Detail

Keywords

Animals, Genetically Modified; Carcinoma, Non-Small-Cell Lung; Inflammation; Kirsten murine sarcoma virus; Receptor, Epidermal Growth Factor

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 lung cancer. Currently, my research group is focused in three main topics:

1) Role of inflammation in KRAS driven lung adenocarcinomas.

2) Targeted and immune-therapies in lung adenocarcinomas .

3) Exploring the possibilities of using BAC-based expression vectors applied to mammalian (e.g. CHO-K1 cells) 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
• Tumor transplant models
• Recombinant protein production

Grants

• Afatinib in KRAS driven lung cancer (2020)
  Source of Funding: FWF (Austrian Science Fund), stand-alone project
  Principal Investigator
• JAK in KRAS driven lung cancer (2020)
  Source of Funding: FWF (Austrian Science Fund), Stand-Alone Project
  Principal Investigator
• 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. Breitenecker, K. et al., 2021. Down-regulation of A20 promotes immune escape of lung adenocarcinomas. Science Translational Medicine, 13(601), p.eabc3911. Available at: http://dx.doi.org/10.1126/scitranslmed.abc3911.
2. Mohrherr, J. et al., 2019. JAK–STAT inhibition impairs K‐RAS‐driven lung adenocarcinoma progression. International Journal of Cancer, 145(12), pp.3376–3388. Available at: http://dx.doi.org/10.1002/ijc.32624.
3. 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.
4. 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.
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.