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23 results on '"Sebens, Susanne"'

1. Epithelial and Mesenchymal-like Pancreatic Cancer Cells Exhibit Different Stem Cell Phenotypes Associated with Different Metastatic Propensities

Author

Philipp, Lisa-Marie, primary, Yesilyurt, Umut-Ulas, additional, Surrow, Arne, additional, Künstner, Axel, additional, Mehdorn, Anne-Sophie, additional, Hauser, Charlotte, additional, Gundlach, Jan-Paul, additional, Will, Olga, additional, Hoffmann, Patrick, additional, Stahmer, Lea, additional, Franzenburg, Sören, additional, Knaack, Hendrike, additional, Schumacher, Udo, additional, Busch, Hauke, additional, and Sebens, Susanne, additional

Published
2024
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2. Epithelial and Mesenchymal Pancreatic Cancer Cells Exhibit Different Stem Cell Phenotypes Being Associated with Different Metastatic Propensity

Author

Philipp, Lisa-Marie, primary, Yesilyurt, Umut-Ulas, additional, Surrow, Arne, additional, Künstner, Axel, additional, Mehdorn, Anne-Sophie, additional, Hauser, Charlotte, additional, Gundlach, Jan-Paul, additional, Will, Olga, additional, Hoffmann, Patrick, additional, Stahmer, Lea, additional, Franzenburg, Sören, additional, Knaack, Hendrike, additional, Schumacher, Udo, additional, Busch, Hauke, additional, and Sebens, Susanne, additional

Published
2023
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3. Monocarboxylate Transporter-1 (MCT1)-Mediated Lactate Uptake Protects Pancreatic Adenocarcinoma Cells from Oxidative Stress during Glutamine Scarcity Thereby Promoting Resistance against Inhibitors of Glutamine Metabolism

Author

Ammar, Nourhane, primary, Hildebrandt, Maya, additional, Geismann, Claudia, additional, Röder, Christian, additional, Gemoll, Timo, additional, Sebens, Susanne, additional, Trauzold, Ania, additional, and Schäfer, Heiner, additional

Published
2023
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4. Combining Solid and Liquid Biopsy for Therapy Monitoring in Esophageal Cancer

Author

Richter, Florian, primary, Henssen, Clara, additional, Steiert, Tim Alexander, additional, Meissner, Tobias, additional, Mehdorn, Anne-Sophie, additional, Röcken, Christoph, additional, Franke, Andre, additional, Egberts, Jan-Hendrik, additional, Becker, Thomas, additional, Sebens, Susanne, additional, and Forster, Michael, additional

Published
2023
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5. Sequential Treatment with Temozolomide Plus Naturally Derived AT101 as an Alternative Therapeutic Strategy: Insights into Chemoresistance Mechanisms of Surviving Glioblastoma Cells

Author

Hellmold, Dana, primary, Kubelt, Carolin, additional, Daunke, Tina, additional, Beckinger, Silje, additional, Janssen, Ottmar, additional, Hauck, Margarethe, additional, Schütt, Fabian, additional, Adelung, Rainer, additional, Lucius, Ralph, additional, Haag, Jochen, additional, Sebens, Susanne, additional, Synowitz, Michael, additional, and Held-Feindt, Janka, additional

Published
2023
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6. Biomarkers in Liquid Biopsies for Prediction of Early Liver Metastases in Pancreatic Cancer

Author

Mehdorn, Anne-Sophie, primary, Gemoll, Timo, additional, Busch, Hauke, additional, Kern, Katharina, additional, Beckinger, Silje, additional, Daunke, Tina, additional, Kahlert, Christoph, additional, Uzunoglu, Faik G., additional, Hendricks, Alexander, additional, Buertin, Florian, additional, Wittel, Uwe A., additional, Sunami, Yoshiaki, additional, Röcken, Christoph, additional, Becker, Thomas, additional, and Sebens, Susanne, additional

Published
2022
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7. Paracrine Interaction of Cholangiocellular Carcinoma with Cancer-Associated Fibroblasts and Schwann Cells Impact Cell Migration

Author

Gundlach, Jan-Paul, primary, Kerber, Jannik, additional, Hendricks, Alexander, additional, Bernsmeier, Alexander, additional, Halske, Christine, additional, Röder, Christian, additional, Becker, Thomas, additional, Röcken, Christoph, additional, Braun, Felix, additional, Sebens, Susanne, additional, and Heits, Nils, additional

