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7 results on '"Junghanss, Christian"'

1. Evaluation of the Synergistic Potential of Simultaneous Pan- or Isoform-Specific BET and SYK Inhibition in B-Cell Lymphoma: An In Vitro Approach

Author

Sender, Sina, primary, Sultan, Ahmad Wael, additional, Palmer, Daniel, additional, Koczan, Dirk, additional, Sekora, Anett, additional, Beck, Julia, additional, Schuetz, Ekkehard, additional, Taher, Leila, additional, Brenig, Bertram, additional, Fuellen, Georg, additional, Junghanss, Christian, additional, and Murua Escobar, Hugo, additional

Published
2022
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2. Inhibition of KRAS, MEK and PI3K Demonstrate Synergistic Anti-Tumor Effects in Pancreatic Ductal Adenocarcinoma Cell Lines

Author

Ma, Yixuan, primary, Schulz, Benjamin, additional, Trakooljul, Nares, additional, Al Ammar, Moosheer, additional, Sekora, Anett, additional, Sender, Sina, additional, Hadlich, Frieder, additional, Zechner, Dietmar, additional, Weiss, Frank, additional, Lerch, Markus, additional, Jaster, Robert, additional, Junghanss, Christian, additional, and Murua Escobar, Hugo, additional

Published
2022
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3. Preclinical Head and Neck Squamous Cell Carcinoma Models for Combined Targeted Therapy Approaches

Author

Schoenwaelder, Nina, primary, Krause, Mareike, additional, Freitag, Thomas, additional, Schneider, Björn, additional, Zonnur, Sarah, additional, Zimpfer, Annette, additional, Becker, Anne Sophie, additional, Salewski, Inken, additional, Strüder, Daniel Fabian, additional, Lemcke, Heiko, additional, Grosse-Thie, Christina, additional, Junghanss, Christian, additional, and Maletzki, Claudia, additional

Published
2022
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4. Longitudinal Humoral and Cellular Immune Responses Following SARS-CoV-2 Vaccination in Patients with Myeloid and Lymphoid Neoplasms Compared to a Reference Cohort: Results of a Prospective Trial of the East German Study Group for Hematology and Oncology (OSHO)

Author

Jotschke, Sabrina, primary, Schulze, Susann, additional, Jaekel, Nadja, additional, Ludwig-Kraus, Beatrice, additional, Engelmann, Robby, additional, Kraus, Frank Bernhard, additional, Zahn, Christina, additional, Nedlitz, Nicole, additional, Prange-Krex, Gabriele, additional, Mohm, Johannes, additional, Peuser, Bettina, additional, Schwarz, Maik, additional, Spohn, Claudia, additional, Behlendorf, Timo, additional, Binder, Mascha, additional, Junghanss, Christian, additional, Böttcher, Sebastian, additional, and Al-Ali, Haifa Kathrin, additional

Published
2022
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6. The Individual Effects of Cyclin-Dependent Kinase Inhibitors on Head and Neck Cancer Cells—A Systematic Analysis

Author

Schoenwaelder, Nina, primary, Salewski, Inken, additional, Engel, Nadja, additional, Krause, Mareike, additional, Schneider, Björn, additional, Müller, Michael, additional, Riess, Christin, additional, Lemcke, Heiko, additional, Skorska, Anna, additional, Grosse-Thie, Christina, additional, Junghanss, Christian, additional, and Maletzki, Claudia, additional

Published
2021
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7. Unraveling the Heterogeneous Mutational Signature of Spontaneously Developing Tumors in MLH1−/− Mice.

Author

Gladbach, Yvonne Saara, Wiegele, Leonie, Hamed, Mohamed, Merkenschläger, Anna-Marie, Fuellen, Georg, Junghanss, Christian, and Maletzki, Claudia

Subjects
TUMOR genetics, ANIMAL experimentation, BIOLOGICAL models, GENOMES, MICE, GENETIC mutation, TRANSCRIPTION factors, NUCLEAR proteins, NEOPLASTIC cell transformation
Abstract

Mismatch repair deficient (MMR-D) tumors exemplify the prototypic hypermutator phenotype. Owing to the high mutation rates, plenty of neo-antigens are present on the tumor cells' surface, ideally shared among different cancer types. The MLH1 knock out mouse represents a preclinical model that resembles features of the human MMR-D counterpart. While these mice develop neoplasias in a sequential twin-peaked manner (lymphomas > gastrointestinal tumors (GIT)) we aimed at identification of underlying molecular mechanisms. Using whole-genome sequencing, we focused on (I) shared and (II) mutually exclusive mutations and describe the process of ongoing mutational events in tumor-derived cell cultures. The landscape of MLH1−/− tumors is heterogeneous with only a few shared mutations being detectable among different tumor entities (ARID1A and IDH2). With respect to coding microsatellite analysis of MMR-D-related target genes, partial overlap was detectable, yet recognizing shared antigens. The present study is the first reporting results of a comparison between spontaneously developing tumors in MMR-D driven tumorigenesis. Additionally to identifying ARID1A as potential causative mutation hotspot, this comprehensive characterization of the mutational landscape may be a good starting point to refine therapeutic concepts. [ABSTRACT FROM AUTHOR]

Published
2019
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