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2. Roflumilast inhibits tumor growth and migration in STK11/LKB1 deficient pancreatic cancer

Author

Zhang, Shuman, Yun, Duo, Yang, Hao, Eckstein, Markus, Elbait, Gihan Daw, Zhou, Yaxing, Lu, Yanxi, Yang, Hai, Zhang, Jinping, Dörflein, Isabella, Britzen-Laurent, Nathalie, Pfeffer, Susanne, Stemmler, Marc P., Dahl, Andreas, Mukhopadhyay, Debabrata, Chang, David, He, Hang, Zeng, Siyuan, Lan, Bin, Frey, Benjamin, Hampel, Chuanpit, Lentsch, Eva, Gollavilli, Paradesi Naidu, Büttner, Christian, Ekici, Arif B., Biankin, Andrew, Schneider-Stock, Regine, Ceppi, Paolo, Grützmann, Robert, and Pilarsky, Christian

Published
2024
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5. Plasma extracellular vesicle messenger RNA profiling identifies prognostic EV signature for non-invasive risk stratification for survival prediction of patients with pancreatic ductal adenocarcinoma

Author

Han, Yi, Drobisch, Pascal, Krüger, Alexander, William, Doreen, Grützmann, Konrad, Böthig, Lukas, Polster, Heike, Seifert, Lena, Seifert, Adrian M., Distler, Marius, Pecqueux, Mathieu, Riediger, Carina, Plodeck, Verena, Nebelung, Heiner, Weber, Georg F., Pilarsky, Christian, Kahlert, Ulf, Hinz, Ulf, Roth, Susanne, Hackert, Thilo, Weitz, Jürgen, Wong, Fang Cheng, and Kahlert, Christoph

Published
2023
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6. N-glycosylation Regulates Intrinsic IFN-γ Resistance in Colorectal Cancer: Implications for Immunotherapy

Author

Krug, Julia, Rodrian, Gabriele, Petter, Katja, Yang, Hai, Khoziainova, Svetlana, Guo, Wei, Bénard, Alan, Merkel, Susanne, Gellert, Susan, Maschauer, Simone, Spermann, Monika, Waldner, Maximilian, Bailey, Peter, Pilarsky, Christian, Liebl, Andrea, Tripal, Philipp, Christoph, Jan, Naschberger, Elisabeth, Croner, Roland, Schellerer, Vera S., Becker, Christoph, Hartmann, Arndt, Tüting, Thomas, Prante, Olaf, Grützmann, Robert, Grivennikov, Sergei I., Stürzl, Michael, and Britzen-Laurent, Nathalie

Published
2023
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7. The glycan CA19-9 promotes pancreatitis and pancreatic cancer in mice

Author

Engle, Dannielle D, Tiriac, Hervé, Rivera, Keith D, Pommier, Arnaud, Whalen, Sean, Oni, Tobiloba E, Alagesan, Brinda, Lee, Eun Jung, Yao, Melissa A, Lucito, Matthew S, Spielman, Benjamin, Da Silva, Brandon, Schoepfer, Christina, Wright, Kevin, Creighton, Brianna, Afinowicz, Lauren, Yu, Kenneth H, Grützmann, Robert, Aust, Daniela, Gimotty, Phyllis A, Pollard, Katherine S, Hruban, Ralph H, Goggins, Michael G, Pilarsky, Christian, Park, Youngkyu, Pappin, Darryl J, Hollingsworth, Michael A, and Tuveson, David A

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Prevention, Cancer, Rare Diseases, Pancreatic Cancer, Digestive Diseases, 2.1 Biological and endogenous factors, Aetiology, Acute Disease, Animals, CA-19-9 Antigen, Carcinogenesis, Carcinoma, Pancreatic Ductal, Cell Line, Tumor, Chronic Disease, ErbB Receptors, Extracellular Matrix Proteins, Fucosyltransferases, Galactosyltransferases, Glycosylation, Humans, Mice, Molecular Targeted Therapy, Pancreatic Neoplasms, Pancreatitis, General Science & Technology
Abstract

