S Weiler
University Hospital Heidelberg
20 Papers
8 Citations
S Weiler is an academic researcher from University Hospital Heidelberg. The author has contributed to research in topics: Biology & Cancer research. The author has an hindex of 5, co-authored 11 publications.
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Papers
Induction of Chromosome Instability by Activation of Yes-Associated Protein and Forkhead Box M1 in Liver Cancer
S Weiler,Federico Pinna,Thomas Wolf,Teresa Lutz,Aman Geldiyev,Carsten Sticht,M Knaub,Stefan Thomann,Michaela Bissinger,S Wan,S Rössler,D Becker,Norbert Gretz,Hauke Lang,Frank Bergmann,Vladimir Ustiyan,Tatiana V. Kalin,Stephan Singer,Ju Seog Lee,Jens U. Marquardt,Peter Schirmacher,Vladimir V. Kalinichenko,Kai Breuhahn +22 more
TL;DR: By analyzing cell lines, genetically modified mice, and HCC tissues, it is found that YAP cooperates with FOXM1 to contribute to chromosome instability and agents that disrupt this pathway might be developed as treatments for liver cancer.
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YAP Orchestrates Heterotypic Endothelial Cell Communication via HGF/c-MET Signaling in Liver Tumorigenesis
Stefan Thomann,S Weiler,Simone Marquard,Fabian Rose,Claudia R. Ball,Marcell Tóth,Teng Wei,Carsten Sticht,Sarah Fritzsche,Stephanie Roessler,Carolina De La Torre,Eduard Ryschich,Olga Ermakova,Carolin Mogler,Daniel Kazdal,Norbert Gretz,Hanno Glimm,Eugen Rempel,Peter Schirmacher,Kai Breuhahn +19 more
TL;DR: YAP-dependent changes of the liver vascular niche comprise the formation of heterologous communication hubs in which tumor cell-derived factors modify the cross-talk between EC subpopulations.
HELLS Is Negatively Regulated by Wild-Type P53 in Liver Cancer by a Mechanism Involving P21 and FOXM1
Stefanie Schuller,Jan Sieker,Philip Riemenschneider,Bianca Köhler,Elisabeth Drucker,S Weiler,Daniel Dauch,Carsten Sticht,Benjamin Goeppert,Stephanie Roessler,Silvia Ribback,Kai Breuhahn,Falko Fend,Frank Dombrowski,Kerstin Singer,Stephan Singer +15 more
TL;DR: It is shown that P53 negatively regulates the expression of Helicase, lymphoid specific (HELLS), previously described as an important pro-tumorigenic epigenetic regulator in hepatocarcinogenesis, as a strong and selective P53 repression target within the SNF2-like helicase family.
Bcl‐xL as prognostic marker and potential therapeutic target in cholangiocarcinoma
Paula Hoffmeister,Andreas Mock,Federico Nichetti,Felix Korell,Christoph Heining,Anna-Lena Scherr,M. Günther,Thomas Albrecht,E. Kelmendi,Kuangfeng Xu,L. Nader,A. Kessler,N. Schmitt,Sarah Fritzsche,S Weiler,B Sobol,Albrecht Stenzinger,Stefan Boeck,C. Benedikt Westphalen,Klaus Schulze-Osthoff,Joerg Trojan,Thomas Kindler,Wilko Weichert,Karsten Spiekermann,Monika Bitzer,Gunnar Folprecht,Anna Lena Illert,Melanie Boerries,Frederick Klauschen,S. Ochsenreiter,Jens T. Siveke,Simone Bauer,Hanno Glimm,Benedikt Brors,Jennifer Hüllein,Daniel Hübschmann,Sebastian Uhrig,Peter Horak,Simon Kreutzfeld,Jesus M. Banales,Christoph Springfeld,Diana Jäger,Peter Schirmacher,Sabine Roessler,Steffen Ormanns,Benjamin Goeppert,Stefan Fröhling,Bruno Köhler +47 more
TL;DR: Observations identify Bcl-xL as a key protein in cell death resistance of CCA and may pave the way for clinical application, as well as indicating a prognostic value of Bcl -xL in CCA depending on the CCA subtype.
Dynamic YAP expression in the non-parenchymal liver cell compartment controls heterologous cell communication
Kaijing Liu,Lilija Wehling,Shan Wan,S Weiler,Marcell Tóth,David Ibberson,Silke Marhenke,Adnan Ali,Macrina Lam,Te Guo,F. Pinna,Fabiola Pedrini,Amruta Damle-Vartak,A Dropmann,Fabian Rose,S. Colucci,Wenxiang Cheng,M. Bissinger,Jennifer Schmitt,Patrizia Birner,Tanja Poth,Peter Angel,Steven Dooley,Martina U Muckenthaler,Thomas Longerich,Arndt Vogel,Mathias Heikenwälder,Peter Schirmacher,Kai Breuhahn +28 more
- 04 Mar 2024
TL;DR: Inactivation of YAP and TAZ in liver cells causes liver damage, inflammation, and fibrosis, but concomitant TAZ deletion reduces this phenotype; YAP expression in non-parenchymal cells contributes to inflammation via TEAD-dependent transcriptional regulation.
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