Cancer, 2009, Vol.8(1), pp.urn:issn:1476-4598
    Description: Background: Chemoresistance acquisition may influence cancer cell biology. Here, bioinformatics analysis of gene expression data was used to identify chemoresistance-associated changes in neuroblastoma biology. Results: Bioinformatics analysis of gene expression data revealed that expression of angiogenesis-associated...
    Keywords: Endothelial Growth-Factor ; In-Vivo ; Melanoma-Cells ; Tumor-Growth ; N-Myc ; Extracellular-Matrix ; Angiogenic Factors ; Cytokine Network ; Vegf Expression ; Blood-Vessels
    ISSN: 1476-4598
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  • 7
    Language: English
    In: PLoS ONE, May 17, 2011, Vol.6(5), p.e19705
    Description: Glycyrrhizin is known to exert antiviral and anti-inflammatory effects. Here, the effects of an approved parenteral glycyrrhizin preparation (Stronger Neo-Minophafen C) were investigated on highly pathogenic influenza A H5N1 virus replication, H5N1-induced apoptosis, and H5N1-induced pro-inflammatory responses in lung epithelial (A549) cells. Therapeutic glycyrrhizin concentrations substantially inhibited H5N1-induced expression of the pro-inflammatory molecules CXCL10, interleukin 6, CCL2, and CCL5 (effective glycyrrhizin concentrations 25 to 50 [micro]g/ml) but interfered with H5N1 replication and H5N1-induced apoptosis to a lesser extent (effective glycyrrhizin concentrations 100 [micro]g/ml or higher). Glycyrrhizin also diminished monocyte migration towards supernatants of H5N1-infected A549 cells. The mechanism by which glycyrrhizin interferes with H5N1 replication and H5N1-induced pro-inflammatory gene expression includes inhibition of H5N1-induced formation of reactive oxygen species and (in turn) reduced activation of NF[kappa]B, JNK, and p38, redox-sensitive signalling events known to be relevant for influenza A virus replication. Therefore, glycyrrhizin may complement the arsenal of potential drugs for the treatment of H5N1 disease.
    Keywords: Antiviral Agents -- Health Aspects ; Virus Replication -- Health Aspects ; Avian Influenza Viruses -- Health Aspects ; Avian Influenza -- Health Aspects ; Genes -- Health Aspects ; Apoptosis -- Health Aspects ; Gene Expression -- Health Aspects
    ISSN: 1932-6203
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  • 8
    Language: English
    In: Int. Journal of Clinical Pharmacology and Therapeutics, 2015, Vol.53(12), pp.1041-1045
    Keywords: Antineoplastic Agents–Pharmacology ; Cell Line, Tumor–Pharmacology ; Cisplatin–Physiology ; Drug Resistance, Neoplasm–Physiology ; Female–Drug Therapy ; Humans–Pathology ; Mitogen-Activated Protein Kinase 1–Pathology ; Mitogen-Activated Protein Kinase 3–Pathology ; Ovarian Neoplasms–Pathology ; Antineoplastic Agents ; Mitogen-Activated Protein Kinase 1 ; Mitogen-Activated Protein Kinase 3 ; Cisplatin;
    ISSN: 0946-1965
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  • 9
    In: Nature Medicine, 2016
    Description: The nucleoside analog cytarabine (Ara-C) is an essential component of primary and salvage chemotherapy regimens for acute myeloid leukemia (AML). After cellular uptake, Ara-C is converted into its therapeutically active triphosphate metabolite, Ara-CTP, which exerts antileukemic effects, primarily by inhibiting DNA synthesis in proliferating cells1. Currently, a substantial fraction of patients with AML fail to respond effectively to Ara-C therapy, and reliable biomarkers for predicting the therapeutic response to Ara-C are lacking2, 3. SAMHD1 is a deoxynucleoside triphosphate (dNTP) triphosphohydrolase that cleaves physiological dNTPs into deoxyribonucleosides and inorganic triphosphate4, 5. Although it has been postulated that SAMHD1 sensitizes cancer cells to nucleoside-analog derivatives through the depletion of competing dNTPs6, we show here that SAMHD1 reduces Ara-C cytotoxicity in AML cells. Mechanistically, dGTP-activated SAMHD1 hydrolyzes Ara-CTP, which results in a drastic reduction of Ara-CTP in leukemic cells. Loss of SAMHD1 activity--through genetic depletion, mutational inactivation of its triphosphohydrolase activity or proteasomal degradation using specialized, virus-like particles7, 8--potentiates the cytotoxicity of Ara-C in AML cells. In mouse models of retroviral AML transplantation, as well as in retrospective analyses of adult patients with AML, the response to Ara-C-containing therapy was inversely correlated with SAMHD1 expression. These results identify SAMHD1 as a potential biomarker for the stratification of patients with AML who might best respond to Ara-C-based therapy and as a target for treating Ara-C-refractory AML.
    Keywords: Leukemia ; Chemotherapy ; Biomarkers ; Medical Prognosis ; Cytotoxicity;
    ISSN: 1078-8956
    E-ISSN: 1546-170X
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  • 10
    Language: English
    In: Medical microbiology and immunology, 2010, Vol.199(2), pp.93-101
    Description: Tumor resistance to lysis by resting natural killer (NK) cells may be overcome by priming of NK cells with cytokines or by binding of NK activating receptors to ligands expressed on target cells. In this study, major histocompatibility complex class I (MHC-I)-negative LNCaP and MHC-I-positive DU145 cells were infected with genetically modified influenza A virus lacking the non-structural gene 1 (∆NS1 IAV). The cells were used to investigate the influence of ∆NS1 IAV infection on NK cell lysis of tumor cells as well as to prime NK cells for lysis of LNCaP and DU145 cells. While LNCaP cells infected with ΔNS1 IAV showed enhanced lysis when compared with mock-infected cells (93% ± 1.47 vs. 52% ± 0.74), both mock-infected and ΔNS1 IAV-infected DU145 cells were resistant to NK cell lysis. Moreover, NK cells primed with ΔNS1 IAV-infected LNCaP/DU145 cells effectively lysed resistant DU145 and sensitive LNCaP cells to a greater extent than NK cells primed with mock-infected LNCaP/DU145 or non-primed NK cells. Also, NK cell priming with ΔNS1 IAV-infected tumor cells enhanced extracellular signal-regulated kinase phosphorylation and increased granule release in NK cells. The increased granule release was specifically mediated by NKp46, which eventually potentiated NK cells primed with ΔNS1 IAV-infected tumor cells to overcome the inhibitory effects posed by MHC-I expression on DU145 cells. These findings show that in addition to direct lytic activity of NK cells, ΔNS1 IAV may influence anti-tumoral responses by priming NK cells. ; Includes references ; p. 93-101.
    Keywords: Tumors -- Health Aspects ; Genetically Modified Organisms -- Health Aspects ; Killer Cells -- Health Aspects ; Influenza -- Health Aspects ; Cytological Research -- Health Aspects;
    ISSN: 0300-8584
    E-ISSN: 14321831
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