Glycosylation alterations are indicative of tissue inflammation and neoplasia, but whether these alterations contribute to disease pathogenesis is largely unknown. To study the role of glycan changes in pancreatic disease, we inducibly expressed human fucosyltransferase 3 and β1,3-galactosyltransferase 5 in mice, reconstituting the glycan sialyl-Lewisa, also known as carbohydrate antigen 19-9 (CA19-9). Notably, CA19-9 expression in mice resulted in rapid and severe pancreatitis with hyperactivation of epidermal growth factor receptor (EGFR) signaling. Mechanistically, CA19-9 modification of the matricellular protein fibulin-3 increased its interaction with EGFR, and blockade of fibulin-3, EGFR ligands, or CA19-9 prevented EGFR hyperactivation in organoids. CA19-9-mediated pancreatitis was reversible and could be suppressed with CA19-9 antibodies. CA19-9 also cooperated with the KrasG12D oncogene to produce aggressive pancreatic cancer. These findings implicate CA19-9 in the etiology of pancreatitis and pancreatic cancer and nominate CA19-9 as a therapeutic target.

Published
2019

10. Targeting DNA Damage Response and Replication Stress in Pancreatic Cancer

Author

Allison, Sarah, Bailey, Peter J., Bailey, Ulla-Maja, Biankin, Andrew V., Beraldi, Dario, Brunton, Holly, Caligiuri, Giuseppina, Cameron, Euan, Chang, David K., Cooke, Susanna L., Cunningham, Richard, Dreyer, Stephan, Grimwood, Paul, Kelly, Shane, Lampraki, Eirini-Maria, Marshall, John, Martin, Sancha, McDade, Brian, McElroy, Daniel, Musgrove, Elizabeth A., Nourse, Craig, Paulus-Hock, Viola, Ramsay, Donna, Upstill-Goddard, Rosie, Wright, Derek, Jones, Marc D., Evers, Lisa, Rebus, Selma, Rahib, Lola, Serrels, Bryan, Hair, Jane, Jamieson, Nigel B., McKay, Colin J., Westwood, Paul, Williams, Nicola, Duthie, Fraser, Johns, Amber L., Mawson, Amanda, Scarlett, Christopher J., Brancato, Mary-Anne L., Rowe, Sarah J., Simpson, Skye H., Martyn-Smith, Mona, Thomas, Michelle T., Chantrill, Lorraine A., Chin, Venessa T., Chou, Angela, Cowley, Mark J., Humphris, Jeremy L., Mead, R. Scott, Nagrial, Adnan M., Pajic, Marina, Pettit, Jessica, Pinese, Mark, Rooman, Ilse, Wu, Jianmin, Tao, Jiang, DiPietro, Renee, Watson, Clare, Steinmann, Angela, Lee, Hong Ching, Wong, Rachel, Pinho, Andreia V., Giry-Laterriere, Marc, Daly, Roger J., Sutherland, Robert L., Grimmond, Sean M., Waddell, Nicola, Kassahn, Karin S., Miller, David K., Wilson, Peter J., Patch, Ann-Marie, Song, Sarah, Harliwong, Ivon, Idrisoglu, Senel, Nourbakhsh, Ehsan, Manning, Suzanne, Wani, Shivangi, Gongora, Milena, Anderson, Matthew, Holmes, Oliver, Leonard, Conrad, Taylor, Darrin, Wood, Scott, Xu, Christina, Nones, Katia, Fink, J. Lynn, Christ, Angelika, Bruxner, Tim, Cloonan, Nicole, Newell, Felicity, Pearson, John V., Bailey, Peter, Quinn, Michael, Nagaraj, Shivashankar, Kazakoff, Stephen, Waddell, Nick, Krisnan, Keerthana, Quek, Kelly, Wood, David, Samra, Jaswinder S., Gill, Anthony J., Pavlakis, Nick, Guminski, Alex, Toon, Christopher, Asghari, Ray, Merrett, Neil D., Pavey, Darren, Das, Amitabha, Cosman, Peter H., Ismail, Kasim, O’Connnor, Chelsie, Lam, Vincent W., McLeod, Duncan, Pleass, Henry C., Richardson, Arthur, James, Virginia, Kench, James G., Cooper, Caroline L., Joseph, David, Sandroussi, Charbel, Crawford, Michael, Gallagher, James, Texler, Michael, Forest, Cindy, Laycock, Andrew, Epari, Krishna P., Ballal, Mo, Fletcher, David R., Mukhedkar, Sanjay, Spry, Nigel A., DeBoer, Bastiaan, Chai, Ming, Zeps, Nikolajs, Beilin, Maria, Feeney, Kynan, Nguyen, Nan Q., Ruszkiewicz, Andrew R., Worthley, Chris, Tan, Chuan P., Debrencini, Tamara, Chen, John, Brooke-Smith, Mark E., Papangelis, Virginia, Tang, Henry, Barbour, Andrew P., Clouston, Andrew D., Martin, Patrick, O’Rourke, Thomas J., Chiang, Amy, Fawcett, Jonathan W., Slater, Kellee, Yeung, Shinn, Hatzifotis, Michael, Hodgkinson, Peter, Christophi, Christopher, Nikfarjam, Mehrdad, Mountain, Angela, Biobank, Victorian Cancer, Eshleman, James R., Hruban, Ralph H., Maitra, Anirban, Iacobuzio-Donahue, Christine A., Schulick, Richard D., Wolfgang, Christopher L., Morgan, Richard A., Hodgin, Mary, Scarpa, Aldo, Lawlor, Rita T., Beghelli, Stefania, Corbo, Vincenzo, Scardoni, Maria, Bassi, Claudio, Tempero, Margaret A., Graham, Janet S., Dreyer, Stephan B., Paris, Clara, Dray, Eloise, Plenker, Dennis, Galluzzo, Zachary, Tesson, Mathias, Jones, Marc, Moran-Jones, Kim, Wright, Derek W., Oien, Karin, McGregor, Grant A., Gulati, Aditi, Brough, Rachel, Bajrami, Ilirjana, Pettitt, Stephan, Dziubinski, Michele L., Candido, Juliana, Balkwill, Frances, Barry, Simon T., Grützmann, Robert, Johns, Amber, Froeling, Fieke E.M., Beer, Phillip, Petersen, Gloria M., Ashworth, Alan, Frame, Margaret C., Crawford, Howard C., Simeone, Diane M., Lord, Chris, Mukhopadhyay, Debabrata, Pilarsky, Christian, Tuveson, David A., Morton, Jennifer P., and Sansom, Owen J.

