Research by Prof. Richard Moriggl and his team at the University of Veterinary Medicine, Vienna and the Paris Lodron University of Salzburg has provided new insights into the development and possible treatment of T-cell acute lymphoblastic leukemia (T-ALL). They discovered that the protein STAT5B, which is activated by mutations in T-ALL patients, promotes cancer growth by stimulating cell division. This finding could lead to new targeted therapies. Pilot experiments in mice have shown that drugs that target STAT5B or inhibit a target protein of it can reduce cancer growth. Such an agent targeting ZAP70 has already been approved for other diseases and could therefore be rapidly tested in clinical trials for T-ALL. The results could also be relevant for other T-cell leukemias and require further research and clinical trials.

Publication in The Journal of Clinical Investigation:

Hyperactive STAT5 Hijacks T-Cell Receptor Signaling and Drives Immature T-Cell Acute Lymphoblastic Leukemia

Tobias Suske, Helena Sorger, Gabriele Manhart, Frank Ruge, Nicole Prutsch, Mark W. Zimmerman, Thomas Eder, Diaaeldin I. Abdallah, Barbara Maurer, Christina Wagner, Susann Schönefeldt, Katrin Spirk, Alexander Pichler, Tea Pemovska, Carmen Schweicker, Daniel Pölöske, Emina Hubanic, Dennis Jungherz, Tony Andreas Müller, Myint Myat Khine Aung, Anna Orlova, Ha Thi Thanh Pham, Kerstin Zimmel, Thomas Krausgruber, Christoph Bock, Mathias Müller, Maik Dahlhoff, Auke Boersma, Thomas Rülicke, Roman Fleck, Elvin Dominic de Araujo, Patrick Thomas Gunning, Tero Aittokallio, Satu Mustjoki, Takaomi Sanda, Sylvia Hartmann, Florian Grebien, Gregor Hoermann, Torsten Haferlach, Philipp Bernhard Staber, Heidi Anne Neubauer, Alfred Thomas Look, Marco Herling, Richard Moriggl