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24 results on '"Gundlach, Jan-Paul"'

3. 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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4. Liver transplantation for HCC in cirrhosis: Are Milan criteria outdated?

Author

Linecker, Michael, primary, Braun, Felix, primary, Gundlach, Jan-Paul, additional, Ellrichmann, Mark, additional, van Rosmalen, Marieke, additional, Vogelaar, Serge, additional, Eimer, Christine, additional, Rheinbay, Corinna, additional, Rösgen, Sabina, additional, Schäfer, Jost-Philipp, additional, and Becker, Thomas, additional

Published
2024
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5. 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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6. Do surgical tumour resection and chemotherapy lead to liver inflammation and outgrowth of liver metastases? Insights from a clinically adapted pancreatic cancer mouse model

Author

Baumann, Leon, primary, Kayser, Charlotte, additional, Hauser, Charlotte, additional, Gundlach, Jan-Paul, additional, Beckinger, Silje, additional, Daunke, Tina, additional, Rahn, Sascha, additional, Röcken, Christoph, additional, Behrens, Hans-Michael, additional, Mehdorn, Anne-Sophie, additional, and Sebens, Susanne, additional

Published
2023
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11. 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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12. Phosphatidylethanol (PEth) for Monitoring Sobriety in Liver Transplant Candidates: Preliminary Results of Differences Between Alcohol-Related and Non-Alcohol-Related Cirrhosis Candidates

Author

Gundlach, Jan-Paul, primary, Braun, Felix, additional, Mötter, Finn, additional, Bernsmeier, Alexander, additional, Barrio, Pablo, additional, Ehmke, Nicola, additional, Günther, Rainer, additional, Hinrichsen, Holger, additional, Becker, Thomas, additional, Weinmann, Wolfgang, additional, Schröck, Alexandra, additional, Yegles, Michel, additional, and Wurst, Friedrich Martin, additional

Published
2022
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14. Indication of Liver Transplantation for Hepatocellular Carcinoma Should Be Reconsidered in Case of Microvascular Invasion and Multilocular Tumor Occurrence

Author

Gundlach, Jan-Paul, primary, Schmidt, Stephan, additional, Bernsmeier, Alexander, additional, Günther, Rainer, additional, Kataev, Victor, additional, Trentmann, Jens, additional, Schäfer, Jost Philipp, additional, Röcken, Christoph, additional, Becker, Thomas, additional, and Braun, Felix, additional

Published
2021
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15. Inferior Vena Cava Constriction After Liver Transplantation Is a Severe Complication Requiring Individually Adapted Treatment: Report of a Single-Center Experience

Author

Gundlach, Jan-Paul, primary, Günther, Rainer, additional, Both, Marcus, additional, Trentmann, Jens, additional, Schäfer, Jost Philipp, additional, Cremer, Jochen T., additional, Röcken, Christoph, additional, Becker, Thomas, additional, Braun, Felix, additional, and Bernsmeier, Alexander, additional

Published
2020
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17. 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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18. Drug Repositioning Inferred from E2F1-Coregulator Interactions Studies for the Prevention and Treatment of Metastatic Cancers

Author

Goody, Deborah, primary, Gupta, Shailendra K., additional, Engelmann, David, additional, Spitschak, Alf, additional, Marquardt, Stephan, additional, Mikkat, Stefan, additional, Meier, Claudia, additional, Hauser, Charlotte, additional, Gundlach, Jan-Paul, additional, Egberts, Jan-Hendrik, additional, Martin, Hubert, additional, Schumacher, Toni, additional, Trauzold, Anna, additional, Wolkenhauer, Olaf, additional, Logotheti, Stella, additional, and Pützer, Brigitte M., additional

Published
2019
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19. Liver metastasis of pancreatic cancer: the hepatic microenvironment impacts differentiation and self-renewal capacity of pancreatic ductal epithelial cells

Author

Knaack, Hendrike, primary, Lenk, Lennart, additional, Philipp, Lisa-Marie, additional, Miarka, Lauritz, additional, Rahn, Sascha, additional, Viol, Fabrice, additional, Hauser, Charlotte, additional, Egberts, Jan-Hendrik, additional, Gundlach, Jan-Paul, additional, Will, Olga, additional, Tiwari, Sanjay, additional, Mikulits, Wolfgang, additional, Schumacher, Udo, additional, Hengstler, Jan G., additional, and Sebens, Susanne, additional

Published
2018
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20. The hepatic microenvironment essentially determines tumor cell dormancy and metastatic outgrowth of pancreatic ductal adenocarcinoma

Author

Lenk, Lennart, primary, Pein, Maren, additional, Will, Olga, additional, Gomez, Beatriz, additional, Viol, Fabrice, additional, Hauser, Charlotte, additional, Egberts, Jan-Hendrik, additional, Gundlach, Jan-Paul, additional, Helm, Ole, additional, Tiwari, Sanjay, additional, Weiskirchen, Ralf, additional, Rose-John, Stefan, additional, Röcken, Christoph, additional, Mikulits, Wolfgang, additional, Wenzel, Patrick, additional, Schneider, Günter, additional, Saur, Dieter, additional, Schäfer, Heiner, additional, and Sebens, Susanne, additional

Published
2017
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22. NF-κB Dependent Chemokine Signaling in Pancreatic Cancer.