Published
2021
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11. IL-3: key orchestrator of inflammation.

Author

Podolska, Malgorzata J., Grützmann, Robert, Pilarsky, Christian, and Bénard, Alan

Subjects
INFLAMMATION, INTERLEUKIN-3
Abstract

Interleukin (IL)-3 has long been known for its hematopoietic properties. However, recent evidence has expanded our understanding of IL-3 function by identifying IL-3 as a critical orchestrator of inflammation in a wide array of diseases. Depending on the type of disease, the course of inflammation, the cell or the tissue involved, IL-3 promotes either pathologic inflammation or its resolution. Here, we describe the cell-specific functions of IL-3 and summarize its role in diseases. We discuss the current treatments targeting IL-3 or its receptor, and highlight the potential and the limitations of targeting IL-3 in clinics. [ABSTRACT FROM AUTHOR]

Published
2024
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16. Interleukin-3 amplifies the development and progression of pancreatic ductal adenocarcinoma

Author

David, Paul, primary, Mittelstädt, Anke, additional, Hansen, Frederik, additional, Cho, Young kwan, additional, Jacobsen, Anne, additional, Anthuber, Anna, additional, Klösch, Bettina, additional, Dörflein, Isabella, additional, Naschberger, Elisabeth, additional, Brunner, Maximilian, additional, Krautz, Christian, additional, Pilarsky, Christian, additional, Lee, Hakho, additional, Grützmann, Robert, additional, and Weber, Georg F., additional

Published
2023
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17. Creation of a GATA transcription factor binding site as underlying pathogenic mechanism of the common SPINK1 p.N34S pancreatitis risk haplotype

Author

Unger, Lara, primary, Wallner, Johanna, additional, Eiseler, Katharina, additional, Manisha, Arumalla, additional, von Törne, Christine, additional, Bhaskar, Seema, additional, Sankareswaran, Alagu, additional, Kolmeder, Daniela, additional, Rauscher, Beate, additional, Truninger, Kaspar, additional, Schmidt, Andreas W., additional, Pilarsky, Christian, additional, Ewers, Maren, additional, Chandak, Giriraj R., additional, Hauck, Stefanie M., additional, Laumen, Helmut, additional, and Witt, Heiko, additional

Published
2023
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19. ecDNA amplification of MYC drives intratumor copy-number heterogeneity and adaptation to stress in PDAC

