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Dr Davide Zecchin
Dr Davide Zecchin profile picture
  • Research Fellow
  • Genetics & Genomic Medicine Dept
  • UCL GOS Institute of Child Health
  • Faculty of Pop Health Sciences

I trained in molecular biotechnology at the University of Turin (Italy), before starting my PhD in Molecular Medicine at the Institute for Cancer Research and Treatment ā€“ Candiolo (Italy) and at the University of Regensburg (Germany), under the supervision of prof. Alberto Bardelli. In 2013 I undertook a post-doctoral fellowship in the lab of Prof. Julian Downward, during  which I moved to the Francis Crick Institute- London (UK). In 2019 I joined the lab of Prof. Veronica Kinsler at UCL Great Ormond Street Institute of Child Health and then Francis Crick Institute- London (UK). During this period, I was granted funds from charities for the study of Sturge Weber Syndrome and melanoma occurring in CMN (Congenital melanocytic nevi) patients.

Research Summary

During my PhD training and post-doctoral experience in Prof. Julian Downward's lab, I have focused on the study of cancer, from functional characterisation of cancer mutations to investigation of targeted ways of intervention. To this aim, I employed a variety of approaches, including cellular and mouse models, and high or low-throughput screening methods designed to answer specific biological questions. My work unveiled targetable vulnerabilities in a G proteins-centred signalling network in PTEN-deficient triple-negative breast cancers.

More recently, under supervision of Prof. Veronica Kinsler, I have been applying my experience to molecular characterisation and identification of therapeutic targets for rare mosaic genetic diseases. Iā€™ m translating my knowledge of aberrant G protein signalling to the study and treatment of Sturge Weber Syndrome, caused by mutations in G protein-coding genes. My research is also currently focusing on identifying therapeutic vulnerabilities in melanoma occurring in CMN (Congenital melanocytic nevi) patients, an inoperable and lethal disease caused in most cases by mosaic mutations on NRAS gene.

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