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Berlin Brandenburg

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  • Oxford Journals (Oxford University Press)  (9)
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  • 1
    In: Neuro-Oncology, 2015, Vol. 17(7), pp.1039-1039
    Description: The question of whether most gliomas are infected with human cytomegalovirus (HCMV) has been under dispute for more than 10 years. We recently reported our failure to detect HCMV in gliomas in Neuro-Oncology.1 Our article was accompanied by 2 related editorials,2,3 one of which boldly criticized our approach.3 Instead of fighting a petty, ivory tower dispute, we would like to lobby for a serious collaborative approach to providing conclusive evidence on the presence of HCMV in glioma (and other cancers). Since we developed the concept of oncomodulation (ie, that HCMV …
    Keywords: Medicine;
    ISSN: 1522-8517
    E-ISSN: 1523-5866
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  • 2
    In: Journal of Antimicrobial Chemotherapy, 2007, Vol. 60(5), pp.981-986
    Description: Objectives West Nile virus (WNV) infection causes severe meningitis and encephalitis in a subset of patients. WNV-induced apoptosis has been suggested to contribute to WNV pathogenesis. Tetracyclines exert antiviral effects against HIV and inhibit apoptosis in different models of neuronal disease. Here, the effects of the tetracyclines minocycline, demeclocycline and chlortetracycline were observed on WNV replication and WNV-induced apoptosis in different human CNS-derived cell types (primary human brain neurons, primary human retinal pigment epithelial cells and T98G human glioma cell line). Methods WNV replication was studied by cytopathic effects and virus yield reduction assay. Cell viability was examined by MTT assay. Apoptosis was investigated by immunostaining for activated caspase 3 and cleaved poly(ADP-ribose) polymerase. Expression and phosphorylation of cellular proteins were examined by western blot. Results Minocycline exerted the strongest anti-WNV activity. Non-toxic minocycline concentrations that can be achieved in human tissues significantly reduced WNV titres in all cell types tested. Minocycline inhibited WNV-induced apoptosis and suppressed virus-induced activation of c-Jun N-terminal kinase (JNK) and its target c-jun. The JNK inhibitor L-JNKi exerted similar effects to minocycline. Conclusions These data suggest that minocycline-induced inhibition of JNK activation contributes to minocycline-induced inhibition of WNV replication and WNV-induced apoptosis. Minocycline is a clinically available, inexpensive and generally very well-tolerated drug. It could be readily evaluated for the treatment of humans with serious WNV infection. [PUBLICATION ]
    Keywords: Antiviral Therapy ; Brain ; Central Nervous System ; Antibiotic ; Encephalitis
    ISSN: 0305-7453
    E-ISSN: 1460-2091
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  • 3
    In: Journal of the National Cancer Institute, Vol. 101(7), pp.441-443
    ISSN: 0027-8874
    E-ISSN: 1460-2105
    Source: Oxford University Press
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  • 4
    In: European Journal of Cardio-Thoracic Surgery, 2014, Vol. 46(5), pp.877-886
    Description: OBJECTIVES: According to the actual treatment strategies of lung cancer, the current therapeutic regimen is an individualized, multidisciplinary concept. The development of chemoresistance in the last decade represents the most important obstacle to an effective treatment. In our study, we examined a new therapeutic alternative in the treatment of multiresistant lung adenocarcinoma via siRNA-specific transfection of six crucial molecules involved in lung carcinogenesis [serum response factor(SFR), E2F1, Survivin, hypoxia inducible factor1 (HIF1), HIF2 and signal transducer and activator of transcription (STAT3)].METHODS: Three chemoresistant A549 adenocarcinoma cells were cultured under standard conditions at 37°C and 5% CO2. The chemoresistance against Vinflunine, Vinorelbine and Methotrexate was induced artificially. The A549 cells were transfected for 2 h at 37°C with specific siRNA targeting SRF, E2F1, Survivin, HIF1, HIF2 and STAT3 in a non-viral manner. The efficiency of siRNA silencing was evaluated via quantitative real-time polymerase chain reaction, whereas the surviving cells after siRNA transfection as predictor factor for tumoural growth were analysed with a CASY cell counter 3 days after transfection.RESULTS: The response of the chemotherapeutic resistant adenocarcinoma cells after siRNA transfection was concentration-dependent at both 25 and 100 nM. The CASY analysis showed a very effective suppression of adenocarcinoma cells in Vinorelbine, Vinflunine and Methotrexate groups, with significantly better results in comparison with the control group.CONCLUSIONS: In our study, we emphasized that siRNA interference might represent a productive platform for further research in order to investigate whether a new regimen in the treatment of multiresistant non-small-cell lung cancer could be established in vivo in the context of a multimodal cancer therapy.