Author

Malinova, Antonia, primary, Schreyer, Daniel, additional, Fiorini, Elena, additional, Pasini, Davide, additional, Bevere, Michele, additional, D'Agosto, Sabrina, additional, Andreani, Silvia, additional, Lupo, Francesca, additional, Veghini, Lisa, additional, Grimaldi, Sonia, additional, Pedron, Serena, additional, Nourse, Craig, additional, Salvia, Roberto, additional, Malleo, Giuseppe, additional, Ruzzenente, Andrea, additional, Guglielmi, Alfredo, additional, Milella, Michele, additional, Lawlor, Rita Teresa, additional, Luchini, Claudio, additional, Pilarsky, Christian, additional, Scarpa, Aldo, additional, Tuveson, David, additional, Bailey, Peter, additional, and Corbo, Vincenzo, additional

Published
2023
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20. ICGC ARGO precision medicine: genomic profiling-informed prediction of immunotherapy response in two patients with metastatic head and neck squamous cell carcinoma

Author

Nocini, Riccardo, primary, Tondulli, Luca, additional, D’Ambrosio, Consuelo, additional, Luchini, Claudio, additional, Biankin, Andrew V, additional, Casolino, Raffaella, additional, Scarpa, Aldo, additional, Milella, Michele, additional, Lawlor, Rita T, additional, Stein, Lincoln D, additional, Park, Keunchil, additional, Johns, Amber L, additional, Korbel, Jan O, additional, Zeps, Nik, additional, Rubin, Mark A, additional, Marra, Marco A, additional, Elemento, Olivier, additional, Gallinger, Steven, additional, Tuveson, David, additional, Trumper, Lorenz, additional, Koch, Raphael, additional, Brennan, Paul, additional, Pilarsky, Christian, additional, Nikolaev, Sergey, additional, Yoon, Sun-Soo, additional, Lee, Eun Sook, additional, Shibata, Tatsuhiro, additional, Wu, Xiaojian, additional, Wu, Jianmin, additional, Zhan, Qimin, additional, Poon, Wai, additional, Yoshino, Takayuki, additional, Al-Kuraya, Khawla S., additional, Eeles, Rosalind, additional, Fitzgerald, Rebecca, additional, Caldas, Carlos, additional, Abraham, Jean, additional, and Chang, David K, additional

Published
2023
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21. Expression and role of the immune checkpoint regulator PD-L1 in the tumor-stroma interplay of pancreatic ductal adenocarcinoma

Author

Daunke, Tina, primary, Beckinger, Silje, additional, Rahn, Sascha, additional, Krüger, Sandra, additional, Heckl, Steffen, additional, Schäfer, Heiner, additional, Wesch, Daniela, additional, Pilarsky, Christian, additional, Eckstein, Markus, additional, Hartmann, Arndt, additional, Röcken, Christoph, additional, Wandmacher, Anna Maxi, additional, and Sebens, Susanne, additional

Published
2023
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22. Precision Oncology in Surgery: Patient Selection for Operable Pancreatic Cancer

Author

Dreyer, Stephan B., Pinese, Mark, Jamieson, Nigel B., Scarlett, Christopher J., Colvin, Emily K., Pajic, Marina, Johns, Amber L., Humphris, Jeremy L., Wu, Jianmin, Cowley, Mark J., Chou, Angela, Nagrial, Adnan M., Chantrill, Lorraine, Chin, Venessa T., Jones, Marc D., Moran-Jones, Kim, Carter, Christopher Ross, Dickson, Euan J., Samra, Jaswinder S., Merrett, Neil D., Gill, Anthony J., Kench, James G., Duthie, Fraser, Miller, David K., Cooke, Susanna, Aust, Daniela, Knösel, Thomas, Rümmele, Petra, Grützmann, Robert, Pilarsky, Christian, Nguyen, Nam Q., Musgrove, Elizabeth A., Bailey, Peter J., McKay, Colin J., Biankin, Andrew V., and Chang, David K.