Author

Geismann, Claudia, Schäfer, Heiner, Gundlach, Jan-Paul, Hauser, Charlotte, Egberts, Jan-Hendrik, Schneider, Günter, and Arlt, Alexander

Subjects
APOPTOSIS, CELLULAR signal transduction, CHEMOKINES, DRUG resistance in cancer cells, GENE expression, ONCOGENES, PANCREATIC tumors, TRANSCRIPTION factors, DNA-binding proteins
Abstract

Pancreatic cancer is one of the carcinomas with the worst prognoses, as shown by its five-year survival rate of 9%. Although there have been new therapeutic innovations, the effectiveness of these therapies is still limited, resulting in pancreatic ductal adenocarcinoma (PDAC) becoming the second leading cause of cancer-related death in 2020 in the US. In addition to tumor cell intrinsic resistance mechanisms, this disease exhibits a complex stroma consisting of fibroblasts, immune cells, neuronal and vascular cells, along with extracellular matrix, all conferring therapeutic resistance by several mechanisms. The NF-κB pathway is involved in both the tumor cell-intrinsic and microenvironment-mediated therapeutic resistance by regulating the transcription of a plethora of target genes. These genes are involved in nearly all scenarios described as the hallmarks of cancer. In addition to classical regulators of apoptosis, NF-κB regulates the expression of chemokines and their receptors, both in the tumor cells and in cells of the microenvironment. These chemokines mediate autocrine and paracrine loops among tumor cells but also cross-signaling between tumor cells and the stroma. In this review, we will focus on NF-κB-mediated chemokine signaling, with an emphasis on therapy resistance in pancreatic cancer. [ABSTRACT FROM AUTHOR]

Published
2019
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23. The hepatic microenvironment essentially determines tumor cell dormancy and metastatic outgrowth of pancreatic ductal adenocarcinoma.

Author

Lenk, Lennart, Pein, Maren, Will, Olga, Gomez, Beatriz, Viol, Fabrice, Hauser, Charlotte, Egberts, Jan-Hendrik, Gundlach, Jan-Paul, Helm, Ole, Tiwari, Sanjay, Weiskirchen, Ralf, Rose-John, Stefan, Röcken, Christoph, Mikulits, Wolfgang, Wenzel, Patrick, Schneider, Günter, Saur, Dieter, Schäfer, Heiner, and Sebens, Susanne

Subjects
ADENOCARCINOMA, LIVER metastasis, STROMAL cells, DIAGNOSIS, THERAPEUTICS
Abstract

Pancreatic ductal adenocarcinoma (PDAC) is often diagnosed when liver metastases already emerged. This study elucidated the impact of hepatic stromal cells on growth behavior of premalignant and malignant pancreatic ductal epithelial cells (PDECs). Liver sections of tumor-bearing KPC mice comprised micrometastases displaying low proliferation located in an unobtrusive hepatic microenvironment whereas macrometastases containing more proliferating cells were surrounded by hepatic myofibroblasts (HMFs). In an age-related syngeneic PDAC mouse model livers with signs of age-related inflammation exhibited significantly more proliferating disseminated tumor cells (DTCs) and micrometastases despite comparable primary tumor growth and DTC numbers. Hepatic stellate cells (HSC), representing a physiologic liver stroma, promoted an IL-8 mediated quiescence-associated phenotype (QAP) of PDECs in coculture. QAP included flattened cell morphology, Ki67-negativity and reduced proliferation, elevated senescence-associated β galactosidase activity and diminished p-Erk/p-p38-ratio. In contrast, proliferation of PDECs was enhanced by VEGF in the presence of HMF. Switching the micromilieu from HSC to HMF or blocking VEGF reversed QAP in PDECs. This study demonstrates how HSCs induce and maintain a reversible QAP in disseminated PDAC cells, while inflammatory HMFs foster QAP reversal and metastatic outgrowth. Overall, the importance of the hepatic microenvironment in induction and reversal of dormancy during PDAC metastasis is emphasized. [ABSTRACT FROM PUBLISHER]

Published
2018
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24. Worse survival of hepatocellular cancer patients with membranous insulin receptor overexpression.

Author

Heckl SM, Schneider C, Kercher L, Behrens HM, Gundlach JP, Bernsmeier A, Schmidt S, Krüger S, Braun F, Günther R, Becker T, Schreiber S, and Röcken C

Subjects
Humans, Male, Female, Middle Aged, Aged, Prognosis, Retrospective Studies, Sorafenib therapeutic use, Adult, Biomarkers, Tumor metabolism, Liver Neoplasms metabolism, Liver Neoplasms mortality, Liver Neoplasms pathology, Receptor, Insulin metabolism, Carcinoma, Hepatocellular metabolism, Carcinoma, Hepatocellular mortality, Carcinoma, Hepatocellular pathology, Receptor, IGF Type 1 metabolism
Abstract

Hepatocellular cancer (HCC) therapy is in need for an ideal companion diagnostic. Preclinical experimental studies have identified the insulin receptor (IR) and its synergistic counterpart, the IGF1 receptor (IGF1R), as relevant in HCC development, and the ligands IGF1 and IGF2 have been found to be elevated in HCC. This study aimed to bridge the gap to the clinical setting and explore whether the IR or the IGF1R would be of prognostic significance and would be associated with clinicopathologic parameters in HCC patients. In our retrospective cohort study located at the University Hospital Schleswig-Holstein, Campus Kiel, Germany, HCC samples of 139 patients were examined for IR and IGF1R expression by immunohistochemistry. A HistoScore was correlated with clinicopathological characteristics and survival. IR overexpression was frequently observed and was associated with clinicopathological parameters and survival. Membranous IR expression was associated with worse tumor specific survival (p = 0.043). Intriguingly, membranous IR expression was associated with worse tumor specific survival (p = 0.017) in the subgroup of patients undergoing sorafenib therapy. IGF1R expression was not associated with survival. In conclusion, our results suggest that membranous IR expression plays a role in HCC prognosis and treatment resistance, inspiring future validation as a potential companion diagnostic in HCC., Competing Interests: Competing interests: The authors declare no competing interests., (© 2025. The Author(s).)

Published
2025
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