Adenocarcinoma; Carcinoma, Hepatocellular; Mice, Transgenic; Recombinant Proteins
- Emilio Casanova
My main research goal is modeling human diseases using genetically modified animals as tools. I have a strong expertise in the generation and characterization of transgenic mice (conditional knock-outs, knock-ins, BAC-based transgenic, etc.) mimicking human diseases with special emphasis in liver cirrhosis and cancer. Currently, my research group is focused in four main topics:
1) The role of the GH (Growth hormone)-STAT5 (Signal transducer and activator of transcription 5)-IGF1 (Insulin-like growth factor 1) axis in liver cirrhosis and hepatocellular carcinoma (HCC).
2) Genetically dissection of the role of the AKT isoforms (AKT1, 2 and 3) in mammary gland tumors.
3) Contribution of STAT3 (Signal transducer and activator of transcription 3) and EGFR (Epidermal growth factor receptor) to K-RAS dependent lung tumors.
4) Exploring the possibilities of using BAC-based expression vectors applied to mammalian recombinant protein production, which could provide anti-cancer treatments, a collaborative project with POLYMUN Scientific Immunobiologische Forschung, an Austrian company in the field of recombinant protein production.
Techniques, methods & infrastructure
- Molecular biology;
- Cell culture;
- Genetically modified mice;
- Recombinant protein production
- EAVI2020 - European AIDS Vaccine Initiative 2020 (project partner) (2015)
Source of Funding: EU, H2020-PHC-2015-single-stage_RTD
- Growth hormone resistance and liver fibrosis (2013)
Source of Funding: FWF (Austrian Science Fund), Stand-Alone Projects
- BAC-based Expression System Technology (2011)
Source of Funding: FFG (Austrian Research Promotion Agency), Bridge
- Zboray, K. et al., 2015. Heterologous protein production using euchromatin-containing expression vectors in mammalian cells. Nucleic Acids Research, 43(16), pp.e102-e102. Available at: http://dx.doi.org/10.1093/nar/gkv475.
- Grabner, B. et al., 2015. Disruption of STAT3 signalling promotes KRAS-induced lung tumorigenesis. Nat Comms, 6, p.6285. Available at: http://dx.doi.org/10.1038/ncomms7285.
- Stiedl, P. et al., 2015. Growth hormone resistance exacerbates cholestasis-induced murine liver fibrosis. Hepatology, 61(2), pp.613-626. Available at: http://dx.doi.org/10.1002/hep.27408.
- Musteanu, M. et al., 2012. A mouse model to identify cooperating signaling pathways in cancer. Nat Meth, 9(9), pp.897-900. Available at: http://dx.doi.org/10.1038/nmeth.2130.
- Blaas, L. et al., 2009. Disruption of the growth hormone-Signal transducer and activator of transcription 5-Insulinlike growth factor 1 axis severely aggravates liver fibrosis in a mouse model of cholestasis. Hepatology, 51(4), pp.1319-1326. Available at: http://dx.doi.org/10.1002/hep.23469.