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1. Three-month life expectancy as inclusion criterion for clinical trials in advanced pancreatic cancer: is it really a valid tool for patient selection?

Author

Weiss, Lena, Heinemann, Volker, Fischer, Laura E., Gieseler, Frank, Hoehler, Thomas, Mayerle, Julia, Quietzsch, Detlef, Reinacher-Schick, Anke, Schenk, Michael, Seipelt, Gernot, Siveke, Jens T., Stahl, Michael, Vehling-Kaiser, Ursula, Waldschmidt, Dirk T., Dorman, Klara, Zhang, Danmei, Westphalen, C. Benedikt, von Bergwelt-Baildon, Michael, Boeck, Stefan, and Haas, Michael

Published
2024
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7. Three-month life expectancy as inclusion criterion for clinical trials in advanced pancreatic cancer: is it really a valid tool for patient selection?

Author

Weiss, Lena, primary, Heinemann, Volker, additional, Fischer, Laura E., additional, Gieseler, Frank, additional, Hoehler, Thomas, additional, Mayerle, Julia, additional, Quietzsch, Detlef, additional, Reinacher-Schick, Anke, additional, Schenk, Michael, additional, Seipelt, Gernot, additional, Siveke, Jens T., additional, Stahl, Michael, additional, Vehling-Kaiser, Ursula, additional, Waldschmidt, Dirk T., additional, Dorman, Klara, additional, Zhang, Danmei, additional, Westphalen, C. Benedikt, additional, von Bergwelt-Baildon, Michael, additional, Boeck, Stefan, additional, and Haas, Michael, additional

Published
2023
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8. Designing a broad-spectrum integrative approach for cancer prevention and treatment

Author

Block, Keith I, Gyllenhaal, Charlotte, Lowe, Leroy, Amedei, Amedeo, Amin, ARM Ruhul, Amin, Amr, Aquilano, Katia, Arbiser, Jack, Arreola, Alexandra, Arzumanyan, Alla, Ashraf, S Salman, Azmi, Asfar S, Benencia, Fabian, Bhakta, Dipita, Bilsland, Alan, Bishayee, Anupam, Blain, Stacy W, Block, Penny B, Boosani, Chandra S, Carey, Thomas E, Carnero, Amancio, Carotenuto, Marianeve, Casey, Stephanie C, Chakrabarti, Mrinmay, Chaturvedi, Rupesh, Chen, Georgia Zhuo, Chen, Helen, Chen, Sophie, Chen, Yi Charlie, Choi, Beom K, Ciriolo, Maria Rosa, Coley, Helen M, Collins, Andrew R, Connell, Marisa, Crawford, Sarah, Curran, Colleen S, Dabrosin, Charlotta, Damia, Giovanna, Dasgupta, Santanu, DeBerardinis, Ralph J, Decker, William K, Dhawan, Punita, Diehl, Anna Mae E, Dong, Jin-Tang, Dou, Q Ping, Drew, Janice E, Elkord, Eyad, El-Rayes, Bassel, Feitelson, Mark A, Felsher, Dean W, Ferguson, Lynnette R, Fimognari, Carmela, Firestone, Gary L, Frezza, Christian, Fujii, Hiromasa, Fuster, Mark M, Generali, Daniele, Georgakilas, Alexandros G, Gieseler, Frank, Gilbertson, Michael, Green, Michelle F, Grue, Brendan, Guha, Gunjan, Halicka, Dorota, Helferich, William G, Heneberg, Petr, Hentosh, Patricia, Hirschey, Matthew D, Hofseth, Lorne J, Holcombe, Randall F, Honoki, Kanya, Hsu, Hsue-Yin, Huang, Gloria S, Jensen, Lasse D, Jiang, Wen G, Jones, Lee W, Karpowicz, Phillip A, Keith, W Nicol, Kerkar, Sid P, Khan, Gazala N, Khatami, Mahin, Ko, Young H, Kucuk, Omer, Kulathinal, Rob J, Kumar, Nagi B, Kwon, Byoung S, Le, Anne, Lea, Michael A, Lee, Ho-Young, Lichtor, Terry, Lin, Liang-Tzung, Locasale, Jason W, Lokeshwar, Bal L, Longo, Valter D, Lyssiotis, Costas A, MacKenzie, Karen L, Malhotra, Meenakshi, Marino, Maria, Martinez-Chantar, Maria L, and Matheu, Ander

