In childhood B-ALL the t(12;21)(p13;q22) chromosomal translocation represents the most frequent rearrangement with an incidence of up to 25% in pediatric patients. The chromosomal translocation results in the ETV6/RUNX1 fusion gene, which is assumed as the “first hit” in ETV6/RUNX1 positive B-ALL, but additional genetic alterations are required for the manifestation of the leukemia. Our goal is to identify secondary hits by developing mouse models for this fatal disease.
Dagmar Stoiber Sakaguchi
Our major interest is to elucidate the molecular basis underlying the development of hematopoietic malignancies. We currently work on three research topics: 1) Acute lymphoblastic leukemia 2) Myeloproliferative disorders 3) Tumor surveillance
The research team of Dagmar Stoiber-Sakaguchi (left) with Jaqueline Horvath and Petra Aigner (right)
About Dagmar Stoiber
Dagmar Stoiber is a founding member of the LBI-CR and heads her independent research team since 2006. As of March 2016 she has contributed to more than 32 PubMed based publications and has an h-factor of 18 according to her google scholar profile. She lectures at the Pharmacology Department and in 2015 she completed her "Habilitation" at the Medical University Vienna.
DS did her PhD with Thomas Decker at the University of Vienna. For her post-doctoral research she joined the team of Tadatsugu Taniguchi at the University of Tokyo and subsequently joined the Institute of Pharmacology at the Medical University Vienna as university assistant.
Please follow the link for a full CV of Dagmar Stoiber.
There are four main myeloproliferative disorders (MPD), - polycythemia vera, essential thrombocytosis, myelofibrosis and chronic myelogenous leukemia (CML). MPD are related to, and may evolve into, myelodysplastic syndrome and acute myeloid leukemia, although the MPD on the whole have a much better prognosis than these conditions. MPD – with the exception of CML – are frequently associated with a mutation of Janus kinase 2 (Jak2 617V>F). We are generating a new mouse model for MPD. With this novel mouse model we intend to elucidate the cooperativity of candidate genes and signaling pathways to interact with constitutive active Jak2 in the development of MPD.
Cells in the human body continuously undergo spontaneous mutations, some of them targeting proto-oncogenes or tumor suppressor genes. These are counteracted by the immune system that is nowadays widely accepted to be able to identify and subsequently eliminate cancerous self. This process is referred to as tumor immune surveillance. We are investigating surveillance of hematopoietic but also solid tumors in mouse models. Our focus lies on the Jak/Stat pathway, in particular interferon signaling, and its role in tumor immune surveillance.
Prof. M. Busslinger, IMP, Vienna, Austria, for the ETV6-RUNX1 project
Dr. T. Decker, Institute of Microbiology and Genetics, Vienna, Austria, for Jak-Stat signaling
Dr. W. Ellmeier, Institute of Immunology, Medical University of Vienna, Austria, for lymphocyte function
Dr. A. Dohnal, Children´s Cancer Research Institute, St. Anna Kinderkrebsforschung, Vienna, Austria