Published
2022
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9. Detection of Cancer Mutations by Urine Liquid Biopsy as a Potential Tool in the Clinical Management of Bladder Cancer Patients

Author

Ibrahim, Nurul Khalida, primary, Eraky, Ahmed, additional, Eggers, Jan, additional, Steiert, Tim Alexander, additional, Sebens, Susanne, additional, Jünemann, Klaus-Peter, additional, Hendricks, Alexander, additional, Bang, Corinna, additional, Stanulla, Martin, additional, Franke, Andre, additional, Hamann, Claudius, additional, Röcken, Christoph, additional, Arnold, Norbert, additional, Hinze, Laura, additional, and Forster, Michael, additional

Published
2022
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12. Programmed Death-Ligand 1 (PD-L1) Expression Is Induced by Insulin in Pancreatic Ductal Adenocarcinoma Cells Pointing to Its Role in Immune Checkpoint Control

Author

Heckl, Steffen M., Mau, Franziska, Senftleben, Anke, Daunke, Tina, Beckinger, Silje, Abdullazade, Samir, Schreiber, Stefan, Röcken, Christoph, Sebens, Susanne, and Schäfer, Heiner

Subjects
endocrine system diseases, T-cells, Article, B7-H1 Antigen, Pancreatic Neoplasms, diabetes mellitus, hyperinsulinemia, Humans, Insulin, Medicine, RNA, Small Interfering, carcinogenesis, signal transduction, Carcinoma, Pancreatic Ductal
Abstract

Simple Summary Type-2 Diabetes is an established risk factor of pancreatic cancer, yet the exact modalities as well as the contribution of hyperinsulinemia are not fully understood. In our study, we explored a possible link between insulin and the immune evasion of pancreatic cancer cells. We could demonstrate that insulin is able to induce expression of Programmed Death-Ligand 1 (PD-L1) representing a key molecule in immune checkpoint control. This effect of insulin greatly depends on insulin receptor-A and/or IGF-receptor-induced ERK signaling and is enhanced via a crosstalk with EGF. Through insulin-induced PD-L1 expression, pancreatic cancer cells suppress proliferation of CD8+ T-cells underscoring the potential of insulin to confer immune evasion through this immune checkpoint regulator. Furthermore, some cases out of a cohort of pancreatic cancer patients reveal coexpression of PD-L1 and the cytoplasmic insulin receptor in the tumor tissue as shown by immunohistochemistry. Abstract Type-2 diabetes (T2DM) is a risk factor for the development of pancreatic ductal adenocarcinoma (PDAC) and is characterized by insulin resistance and hyperinsulinemia. Besides the well-known growth-promoting activity of insulin or the other members of the Insulin/Insulin-like Growth factor (IGF) axis, we here describe an inducing effect of insulin on PD-L1 expression in PDAC cells. Treatment of the PDAC cell lines BxPc3, A818-6, and T3M4 with insulin increased PD-L1 expression in a time- and dose dependent fashion, as shown by Western blot and qPCR analysis. siRNA mediated knock-down showed that the effects of insulin on PD-L1 depend on the insulin and IGF receptors (InsR and IGFR, respectively). In addition, a crosstalk of insulin-induced ERK activation and Epidermal Growth Factor (EGF) triggered PD-L1 expression. This involves different mechanisms in the three cell lines including upregulation of InsR-A expression in A818-6 and modulation of the adaptor protein Gab1 in BxPc3 cells. As a consequence of the insulin-induced PD-L1 expression, PDAC cells suppress the proliferation of activated human CD8+ T-cells in coculture experiments. The suppression of CD8+ cell proliferation by insulin-pretreated PDAC cells was reversed by PD-1 blockade with Pembrolizumab or by PD-L1 siRNA. Furthermore, the clinical relevance of these observations was supported by detecting a coexpression of cytoplasmic InsR (characteristic for its activation) and PD-L1 in tumor tissues from PDAC patients. Our findings provide a novel insight into the protumorigenic role of insulin in PDAC. Recognizing the impact of insulin on PD-L1 expression as part of the immune privilege, strategies to interfere with this mechanism could pave the way towards a more efficient immunotherapy of PDAC.