    Keywords: Sirna ; Nsclc ; Target Molecules ; Chemoresistance ; Multimodality Concept
    ISSN: 1010-7940
    E-ISSN: 1873-734X
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  • 5
    In: Neuro-Oncology, 2014, Vol. 16(11), pp.1469-1477
    Description: BACKGROUND: Experimental findings have suggested that human cytomegalovirus (HCMV) infection of tumor cells may exert oncomodulatory effects that enhance tumor malignancy. However, controversial findings have been published on the presence of HCMV in malignant tumors. Here, we present the first study that systematically investigates HCMV infection in human nervous system tumors by highly sensitive immunohistochemistry in correlation with the HCMV serostatus of the patients.METHODS: Immunohistochemical and quantitative PCR-based methods to detect different HCMV antigens and genomic HCMV DNA were optimized prior to the investigation of pathological samples. Moreover, the pathological results were matched with the HCMV serostatus of the patients.RESULTS: HCMV immediate-early, late, and pp65 antigens could be detected in single cells from HCMV strain Hi91-infected UKF-NB-4 neuroblastoma cells after 1:1024 dilution with noninfected UKF-NB-4 cells. Genomic HCMV DNA could be detected in copy numbers as low as 430 copies/mL. However, we did not detect HCMV in tumors from a cohort of 123 glioblastoma, medulloblastoma, or neuroblastoma patients. Notably, we detected nonspecifically positive staining in tumor tissues of HCMV seropositive and seronegative glioblastoma patients. The HCMV serostatus of 67 glioblastoma patients matched the general epidemiological prevalence data for Western countries (72% of female and 57% of male glioblastoma patients were HCMV seropositive). Median survival was not significantly different in HCMV seropositive versus seronegative glioblastoma patients.CONCLUSIONS: The prevalence of HCMV-infected tumor cells may be much lower than previously reported based on highly sensitive detection methods.
    Keywords: Cytomegalovirus ; Glioma ; Oncomodulation
    ISSN: 1522-8517
    E-ISSN: 1523-5866
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  • 6
    In: Journal of the National Cancer Institute, 2009, Vol. 101(22), pp.1562-1574
    Description: Background Restoring p53 function by antagonizing its interaction with the negative regulator MDM2 is an appealing nongenotoxic approach to treating tumors with wild-type p53. Mutational inactivation of p53 is rare in neuroblastoma tumors at diagnosis and occurs in only a subset of multidrug-resistant neuroblastomas. Methods The antiproliferative and cytotoxic effect of nutlin-3, a small-molecule MDM2 antagonist, was examined in chemosensitive (UKF-NB-3) and matched chemoresistant neuroblastoma cells with wild-type p53 (UKF-NB-3r[DOX.sup.20]) or with mutant p53 (UKF-NB-[3.sup.r][VCR.sup.10]). Activation of the p53 pathway was assessed by expression analysis of p53 target genes, flow cytometric cell cycle analysis, and apoptosis assays. Mice with established chemoresistant tumor xenografts were treated orally with nutlin-3 or vehicle control (n = 5-10 mice per group) and were used to evaluate effects on tumor growth, p53 pathway activity, and metastatic tumor burden. All statistical tests were two-sided. Results Nutlin-3 induced a similar activation of the p53 pathway in UKF-NB-3 and UKF-NB-[3.sup.r][DOX.sup.20] cells, as evidenced by increased expression of p53 target genes, [G.sub.1] cell cycle arrest, and induction of apoptosis. No such response was observed in UKF-NB-[3.sup.r][VCR.sup.10] cells with mutant p53. Oral administration of nutlin-3 to UKF-NB-[3.sup.r][DOX.sup.20] xenograft-bearing mice led to inhibition of primary tumor growth (mean tumor volume after 3 weeks of treatment, nutlin-3-vs vehicle-treated mice: 772 vs 1661 [mm.sup.3], difference = 890 [mm.sup.3], 95% confidence interval = 469 to 1311 [mm.sup.3], P 〈 .001), p53 pathway activation, and reduction in the extent of metastatic disease. The growth of UKF-NB-[3.sup.r][VCR.sup.10] xenografts was unaffected by nutlin-3. Conclusions Nutlin-3 activates the p53 pathway and suppresses tumor growth in this model system of chemoresistant neuroblastoma, provided that wild-type p53 is present. J Natl Cancer Inst 2009;101:1562-1574 DOI: 10.1093/jnci/djp355 [C] The Author 2009. Published by Oxford University Press. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org. Advance Access publication on November 10, 2009.
