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Your search keyword '"Weiss, Christel"' showing total 8 results
Start Over Author "Weiss, Christel" Journal international journal of molecular sciences
8 results on '"Weiss, Christel"'

1. Different Involvement of Vimentin during Invasion by Listeria monocytogenes at the Blood–Brain and the Blood–Cerebrospinal Fluid Barriers In Vitro

Author

Banovic, Franjo, primary, Schulze, Sandrin, additional, Abu Mraheil, Mobarak, additional, Hain, Torsten, additional, Chakraborty, Trinad, additional, Orian-Rousseau, Véronique, additional, Moroniak, Selina, additional, Weiss, Christel, additional, Ishikawa, Hiroshi, additional, Schroten, Horst, additional, Adam, Rüdiger, additional, and Schwerk, Christian, additional

Published
2022
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3. Proteins Marking the Sequence of Genotoxic Signaling from Irradiated Mesenchymal Stromal Cells to CD34+ Cells

Author

Kohl, Vanessa, primary, Drews, Oliver, additional, Costina, Victor, additional, Bierbaum, Miriam, additional, Jawhar, Ahmed, additional, Roehl, Henning, additional, Weiss, Christel, additional, Brendel, Susanne, additional, Kleiner, Helga, additional, Flach, Johanna, additional, Spiess, Birgit, additional, Seifarth, Wolfgang, additional, Nowak, Daniel, additional, Hofmann, Wolf-Karsten, additional, Fabarius, Alice, additional, and Popp, Henning D., additional

Published
2021
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4. Adverse Prognostic Impact of the KIT D816V Transcriptional Activity in Advanced Systemic Mastocytosis

Author

Naumann, Nicole, primary, Lübke, Johannes, additional, Baumann, Sofie, additional, Schwaab, Juliana, additional, Hoffmann, Oliver, additional, Kreil, Sebastian, additional, Dangelo, Vito, additional, Reiter, Lukas, additional, Bugert, Peter, additional, Kristensen, Thomas, additional, Sotlar, Karl, additional, Haselmann, Verena, additional, Schneider, Sven, additional, Metzgeroth, Georgia, additional, Weiss, Christel, additional, Popp, Henning D., additional, Fabarius, Alice, additional, Hofmann, Wolf-Karsten, additional, Cross, Nicholas C. P., additional, Reiter, Andreas, additional, and Jawhar, Mohamad, additional

Published
2021
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6. The Impact of Small Extracellular Vesicles on Lymphoblast Trafficking across the Blood-Cerebrospinal Fluid Barrier In Vitro

Author

Erb, Ulrike, primary, Hikel, Julia, additional, Meyer, Svenja, additional, Ishikawa, Hiroshi, additional, Worst, Thomas S., additional, Nitschke, Katja, additional, Nuhn, Philipp, additional, Porubsky, Stefan, additional, Weiss, Christel, additional, Schroten, Horst, additional, Adam, Rüdiger, additional, and Karremann, Michael, additional

Published
2020
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7. Individual Assessment of Brain Tissue Changes in MS and the Effect of Focal Lesions on Short-Term Focal Atrophy Development in MS: A Voxel-Guided Morphometry Study

Author

Fox, Jan, primary, Kraemer, Matthias, additional, Schormann, Thorsten, additional, Dabringhaus, Andreas, additional, Hirsch, Jochen, additional, Eisele, Philipp, additional, Szabo, Kristina, additional, Weiss, Christel, additional, Amann, Michael, additional, Weier, Katrin, additional, Naegelin, Yvonne, additional, Kappos, Ludwig, additional, and Gass, Achim, additional

Published
2016
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8. DNA Damage and DNA Damage Response in Chronic Myeloid Leukemia.

Author

Popp, Henning D., Kohl, Vanessa, Naumann, Nicole, Flach, Johanna, Brendel, Susanne, Kleiner, Helga, Weiss, Christel, Seifarth, Wolfgang, Saussele, Susanne, Hofmann, Wolf-Karsten, and Fabarius, Alice

Subjects
DNA repair, CHRONIC myeloid leukemia, DNA damage, DASATINIB, DOUBLE-strand DNA breaks, BLOOD testing
Abstract

DNA damage and alterations in the DNA damage response (DDR) are critical sources of genetic instability that might be involved in BCR-ABL1 kinase-mediated blastic transformation of chronic myeloid leukemia (CML). Here, increased DNA damage is detected by γH2AX foci analysis in peripheral blood mononuclear cells (PBMCs) of de novo untreated chronic phase (CP)-CML patients (n = 5; 2.5 γH2AX foci per PBMC ± 0.5) and blast phase (BP)-CML patients (n = 3; 4.4 γH2AX foci per PBMC ± 0.7) as well as CP-CML patients with loss of major molecular response (MMR) (n = 5; 1.8 γH2AX foci per PBMC ± 0.4) when compared to DNA damage in PBMC of healthy donors (n = 8; 1.0 γH2AX foci per PBMC ± 0.1) and CP-CML patients in deep molecular response or MMR (n = 26; 1.0 γH2AX foci per PBMC ± 0.1). Progressive activation of erroneous non-homologous end joining (NHEJ) repair mechanisms during blastic transformation in CML is indicated by abundant co-localization of γH2AX/53BP1 foci, while a decline of the DDR is suggested by defective expression of (p-)ATM and (p-)CHK2. In summary, our data provide evidence for the accumulation of DNA damage in the course of CML and suggest ongoing DNA damage, erroneous NHEJ repair mechanisms, and alterations in the DDR as critical mediators of blastic transformation in CML. [ABSTRACT FROM AUTHOR]

Published
2020
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