Published
2020
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23. Expression and role of the immune checkpoint regulator PD-L1 in the tumor-stroma interplay of pancreatic ductal adenocarcinoma

Author

Daunke, Tina, Beckinger, Silje, Rahn, Sascha, Krüger, Sandra, Heckl, Steffen, Schäfer, Heiner, Wesch, Daniela, Pilarsky, Christian, Eckstein, Markus, Hartmann, Arndt, Röcken, Christoph, Wandmacher, Anna Maxi, and Sebens, Susanne

Subjects
ddc:610
Abstract

Introduction: Immune checkpoint inhibitors (ICI), e.g., targeting programmed cell death protein 1-ligand 1 (PD-L1) or its receptor PD-1, have markedly improved the therapy of many cancers but so far failed in pancreatic ductal adenocarcinoma (PDAC). Macrophages represent one of the most abundant immune cell populations within the tumor microenvironment (TME) of PDAC being able to either support or restrain tumor progression depending on their phenotype. To better understand treatment failure of PD-L1/PD-1 inhibitors in PDAC, this study examined PD-L1 expression in the context of a dynamic TME in PDAC with a particular focus on the impact of macrophages. Methods: Formalin-fixed and paraffin embedded tissue samples of primary PDAC tissues and corresponding liver metastases were used for immunohistochemical analyses. Serial sections were stained with antibodies detecting Pan-Cytokeratin, CD68, CD163, CD8, and PD-L1.To investigate whether the PD-1/PD-L1 axis and macrophages contribute to immune escape of PDAC cells, a stroma enriched 3D spheroid coculture model was established in vitro, using different PDAC cell lines and macrophages subtypes as well as CD8+ T cells. Functional and flow cytometry analyses were conducted to characterize cell populations. Results: Immunohistochemical analyses revealed that PD-L1 is mainly expressed by stroma cells, including macrophages and not PDAC cells in primary PDAC tissues and corresponding liver metastases. Notably, high local abundance of macrophages and strong PD-L1 staining were commonly found at invasion fronts of tumoral lesions between CD8+ T cells and tumor cells. In order to investigate whether PD-L1 expressing macrophages impact the response of PDAC cells to treatment with PD-L1/PD-1 inhibitors, we developed a spheroid model comprising two different PDAC cell lines and different ratios of in vitro differentiated primary M1- or M2-like polarized macrophages. In line with our in situ findings, high PD-L1 expression was observed in macrophages rather than PDAC cells, which was further increased by the presence of PDAC cells. The effector phenotype of co-cultured CD8+ T cells exemplified by expression of activation markers and release of effector molecules was rather enhanced by PDAC macrophage spheroids, particularly with M1-like macrophages compared to mono-culture spheroids. However, this was not associated with enhanced PDAC cell death. ICI treatment with either Durvalumab or Pembrolizumab alone or in combination with Gemcitabine hardly affected the effector phenotype of CD8+ T cells along with PDAC cell death. Thus, despite strong PD-L1 expression in macrophages, ICI treatment did not result in an enhanced activation and cytotoxic phenotype of CD8+ T cells. Conclusion: Overall, our study revealed novel insights into the interplay of PDAC cells and macrophages in the presence of ICI.

Published
2023

28. Supplementary Table S4 from Identification and Validation of Colorectal Neoplasia–Specific Methylation Markers for Accurate Classification of Disease

Author

Model, Fabian, primary, Osborn, Neal, primary, Ahlquist, David, primary, Gruetzmann, Robert, primary, Molnar, Bela, primary, Sipos, Ferenc, primary, Galamb, Orsolya, primary, Pilarsky, Christian, primary, Saeger, Hans-Detlev, primary, Tulassay, Zsolt, primary, Hale, Kari, primary, Mooney, Suzanne, primary, Lograsso, Joseph, primary, Adorjan, Peter, primary, Lesche, Ralf, primary, Dessauer, Andreas, primary, Kleiber, Joerg, primary, Porstmann, Baerbel, primary, Sledziewski, Andrew, primary, and Lofton-Day, Catherine, primary

Published
2023
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32. Supplementary Data from Tumor-associated CD75s- and iso-CD75s-gangliosides are potential targets for adjuvant therapy in pancreatic cancer

Author

Distler, Ute, primary, Souady, Jamal, primary, Hülsewig, Marcel, primary, Drmić-Hofman, Irena, primary, Haier, Jörg, primary, Denz, Axel, primary, Grützmann, Robert, primary, Pilarsky, Christian, primary, Senninger, Norbert, primary, Dreisewerd, Klaus, primary, Berkenkamp, Stefan, primary, Schmidt, M. Alexander, primary, Peter-Katalinić, Jasna, primary, and Müthing, Johannes, primary

Published
2023
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36. Additional file 1 of Plasma extracellular vesicle messenger RNA profiling identifies prognostic EV signature for non-invasive risk stratification for survival prediction of patients with pancreatic ductal adenocarcinoma

Author

Han, Yi, Drobisch, Pascal, Krüger, Alexander, William, Doreen, Grützmann, Konrad, Böthig, Lukas, Polster, Heike, Seifert, Lena, Seifert, Adrian M., Distler, Marius, Pecqueux, Mathieu, Riediger, Carina, Plodeck, Verena, Nebelung, Heiner, Weber, Georg F., Pilarsky, Christian, Kahlert, Ulf, Hinz, Ulf, Roth, Susanne, Hackert, Thilo, Weitz, Jürgen, Wong, Fang Cheng, and Kahlert, Christoph

Abstract

Additional file 1. Supplementary figures (Fig. S1–S5) and tables (Table S1–S2).