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Cancer, Rare Diseases, Precision Medicine, Aetiology, 5.1 Pharmaceuticals, Development of treatments and therapeutic interventions, 2.1 Biological and endogenous factors, Good Health and Well Being, Antineoplastic Agents, Phytogenic, Drug Resistance, Neoplasm, Genetic Heterogeneity, Humans, Molecular Targeted Therapy, Neoplasms, Signal Transduction, Tumor Microenvironment, Multi-targeted, Cancer hallmarks, Phytochemicals, Targeted therapy, Integrative medicine, Oncology & Carcinogenesis, Biochemistry and cell biology, Oncology and carcinogenesis
Abstract

Targeted therapies and the consequent adoption of "personalized" oncology have achieved notable successes in some cancers; however, significant problems remain with this approach. Many targeted therapies are highly toxic, costs are extremely high, and most patients experience relapse after a few disease-free months. Relapses arise from genetic heterogeneity in tumors, which harbor therapy-resistant immortalized cells that have adopted alternate and compensatory pathways (i.e., pathways that are not reliant upon the same mechanisms as those which have been targeted). To address these limitations, an international task force of 180 scientists was assembled to explore the concept of a low-toxicity "broad-spectrum" therapeutic approach that could simultaneously target many key pathways and mechanisms. Using cancer hallmark phenotypes and the tumor microenvironment to account for the various aspects of relevant cancer biology, interdisciplinary teams reviewed each hallmark area and nominated a wide range of high-priority targets (74 in total) that could be modified to improve patient outcomes. For these targets, corresponding low-toxicity therapeutic approaches were then suggested, many of which were phytochemicals. Proposed actions on each target and all of the approaches were further reviewed for known effects on other hallmark areas and the tumor microenvironment. Potential contrary or procarcinogenic effects were found for 3.9% of the relationships between targets and hallmarks, and mixed evidence of complementary and contrary relationships was found for 7.1%. Approximately 67% of the relationships revealed potentially complementary effects, and the remainder had no known relationship. Among the approaches, 1.1% had contrary, 2.8% had mixed and 62.1% had complementary relationships. These results suggest that a broad-spectrum approach should be feasible from a safety standpoint. This novel approach has potential to be relatively inexpensive, it should help us address stages and types of cancer that lack conventional treatment, and it may reduce relapse risks. A proposed agenda for future research is offered.

Published
2015

11. Ambrisentan, an endothelin receptor type A-selective antagonist, inhibits cancer cell migration, invasion, and metastasis

Author

Kappes, Lucy, Amer, Ruba L., Sommerlatte, Sabine, Bashir, Ghada, Plattfaut, Corinna, Gieseler, Frank, Gemoll, Timo, Busch, Hauke, Altahrawi, Abeer, Al-Sbiei, Ashraf, Haneefa, Shoja M., Arafat, Kholoud, Schimke, Lena F., Khawanky, Nadia El, Schulze-Forster, Kai, Heidecke, Harald, Kerstein-Staehle, Anja, Marschner, Gabriele, Pitann, Silke, Ochs, Hans D., Mueller, Antje, Attoub, Samir, Fernandez-Cabezudo, Maria J., Riemekasten, Gabriela, al-Ramadi, Basel K., and Cabral-Marques, Otavio

Published
2020
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16. GPCR-specific autoantibody signatures are associated with physiological and pathological immune homeostasis

Author

Cabral-Marques, Otavio, Marques, Alexandre, Giil, Lasse Melvær, De Vito, Roberta, Rademacher, Judith, Günther, Jeannine, Lange, Tanja, Humrich, Jens Y., Klapa, Sebastian, Schinke, Susanne, Schimke, Lena F., Marschner, Gabriele, Pitann, Silke, Adler, Sabine, Dechend, Ralf, Müller, Dominik N., Braicu, Ioana, Sehouli, Jalid, Schulze-Forster, Kai, Trippel, Tobias, Scheibenbogen, Carmen, Staff, Annetine, Mertens, Peter R., Löbel, Madlen, Mastroianni, Justin, Plattfaut, Corinna, Gieseler, Frank, Dragun, Duska, Engelhardt, Barbara Elizabeth, Fernandez-Cabezudo, Maria J., Ochs, Hans D., al-Ramadi, Basel K., Lamprecht, Peter, Mueller, Antje, Heidecke, Harald, and Riemekasten, Gabriela

