One of the key pathways in cancer development is the Janus kinase (JAK) – signal transducer and activator of transcription (STAT) signaling pathway. One component of this pathway, STAT3 has been proposed as an oncogene, but recently it was also demonstrated as a tumor suppressor in different tumor models. In hematologic malignancies persistent STAT3 activation has frequently been detected suggesting an important role therein. Stat3 produces two isoforms (STAT3α and β) by alternative splicing that exhibit overlapping but distinct transcriptional activity.
Dagmar Stoiber Sakaguchi
Please note this website is not updated anymore as the LBI-CR was integrated into its partner universities.
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 has now moved to the Karl Landsteiner University, Krems.
The research team of Dagmar Stoiber-Sakaguchi (from left) Jaqueline Horvath (Research assistant), Verena Greß (Master student), Lena Müller (PhD student), Petra Aigner (PhD student), Dagmar Stoiber-Sakaguchi (Key researcher)
About Dagmar Stoiber
Dagmar Stoiber is a founding member of the LBI-CR and heads her independent research team since 2006. As of March 2017 she has contributed to more than 34 PubMed based publications and has an h-factor of 21 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.
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.
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. M. Müller, Institute of Animal Breeding and Genetics, University of Veterinary Medicine, Vienna, Austria, for Jak-Stat signaling