Published
2023
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37. Independent Validation and Assay Standardization of Improved Metabolic Biomarker Signature to Differentiate Pancreatic Ductal Adenocarcinoma From Chronic Pancreatitis

Author

Mahajan, Ujjwal M., primary, Oehrle, Bettina, additional, Sirtl, Simon, additional, Alnatsha, Ahmed, additional, Goni, Elisabetta, additional, Regel, Ivonne, additional, Beyer, Georg, additional, Vornhülz, Marlies, additional, Vielhauer, Jakob, additional, Chromik, Ansgar, additional, Bahra, Markus, additional, Klein, Fritz, additional, Uhl, Waldemar, additional, Fahlbusch, Tim, additional, Distler, Marius, additional, Weitz, Jürgen, additional, Grützmann, Robert, additional, Pilarsky, Christian, additional, Weiss, Frank Ulrich, additional, Adam, M. Gordian, additional, Neoptolemos, John P., additional, Kalthoff, Holger, additional, Rad, Roland, additional, Christiansen, Nicole, additional, Bethan, Bianca, additional, Kamlage, Beate, additional, Lerch, Markus M., additional, and Mayerle, Julia, additional

Published
2022
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39. GATA4 and GATA6 loss-of-expression is associated with extinction of the classical programme and poor outcome in pancreatic ductal adenocarcinoma

Author

de Andrés, Mónica P, primary, Jackson, Richard J, additional, Felipe, Irene, additional, Zagorac, Sladjana, additional, Pilarsky, Christian, additional, Schlitter, Anna Melissa, additional, Martinez de Villareal, Jaime, additional, Jang, Gun Ho, additional, Costello, Eithne, additional, Gallinger, Steve, additional, Ghaneh, Paula, additional, Greenhalf, William, additional, Knösel, Thomas, additional, Palmer, Daniel H, additional, Ruemmele, Petra, additional, Weichert, Wilko, additional, Buechler, Markus, additional, Hackert, Thilo, additional, Neoptolemos, John P, additional, Notta, Faiyaz, additional, Malats, Núria, additional, Martinelli, Paola, additional, and Real, Francisco X, additional

Published
2022
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42. Genomic analyses identify molecular subtypes of pancreatic cancer

Author

Bailey, Peter, Chang, David K., Nones, Katia, Johns, Amber L., Patch, Ann-Marie, Gingras, Marie-Claude, Miller, David K., Christ, Angelika N., Bruxner, Tim J. C., Quinn, Michael C., Nourse, Craig, Murtaugh, L. Charles, Harliwong, Ivon, Idrisoglu, Senel, Manning, Suzanne, Nourbakhsh, Ehsan, Wani, Shivangi, Fink, Lynn, Holmes, Oliver, Chin, Venessa, Anderson, Matthew J., Kazakoff, Stephen, Leonard, Conrad, Newell, Felicity, Waddell, Nick, Wood, Scott, Xu, Qinying, Wilson, Peter J., Cloonan, Nicole, Kassahn, Karin S., Taylor, Darrin, Quek, Kelly, Robertson, Alan, Pantano, Lorena, Mincarelli, Laura, Sanchez, Luis N., Evers, Lisa, Wu, Jianmin, Pinese, Mark, Cowley, Mark J., Jones, Marc D., Colvin, Emily K., Nagrial, Adnan M., Humphrey, Emily S., Chantrill, Lorraine A., Mawson, Amanda, Humphris, Jeremy, Chou, Angela, Pajic, Marina, Scarlett, Christopher J., Pinho, Andreia V., Giry-Laterriere, Marc, Rooman, Ilse, Samra, Jaswinder S., Kench, James G., Lovell, Jessica A., Merrett, Neil D., Toon, Christopher W., Epari, Krishna, Nguyen, Nam Q., Barbour, Andrew, Zeps, Nikolajs, Moran-Jones, Kim, Jamieson, Nigel B., Graham, Janet S., Duthie, Fraser, Oien, Karin, Hair, Jane, Grützmann, Robert, Maitra, Anirban, Iacobuzio-Donahue, Christine A., Wolfgang, Christopher L., Morgan, Richard A., Lawlor, Rita T., Corbo, Vincenzo, Bassi, Claudio, Rusev, Borislav, Capelli, Paola, Salvia, Roberto, Tortora, Giampaolo, Mukhopadhyay, Debabrata, Petersen, Gloria M., Munzy, Donna M., Fisher, William E., Karim, Saadia A., Eshleman, James R., Hruban, Ralph H., Pilarsky, Christian, Morton, Jennifer P., Sansom, Owen J., Scarpa, Aldo, Musgrove, Elizabeth A., Bailey, Ulla-Maja Hagbo, Hofmann, Oliver, Sutherland, Robert L., Wheeler, David A., Gill, Anthony J., Gibbs, Richard A., Pearson, John V., Waddell, Nicola, Biankin, Andrew V., and Grimmond, Sean M.

