Hematopoietic cancer

We are studying normal and abnormal hematopoiesis. We and others have described an essential role for STAT5 activation in regulation of survival genes in myeloid leukemias with a link to PI3K-AKT-mTOR activation. We were the first to link serine phosphorylation and oligomerization of STAT5 to myeloid transformation. We have related the findings to human MPN. Currently, we study how increased levels of hyperactive STAT5 signalling drive leukemia and lymphoma development in association with chromatin modifiers.  The RM lab is further involved in therapeutic cancer intervention studies, also within the context of an SFB F47, where our mission is to pioneer preclinical work with lead inhibitors tested in international collaboration with the group of Prof. Patrick Gunning, Toronto, Canada, to target STAT5. These projects are conducted in close collaboration with Medical and Veterinary Medicine universities, IMP, CeMM, CCRI (Weblink to Ludwig Boltzmann-Institute, Partnerships 1) and University Vienna.

The Recurrent STAT5B Driver Mutation Causes Rapid Lymphoma/Leukemia in Juvenile Mice: A Schematic of STAT5B together with reported recurrent, somatic mutations. B Kaplan–Meier survival curve of mice which harbor the STAT5B mutation shows that the mice were terminally ill at the age of 60 days. C Peripheral blood smear of the mutant mice shows a severe degree of white blood cell expansion. D Mutant STAT5B transgenic mice suffer from splenomegaly with eight fold increase in spleen weight (data not shown). E STAT5 expression and activation was increased in LN of transgenic mice as analyzed by immunoblotting. F Further analysis revealed that the LSK population in the transgenic mice is significantly increased in comparison to WT mice. G Interestingly, the population of the common lymphoid progenitor cells is also increased.
The Recurrent STAT5B Driver Mutation Causes Rapid Lymphoma/Leukemia in Juvenile Mice 2

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