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Group Mikulits

Stat Activation in Liver Fibrosis and Late Stage Hepatocarcinogenesis


We investigate the role of Stat3 in hepatic fibrosis and liver carcinoma progression and focus on Stat3 as the molecular link between these different but related liver diseases. Advanced hepatocellular systems combined with animal tumour models allow us to analyse the impact of Stat3 activation in these pathophysiological changes of both parenchymal and mesenchymal compartments. In particular, we employ the epithelial to mesenchymal transition (EMT) of hepatocytes as a close in vitro correlate of liver carcinoma progression and metastasis. Studies on epithelial-mesenchymal interactions further address the involvement of Stat3 in the communication between malignant hepatocytes and stromal cells of the tumour microenvironment, and thus deal with the molecular and cellular implications of Stat3 activation in the tumour-host crosstalk.

Key Hypothesis:

  • Stat3 is the molecular link between hepatic fibrosis and liver carcinoma progression. Other important signal transduction pathways like TGF-ß/PGDF/PI3K/Ras and/or ß-catenin signalling might co-operate with Stat3 activation in tumourigenesis.
Antwort auf/zuklappen Report on funding period 1 (03/2006-03/2010)

Antwort auf/zuklappen Proposal for funding period 2 (03/2010-03/2013)


Department of Medicine I, Division: Institute of Cancer Research,
Medical University of Vienna
Broschke-Gasse 8a
A-1090 Vienna


phone: +43(0)1 4277 65250
fax: +43(0)1 4277-65239