Published
2016
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43. Structural Protein Interactions Predict Kinase-Inhibitor Interactions in Upregulated Pancreas Tumour Genes Expression Data

Author

Dawelbait, Gihan, Pilarsky, Christian, Zhang, Yanju, Grützmann, Robert, Schroeder, Michael, Hutchison, David, editor, Kanade, Takeo, editor, Kittler, Josef, editor, Kleinberg, Jon M., editor, Mattern, Friedemann, editor, Mitchell, John C., editor, Naor, Moni, editor, Nierstrasz, Oscar, editor, Pandu Rangan, C., editor, Steffen, Bernhard, editor, Sudan, Madhu, editor, Terzopoulos, Demetri, editor, Tygar, Dough, editor, Vardi, Moshe Y., editor, Weikum, Gerhard, editor, Istrail, Sorin, editor, Pevzner, Pavel, editor, Waterman, Michael, editor, R. Berthold, Michael, editor, Glen, Robert C., editor, Diederichs, Kay, editor, Kohlbacher, Oliver, editor, and Fischer, Ingrid, editor

Published
2005
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45. A Novel Anti-Cancer Therapy: CRISPR/Cas9 Gene Editing

Author

Chen, Xin-Zhu, primary, Guo, Rong, additional, Zhao, Cong, additional, Xu, Jing, additional, Song, Hang, additional, Yu, Hua, additional, Pilarsky, Christian, additional, Nainu, Firzan, additional, Li, Jing-Quan, additional, Zhou, Xin-Ke, additional, and Zhang, Jian-Ye, additional

Published
2022
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46. Genome-Wide CRISPR Screening Identifies DCK and CCNL1 as Genes That Contribute to Gemcitabine Resistance in Pancreatic Cancer

Author

Yang, Hai, primary, Liu, Bin, additional, Liu, Dongxue, additional, Yang, Zhirong, additional, Zhang, Shuman, additional, Xu, Pengyan, additional, Xing, Yuming, additional, Kutschick, Isabella, additional, Pfeffer, Susanne, additional, Britzen-Laurent, Nathalie, additional, Grützmann, Robert, additional, and Pilarsky, Christian, additional

Published
2022
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49. Intracellular Quantification and Localization of Label-Free Iron Oxide Nanoparticles by Holotomographic Microscopy

Author

Friedrich, Ralf P, Schreiber, Eveline, Tietze, Rainer, Yang, Hai, Pilarsky, Christian, and Alexiou, Christoph

Subjects
cellular SPION uptake, flow cytometry, atomic emission spectroscopy, superparamagnetic iron oxide nanoparticles, cytotoxicity, ddc:610, Nanotechnology, Science and Applications, Original Research
Abstract

