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Your search keyword '"Buchberger, Elisabeth"' showing total 22 results
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22 results on '"Buchberger, Elisabeth"'

7. Inhibition of the transcriptional repressor complex Bcl-6/BCoR induces endothelial sprouting but does not promote tumor growth

Author

Buchberger, Elisabeth, primary, Payrhuber, Dietmar, additional, Harchi, Miriam El, additional, Zagrapan, Branislav, additional, Scheuba, Katharina, additional, Zommer, Anna, additional, Bugyik, Edina, additional, Dome, Balazs, additional, Kral, Julia Barbara, additional, Schrottmaier, Waltraud Cornelia, additional, Schabbauer, Gernot, additional, Petzelbauer, Peter, additional, Gröger, Marion, additional, Bilban, Martin, additional, and Brostjan, Christine, additional

Published
2016
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8. The VEGF rise in blood of bevacizumab patients is not based on tumor escape but a host-blockade of VEGF clearance

Author

Alidzanovic, Lejla, primary, Starlinger, Patrick, additional, Schauer, Dominic, additional, Maier, Thomas, additional, Feldman, Alexandra, additional, Buchberger, Elisabeth, additional, Stift, Judith, additional, Koeck, Ulrike, additional, Pop, Lorand, additional, Gruenberger, Birgit, additional, Gruenberger, Thomas, additional, and Brostjan, Christine, additional

Published
2016
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9. Botulinum Toxin A

Author

Gugerell, Alfred, primary, Kober, Johanna, additional, Schmid, Melanie, additional, Buchberger, Elisabeth, additional, Kamolz, Lars-Peter, additional, and Keck, Maike, additional

Published
2016
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11. Chemotherapy of colorectal liver metastases induces a rapid rise in intermediate blood monocytes which predicts treatment response

Author

Schauer, Dominic, primary, Starlinger, Patrick, additional, Alidzanovic, Lejla, additional, Zajc, Philipp, additional, Maier, Thomas, additional, Feldman, Alexandra, additional, Padickakudy, Robin, additional, Buchberger, Elisabeth, additional, Elleder, Vanessa, additional, Spittler, Andreas, additional, Stift, Judith, additional, Pop, Lorand, additional, Gruenberger, Birgit, additional, Gruenberger, Thomas, additional, and Brostjan, Christine, additional

Published
2016
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12. Levosimendan exerts anti-inflammatory effects on cardiac myocytes and endothelial cells in vitro

Author

Krychtiuk, Konstantin A., primary, Watzke, Lukas, primary, Kaun, Christoph, primary, Buchberger, Elisabeth, primary, Hofer-Warbinek, Renate, primary, Demyanets, Svitlana, primary, Pisoni, Julia, primary, Kastl, Stefan P., primary, Rauscher, Sabine, primary, Gröger, Marion, primary, Aliabadi, Arezu, primary, Zuckermann, Andreas, primary, Maurer, Gerald, primary, Martin, Rainer de, primary, Huber, Kurt, primary, Speidl, Walter S., primary, and Wojta, Johann, additional

Published
2015
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13. Neutralizing Type I Interferon Antibodies trigger an Interferon-Like Response in Endothelial Cells1

Author

Moll, Herwig Peter, Freudenthaler, Harald, Zommer, Anna, Buchberger, Elisabeth, and Brostjan, Christine

Subjects
Immunoglobulin Fab Fragments, Gene Expression Regulation, immune system diseases, Interferon Type I, Cell Culture Techniques, Endothelial Cells, Humans, Receptor, Interferon alpha-beta, skin and connective tissue diseases, Article, Antibodies, Interferon-Stimulated Gene Factor 3, gamma Subunit
Abstract