Published
2018
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25. The role of family confidants and caregivers in the care of older cancer patients: Extending the concept of “shared decision‐making”

Author

Gieseler, Frank, primary, Heidenreich, Andreas, additional, Schubert, Jacqueline, additional, Frielitz, Fabian, additional, Rehmann‐Sutter, Christoph, additional, Wörler, Frank, additional, Schües, Christina, additional, Hübner, Joachim, additional, Elsner, Susanne, additional, Block, Katarina, additional, Rody, Achim, additional, Bubnoff, Nikolas, additional, Keck, Tobias, additional, Steimann, Monika, additional, Endsin, Gero, additional, and Katalinic, Alexander, additional

Published
2021
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36. Extracellular Vesicles as biomarkers for cancer progression and cancer associated VTE

Author

Gieseler, Frank and Ender, Fanny

Abstract

Microvesicles (MVs) represent a subgroup of extracellular vesicles (EVs) emerging from various cells by blebbing of their outer membrane. Therefore, they share features such as membrane composition and antigenicity with their parental cells. Released by many immune and tumor cells, MVs act as intercellular messengers, account for horizontal gene transfer and can activate the coagulation system. With the aim to investigate their relevance for tumor cell biology, we characterized MVs released by human tumor cell lines of various origins in the absence or presence of TNF-a. After stimulation, we used the combination of low and high-speed centrifugation to enrich MVs from cell culture supernatants. We analyzed the presentation of phosphatidylserine (PS) and tissue factor (TF) activity on the cell surface and investigated their potency to induce tumor cell migration. In all tumor cell lines, TNF-a stimulation enhanced the release of MVs. While the expression of PS was universally increased, an elevated activity of procoagulant TF could be detected on MVs from lung, pancreatic, and colon carcinoma, but not from breast and ovarian cancer cell lines. Functionally, TNF-a stimulation significantly increased the potency of MVs to induce tumor cell migration. In conclusion, inflammatory conditions promote the release of MVs with increased procoagulant activity from tumor cell lines in vitro. PS-containing and TF-expressing MVs may account for systemic activation of the coagulation system as seen in cancer patients and, since they induce tumor cell migration, they may serve as biomarkers for tumor progression. Publication: Cell Biology International 2018., Proceedings on Cancer-Immuno-Oncology, Vol 1 No 1 (2018)

Published
2018
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37. Randomized Phase III Trial of Gemcitabine Plus Cisplatin Compared With Gemcitabine Alone in Advanced Pancreatic Cancer

Author

Heinemann, Volker, Quietzsch, Detlef, Gieseler, Frank, Gonnermann, Michael, Schönekäs, Herbert, Rost, Andreas, Neuhaus, Horst, Haag, Caroline, Clemens, Michael, Heinrich, Bernard, Vehling-Kaiser, Ursula, Fuchs, Martin, Fleckenstein, Doris, Gesierich, Wolfgang, Uthgenannt, Dirk, Einsele, Hermann, Holstege, Axel, Hinke, Axel, Schalhorn, Andreas, and Wilkowski, Ralf

Published
2006
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40. Signaling Crosstalk of TGF-β/ALK5 and PAR2/PAR1: A Complex Regulatory Network Controlling Fibrosis and Cancer

Author

Ungefroren, Hendrik, Gieseler, Frank, Kaufmann, Roland, Settmacher, Utz, Lehnert, Hendrik, and Rauch, Bernhard H.

Subjects
Liver Cirrhosis, TGF-β, Receptor, Transforming Growth Factor-beta Type I, Review, Protein Serine-Threonine Kinases, Kidney, ALK5, lcsh:Chemistry, Transforming Growth Factor beta, Neoplasms, Animals, Humans, Receptor, PAR-2, cancer, Receptor, PAR-1, Lung, lcsh:QH301-705.5, fibrosis, PAR2, PAR1, serine proteinases, lcsh:Biology (General), lcsh:QD1-999, signaling, Receptors, Transforming Growth Factor beta, Signal Transduction
Abstract

