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B. Maurer et al.
here represents a tool to investigate molecular mecha- nisms of PTCL development. Our model serves for identi- fication and pre-clinical testing of novel interventional strategies to target STAT5-dependent PTCL. We conclude that both STAT5A and STAT5B are oncogenes in PTCL, and STAT5B is more transforming. Overall, mutation induced-cytokine sensitivity drives PTCL due to enhanced STAT3/STAT5 signaling.
Acknowledgments
Jerry Adams (WEHI, Australia) kindly provided us with the
vav-hCD4 (HS21/45) plasmid and Dagmar Stoiber (LBI-CR, Vienna, Austria) with the E.G7 cell line. We thank Safia Zahma (LBI-CR, Vienna, Austria), Elisabeth Gurnhofer, Sigurd Krieger (both at the Department of Clinical Pathology, Medical University Vienna, Austria), Sabine Fajmann (Institute of Pharmacology and Toxicology, University of Veterinary Medicine, Vienna, Austria), and Boris Kovacic (Institute of Medical Genetics, Medical University of Vienna, Vienna, Austria) for technical support. We thank also our mouse facility team and Jisung Park (Department of Chemistry, University of Toronto Mississauga, Canada) for synthesizing the inhibitor AC-3-19 used in this study.
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