Ralf P Friedrich,1 Eveline Schreiber,1 Rainer Tietze,1 Hai Yang,2 Christian Pilarsky,2 Christoph Alexiou1 1Department of Otorhinolaryngology, Head and Neck Surgery, Section of Experimental Oncology and Nanomedicine (SEON), Else Kröner-Fresenius-Stiftung-Professorship, Universitätsklinikum Erlangen, Erlangen, 91054, Germany; 2Department of Surgery, Universitätsklinikum Erlangen, Erlangen 91054, GermanyCorrespondence: Ralf P FriedrichDepartment of Otorhinolaryngology, Head and Neck Surgery, Section of Experimental Oncology and Nanomedicine (SEON), Else Kröner-Fresenius-Stiftung-Professorship, Universitätsklinikum Erlangen, Glückstrasse 10a, Erlangen 91054, GermanyTel +49 9131 85 43943Fax +49 9131 85 34828Email ralf.friedrich@uk-erlangen.deBackground: The limitations of optical microscopy to determine the cellular localization of label-free nanoparticles prevent a solid prediction of the cellular effect of particles intended for medical applications. To avoid the strong physicochemical changes associated with fluorescent labelling, which often result in differences in cellular uptake, efficiency and toxicity of particles, novel detection techniques are required.Methods: In the present study, we determined the intracellular content of unlabeled SPIONs by analyzing refractive index (RI)-based images from holotomographic three-dimensional (3D) microscopy and side scatter data measured by flow cytometry. The results were compared with the actual cellular SPION amount as quantified by atomic emission spectroscopy (AES).Results: Live cell imaging by 3D holotomographic microscopy demonstrated cell-specific differences in intracellular nanoparticle uptake in different pancreatic cell lines. Thus, treatment of PANC-1SMAD4 (1− 4) and PANC-1SMAD4 (2− 6) with SPIONs resulted in a significant increase in number of areas with higher RI, whereas in PANC-1, SUIT-2 and PaCa DD183, only a minimal increase of spots with high RI was observed. The increase in areas with high RI was in accordance with the SPION content determined by quantitative iron measurements using AES. In contrast, determination of the SPION amount by flow cytometry was strongly cell type-dependent and did not allow the discrimination between intracellular and membrane-bound SPIONs. However, flow cytometry is a very rapid and reliable method to assess the cellular toxicity and allows an estimation of the cell-associated SPION content.Conclusion: Holotomographic 3D microscopy is a useful method to distinguish between intracellular and membrane-associated particles. Thus, it provides a valuable tool for scientists to evaluate the cellular localization and the particle load, which facilitates prediction of potential toxicity and efficiency of nanoparticles for medical applications.Keywords: superparamagnetic iron oxide nanoparticles, cellular SPION uptake, cytotoxicity, flow cytometry, atomic emission spectroscopy

Published
2020

50. Glypican-1 identifies cancer exosomes and detects early pancreatic cancer

Author

Melo, Sonia A., Luecke, Linda B., Kahlert, Christoph, Fernandez, Agustin F., Gammon, Seth T., Kaye, Judith, LeBleu, Valerie S., Mittendorf, Elizabeth A., Weitz, Juergen, Rahbari, Nuh, Reissfelder, Christoph, Pilarsky, Christian, Fraga, Mario F., Piwnica-Worms, David, and Kalluri, Raghu

Subjects
Cancer -- Diagnosis, Pancreatic cancer -- Diagnosis, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

Exosomes are lipid-bilayer-enclosed extracellular vesicles that contain proteins and nucleic acids. They are secreted by all cells and circulate in the blood. Specific detection and isolation of cancer-cell-derived exosomes in the circulation is currently lacking. Using mass spectrometry analyses, we identify a cell surface proteoglycan, glypican-1 (GPC1), specifically enriched on cancer-cell-derived exosomes. [GPC1.sup.+] circulating exosomes (crExos) were monitored and isolated using flow cytometry from the serum of patients and mice with cancer. [GPC1.sup.+] crExos were detected in the serum of patients with pancreatic cancer with absolute specificity and sensitivity, distinguishing healthy subjects and patients with a benign pancreatic disease from patients with early- and late-stage pancreatic cancer. Levels of GPC11 crExos correlate with tumour burden and the survival of pre- and post-surgical patients. [GPC1.sup.+] crExos from patients and from mice with spontaneous pancreatic tumours carry specific KRAS mutations, and reliably detect pancreatic intraepithelial lesions in mice despite negative signals by magnetic resonance imaging. [GPC1.sup.+] crExos may serve as a potential non-invasive diagnostic and screening tool to detect early stages of pancreatic cancer to facilitate possible curative surgical therapy., Exosomes are secreted membrane enclosed vesicles (extracellular vesicles) of 50-150 nm diameter (1). Formed during the inward budding of late endosomes, they develop into intracellular multivesicular endosomes and contain nucleic [...]

Published
2015
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