Neutralizing Abs to type I IFNs are of therapeutic significance, i.e., are currently evaluated for the treatment of autoimmune diseases with pathogenic IFN-alpha production such as for systemic lupus erythematosus. Unexpectedly, we observed that several neutralizing Abs reportedly known to counteract IFN-alpha or IFN-beta activity triggered an "IFN-like" response in quiescent primary human endothelial cells leading to activation of the transcription factor IFN-stimulated gene factor 3 and the expression of IFN-responsive genes. Furthermore, these Abs were found to enhance rather than inhibit type I IFN signals, and the effect was also detectable for distinct other cell types such as PBMCs. The stimulatory capacity of anti-IFN-alpha/beta Abs was mediated by the constitutive autocrine production of "subthreshold" IFN levels, involved the type I IFNR and was dependent on the Fc Ab domain, as Fab or F(ab')(2) fragments potently inhibited IFN activity. We thus propose that a combined effect of IFN recognition by the Ab paratope and the concomitant engagement of the Fc domain may trigger an IFN signal via the respective type I IFNR, which accounts for the observed IFN-like response to the neutralizing Abs. With respect to clinical applications, the finding may be of importance for the design of recombinant Abs vs Fab or F(ab')(2) fragments to efficiently counteract IFN activity without undesirable activating effects.

Published
2008

18. Intermediate Monocytes but Not TIE2-Expressing Monocytes Are a Sensitive Diagnostic Indicator for Colorectal Cancer

Author

Schauer, Dominic, primary, Starlinger, Patrick, additional, Reiter, Christian, additional, Jahn, Nikolaus, additional, Zajc, Philipp, additional, Buchberger, Elisabeth, additional, Bachleitner-Hofmann, Thomas, additional, Bergmann, Michael, additional, Stift, Anton, additional, Gruenberger, Thomas, additional, and Brostjan, Christine, additional

Published
2012
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22. Inhibition of the transcriptional repressor complex Bcl-6/BCoR induces endothelial sprouting but does not promote tumor growth.

Author

Buchberger E, Payrhuber D, El Harchi M, Zagrapan B, Scheuba K, Zommer A, Bugyik E, Dome B, Kral JB, Schrottmaier WC, Schabbauer G, Petzelbauer P, Gröger M, Bilban M, and Brostjan C

Subjects
Animals, Cell Cycle, Cell Line, Cell Proliferation, Disease Models, Animal, Gene Expression, Gene Expression Regulation, Neoplastic, Gene Silencing, Heterografts, Humans, Mice, Neoplasms genetics, Neovascularization, Pathologic, Protein Binding, Proto-Oncogene Proteins genetics, Proto-Oncogene Proteins c-bcl-6 antagonists & inhibitors, Proto-Oncogene Proteins c-bcl-6 genetics, RNA, Messenger genetics, Receptors, Notch metabolism, Repressor Proteins genetics, Signal Transduction, Endothelial Cells metabolism, Neoplasms metabolism, Neoplasms pathology, Proto-Oncogene Proteins metabolism, Proto-Oncogene Proteins c-bcl-6 metabolism, Repressor Proteins metabolism
Abstract

The oncogenic potential of the transcriptional repressor Bcl-6 (B-cell lymphoma 6) was originally discovered in non-Hodgkin patients and the soluble Bcl-6 inhibitor 79-6 was developed to treat diffuse large B-cell lymphomas with aberrant Bcl-6 expression. Since we found Bcl-6 and its co-repressor BCoR (Bcl-6 interacting co-repressor) to be regulated in human microvascular endothelium by colorectal cancer cells, we investigated their function in sprouting angiogenesis which is central to tumor growth. Based on Bcl-6/BCoR gene silencing we found that the transcriptional repressor complex in fact constitutes an endogenous inhibitor of vascular sprouting by supporting the stalk cell phenotype: control of Notch target genes (HES1, HEY1, DLL4) and cell cycle regulators (cyclin A and B1). Thus, when endothelial cells were transiently transfected with Bcl-6 and/or BCoR siRNA, vascular sprouting was prominently induced. Comparably, when the soluble Bcl-6 inhibitor 79-6 was applied in the mouse retina model of physiological angiogenesis, endothelial sprouting and branching were significantly enhanced. To address the question whether clinical treatment with 79-6 might therefore have detrimental therapeutic effects by promoting tumor angiogenesis, mouse xenograft models of colorectal cancer and diffuse large B-cell lymphoma were tested. Despite a tendency to increased tumor vessel density, 79-6 therapy did not enhance tumor expansion. In contrast, growth of colorectal carcinomas was significantly reduced which is likely due to a combined 79-6 effect on cancer cells and tumor stroma. These findings may provide valuable information regarding the future clinical development of Bcl-6 inhibitors.

Published
2017
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