    Keywords: Antineoplastic Agents -- Dosage And Administration ; Antineoplastic Agents -- Genetic Aspects ; Neuroblastoma -- Genetic Aspects ; Neuroblastoma -- Drug Therapy ; Neuroblastoma -- Research ; Tumor Suppressor Genes -- Physiological Aspects;
    ISSN: 0027-8874
    E-ISSN: 1460-2105
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  • 7
    In: Cardiovascular Research, 2008, Vol. 77(3), pp.544-550
    Description: AIMS: The endothelium represents a natural site of human cytomegalovirus (HCMV) infection involved in viral spreading and persistence. Moreover, HCMV infection of endothelial cells has been associated with different pathological conditions of the cardiovascular system. Here, the influence of the antiepileptic drug valproic acid (VPA) was investigated on HCMV replication in human umbilical vein endothelial cells alone or in combination with the antiviral drugs ganciclovir, cidofovir or foscarnet.METHODS AND RESULTS: HCMV replication was observed by immunostaining for viral antigens and by virus yield assay. Protein expression and phosphorylation were examined by western blot. Cell viability was assessed using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide dye reduction assay. Therapeutic VPA concentrations (〈 or =1 mM) increased HCMV immediate early antigen, late antigen, and viral titres of different endotheliotropic and non-endotheliotropic HCMV strains in a concentration- and time-dependent manner up to 30-fold. Moreover, VPA impaired the antiviral activity of the anti-HCMV drugs ganciclovir, cidofovir, and foscarnet. VPA inhibits histone deacetylases (HDAC) and induces HDAC-independently extracellular signal-regulated kinases 1/2 (ERK 1/2) phosphorylation in endothelial cells. Both effects observed, HCMV stimulation and interference with antiviral drugs, depend on HDAC inhibition but not on ERK 1/2 phosphorylation.CONCLUSION: These findings suggest to carefully monitor the frequency of HCMV reactivation in cardiovascular patients treated with VPA (or other HDAC inhibitors) in comparison to control individuals.
    Keywords: Human Cytomegalovirus ; Antiviral Therapy ; Endothelium
    ISSN: 0008-6363
    E-ISSN: 1755-3245
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  • 8
    In: Annals of Occupational Hygiene, 2008, 2008, Vol. 52(7), pp.615-622
    Description: Objectives: Our paper measures the prevalence of hepatitis B virus (HBV), hepatitis C virus (HCV) and human immunodeficiency virus (HIV) in patients at the University Hospital of Frankfurt/Main, and correlates the prevalence with risk factors for exposure to and infection of healthcare workers (HCWs). Individual risk assessments were calculated for exposed HCWs. Methods: Survey of patients admitted to a German University Hospital. Markers for HBV, HCV and HIV were studied and evaluated statistically. Data on needlestick injuries (NSIs) among HCWs were correlated with the prevalence of infectious patients. Results: The HBV, HCV and HIV prevalence among patients at the University Hospital were 5.3% ( n  = 709/13 358), 5.8% ( n  = 1167/20 163) and 4.1% ( n  = 552/13 381), respectively. Our results indicate that the prevalence of blood-borne infections in patients was about nine times higher for HBV, ∼15 times higher for HCV and ∼82 times higher for HIV than in the overall German population. The highest risk of acquiring a blood-borne infection via NSI was found in the department of internal medicine due to increased prevalence of blood-borne pathogens in patients under treatment. Conclusions: While accidental NSIs were most frequent in surgery, the nominal risk of blood-borne virus infection was greatest in the field of internal medicine. The study underlines the importance of HBV vaccinations and access to HIV-post-exposure prophylaxis for HCWs as well as the use of anti-needlestick devices.
    Keywords: Blood - Borne Viruses ; Healthcare Workers ; Occupational Infections
    ISSN: 0003-4878
    E-ISSN: 1475-3162
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  • 9
    In: FEMS Microbiology Reviews, February 2004, Vol.28(1), pp.59-77
    Description: A high frequency of human cytomegalovirus (HCMV) genome and antigens in tumor samples of patients with different malignancies is now well documented, although the causative role for HCMV in the development of the neoplasias remains to be established. HCMV infection can modulate multiple cellular regulatory and signalling pathways in a manner similar to that of oncoproteins of small DNA tumor viruses such as human papilloma virus or adenoviruses. However, in contrast to these DNA tumor viruses, HCMV infection fails to transform susceptible normal human cells. There is now growing evidence that tumor cells with disrupted regulatory and signalling pathways enable HCMV to modulate their properties including stimulation of cell proliferation, survival, invasion, production of angiogenic factors, and immunogenic properties. In contrast to previously suggested “hit and run” transformation we suggest that persistence in tumor cells is essential for HCMV to fully express its oncomodulatory effects. These effects are observed particularly in persistent HCMV infection and are mediated mainly by activity of HCMV regulatory proteins. In persistently HCMV‐infected tumor cell lines – a selection of novel, slowly growing virus variants with changes in coding sequences for virus regulatory proteins takes place. As a result, oncomodulatory effects of HCMV infection may lead to a shift to more malignant phenotype of tumor cells contributing to tumor progression.
    Keywords: Human Cytomegalovirus ; Oncomodulation ; Tumor ; Dna‐Virus ; Apoptosis ; Angiogenesis
    ISSN: 0168-6445
    E-ISSN: 1574-6976
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