Detail

Keywords

Adenocarcinoma; Carcinoma, Hepatocellular; Mice, Transgenic; Recombinant Proteins

Research group(s)

• Emilio Casanova
  Members:
  • Emilio Casanova

Research interests

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;
• Xenografts;
• Recombinant protein production

Grants

• Carbohydrate libraries for improved innate immunity binding (2016)
  Source of Funding: FFG (Austrian Research Promotion Agency), BRIDGE
  Principal Investigator
• EAVI2020 - European AIDS Vaccine Initiative 2020 (project partner) (2015)
  Source of Funding: EU, H2020-PHC-2015-single-stage_RTD
  Principal Investigator
• Growth hormone resistance and liver fibrosis (2013)
  Source of Funding: FWF (Austrian Science Fund), Stand-Alone Projects
  Principal Investigator
• BAC-based Expression System Technology (2011)
  Source of Funding: FFG (Austrian Research Promotion Agency), Bridge
  Principal Investigator

Selected publications

1. Moll, H.P. et al., 2018. Afatinib restrains K-RAS-driven lung tumorigenesis. Science Translational Medicine, 10(446), p.eaao2301. Available at: http://dx.doi.org/10.1126/scitranslmed.aao2301.
2. 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.
3. Grabner, B. et al., 2015. Disruption of STAT3 signalling promotes KRAS-induced lung tumorigenesis. Nature Communications, 6(1). Available at: http://dx.doi.org/10.1038/ncomms7285.
4. 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.
5. Musteanu, M. et al., 2012. A mouse model to identify cooperating signaling pathways in cancer. Nature Methods, 9(9), pp.897-900. Available at: http://dx.doi.org/10.1038/nmeth.2130.