Published
2021

15. Initiation of Pancreatic Cancer: The Interplay of Hyperglycemia and Macrophages Promotes the Acquisition of Malignancy-Associated Properties in Pancreatic Ductal Epithelial Cells

Author

Otto, Lilli, primary, Rahn, Sascha, additional, Daunke, Tina, additional, Walter, Frederik, additional, Winter, Elsa, additional, Möller, Julia Luisa, additional, Rose-John, Stefan, additional, Wesch, Daniela, additional, Schäfer, Heiner, additional, and Sebens, Susanne, additional

Published
2021
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16. ADAM17 Inhibition Increases the Impact of Cisplatin Treatment in Ovarian Cancer Spheroids

Author

Hedemann, Nina, primary, Herz, Andreas, additional, Schiepanski, Jan Hendrik, additional, Dittrich, Jan, additional, Sebens, Susanne, additional, Dempfle, Astrid, additional, Feuerborn, Julia, additional, Rogmans, Christoph, additional, Tribian, Nils, additional, Flörkemeier, Inken, additional, Weimer, Jörg, additional, Krüger, Sandra, additional, Maass, Nicolai, additional, and Bauerschlag, Dirk O., additional

Published
2021
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20. Inflammation Associated Pancreatic Tumorigenesis: Upregulation of Succinate Dehydrogenase (Subunit B) Reduces Cell Growth of Pancreatic Ductal Epithelial Cells

Author

Rahn, Sascha, primary, Dänzer Barbosa, Philippe, additional, Möller, Julia Luisa, additional, Ammar, Nourhane, additional, Demetrowitsch, Tobias, additional, Helm, Ole, additional, Wesch, Daniela, additional, Sipos, Bence, additional, Röcken, Christoph, additional, Schwarz, Karin, additional, Schäfer, Heiner, additional, and Sebens, Susanne, additional

Published
2019
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21. The Hepatic Microenvironment and TRAIL-R2 Impact Outgrowth of Liver Metastases in Pancreatic Cancer after Surgical Resection

Author

Miarka, Lauritz, primary, Hauser, Charlotte, additional, Helm, Ole, additional, Holdhof, Dörthe, additional, Beckinger, Silje, additional, Egberts, Jan-Hendrik, additional, Gundlach, Jan-Paul, additional, Lenk, Lennart, additional, Rahn, Sascha, additional, Mikulits, Wolfgang, additional, Trauzold, Anna, additional, and Sebens, Susanne, additional

Published
2019
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23. Analysis of Single- and Double-Stranded DNA Damage in Osteoblastic Cells after Hyperbaric Oxygen Exposure.

Author

Schönrock N, Tillmans F, Sebens S, Kähler W, Klapa S, Rieger B, Scherthan H, and Koch A

Abstract

(1) Background: Hyperbaric oxygen (HBO) exposure induces oxidative stress that may lead to DNA damage, which has been observed in human peripheral blood lymphocytes or non-human cells. Here, we investigated the impact of hyperbaric conditions on two human osteoblastic cell lines: primary human osteoblasts, HOBs, and the osteogenic tumor cell line SAOS-2. (2) Methods: Cells were exposed to HBO in an experimental hyperbaric chamber (4 ATA, 100% oxygen, 37 °C, and 4 h) or sham-exposed (1 ATA, air, 37 °C, and 4 h). DNA damage was examined before, directly after, and 24 h after exposure with an alkaline comet assay and detection of γH2AX+53BP1 colocalizing double-strand break (DSB) foci and apoptosis. The gene expression of TGFß-1, HO-1, and NQO1, involved in antioxidative functions, was measured with qRT-PCR. (3) Results: The alkaline comet assay showed significantly elevated levels of DNA damage in both cell lines after 4 h of HBO, while the DSB foci were similar to sham. γH2AX analysis indicated a slight increase in apoptosis in both cell lines. The increased expression of HO-1 in HOB and SAOS-2 directly after exposure suggested the induction of an antioxidative response in these cells. Additionally, the expression of TGF-ß1 was negatively affected in HOB cells 4 h after exposure. (4) Conclusions: in summary, this study indicates that osteoblastic cells are sensitive to the DNA-damaging effects of hyperbaric hyperoxia, with the HBO-induced DNA damage consisting largely of single-strand DNA breaks that are rapidly repaired.

Published
2023
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