Both signaling by transforming growth factor-β (TGF-β) and agonists of the G Protein-coupled receptors proteinase-activated receptor-1 (PAR1) and -2 (PAR2) have been linked to tissue fibrosis and cancer. Intriguingly, TGF-β and PAR signaling either converge on the regulation of certain matrix genes overexpressed in these pathologies or display mutual regulation of their signaling components, which is mediated in part through sphingosine kinases and sphingosine-1-phosphate and indicative of an intimate signaling crosstalk between the two pathways. In the first part of this review, we summarize the various regulatory interactions that have been discovered so far according to the organ/tissue in which they were described. In the second part, we highlight the types of signaling crosstalk between TGF-β on the one hand and PAR2/PAR1 on the other hand. Both ligand–receptor systems interact at various levels and by several mechanisms including mutual regulation of ligand–ligand, ligand–receptor, and receptor–receptor at the transcriptional, post-transcriptional, and receptor transactivation levels. These mutual interactions between PAR2/PAR1 and TGF-β signaling components eventually result in feed-forward loops/vicious cycles of matrix deposition and malignant traits that exacerbate fibrosis and oncogenesis, respectively. Given the crucial role of PAR2 and PAR1 in controlling TGF-β receptor activation, signaling, TGF-β synthesis and bioactivation, combining PAR inhibitors with TGF-β blocking agents may turn out to be more efficient than targeting TGF-β alone in alleviating unwanted TGF-β-dependent responses but retaining the beneficial ones.

Published
2018

44. Differential roles of Smad2 and Smad3 in the regulation of TGF-β1-mediated growth inhibition and cell migration in pancreatic ductal adenocarcinoma cells: control by Rac1

Author

Lehnert Hendrik, Sebens Susanne, Groth Stephanie, Ungefroren Hendrik, Gieseler Frank, and Fändrich Fred

Subjects
Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract

Abstract Background Progression of pancreatic ductal adenocarcinoma (PDAC) is largely the result of genetic and/or epigenetic alterations in the transforming growth factor-beta (TGF-β)/Smad signalling pathway, eventually resulting in loss of TGF-β-mediated growth arrest and an increase in cellular migration, invasion, and metastasis. These cellular responses to TGF-β are mediated solely or partially through the canonical Smad signalling pathway which commences with activation of receptor-regulated Smads (R-Smads) Smad2 and Smad3 by the TGF-β type I receptor. However, little is known on the relative contribution of each R-Smad, the possible existence of functional antagonism, or the crosstalk with other signalling pathways in the control of TGF-β1-induced growth inhibition and cell migration. Using genetic and pharmacologic approaches we have inhibited in PDAC cells endogenous Smad2 and Smad3, as well as a potential regulator, the small GTPase Rac1, and have analysed the consequences for TGF-β1-mediated growth inhibition and cell migration (chemokinesis). Results SiRNA-mediated silencing of Smad3 in the TGF-β responsive PDAC cell line PANC-1 reduced TGF-β1-induced growth inhibition but increased the migratory response, while silencing of Smad2 enhanced growth inhibition but decreased chemokinesis. Interestingly, siRNA-mediated silencing of the small GTPase Rac1, or ectopic expression of a dominant-negative Rac1 mutant largely mimicked the effect of Smad2 silencing on both TGF-β1-induced growth inhibition, via upregulation of the cdk inhibitor p21WAF1, and cell migration. Inhibition of Rac1 activation reduced both TGF-β1-induction of a Smad2-specific transcriptional reporter and Smad2 C-terminal phosphorylation in PDAC cells while Smad3-specific transcriptional activity and Smad3 C-terminal phosphorylation appeared increased. Disruption of autocrine TGF-β signalling in PANC-1 cells rendered cells less susceptible to the growth-suppressive effect of Rac1 inhibition, suggesting that the decrease in "basal" proliferation upon Rac1 inhibition was caused by potentiation of autocrine TGF-β growth inhibition. Conclusions In malignant cells with a functional TGF-β signalling pathway Rac1 antagonizes the TGF-β1 growth inhibitory response and enhances cell migration by antagonistically regulating Smad2 and Smad3 activation. This study reveals that Rac1 is prooncogenic in that it can alter TGF-β signalling at the R-Smad level from a tumour-suppressive towards a tumour-promoting outcome. Hence, Rac1 might represent a viable target for therapeutic intervention to inhibit PDAC progression.

Published
2011
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