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Dr. rer. nat. Gianmaria Liccardi
Dr. rer. nat. Gianmaria Liccardi

Institute of Biochemistry

University of Cologne

Albertus-Magnus-Platz

50923 Cologne

CV

Scientific degrees

2006 - 2011 PhD in Molecular Oncology, University College London (UCL), London, UK
2003 - 2004 MSc Molecular Medicine, Imperial College, London, UK
2000 - 2003 BSc Molecular Genetics in Biotechnology, University of Sussex, Brighton, UK

 

Scientific career

03/2021 - present Junior Group Leader, Center for Biochemistry, University of Cologne
2020 - 2021   Senior Post-doctoral Fellow, CECAD Research Centre, University of Cologne
2012 - 2019 Post-doctoral Fellow, The Institute of Cancer Research, London, UK
2018 - present Lecturer for MSc Oncology, The Institute of Cancer Research, London, UK
2011 - 2012 Post-doctoral Fellow, UCL Cancer Institute, UCL, London, UK
2006 - 2011 PhD student, UCL Cancer Institute, UCL, London, UK
2010 - present Lecturer, Faculty of Life Science, UCL, London, UK
2010 - 2012 Lecturer for MSc Cancer, UCL Cancer Institute, UCL, London, UK
2006 - 2010 Teaching Assistant, Faculty of Life Science, UCL, London, UK
2005 - 2006 Research Assistant, Imperial College, London, UK
2003 - 2004 MSc student, Imperial College, London, UK
2002 - 2003 Intern, Genome Damage & Stability Centre, University of Sussex, Brighton, UK

 

Honors/ Awards/ Memberships

2018 - present Editorial board member of Cell Death Disease
2016 Talk prize, ECDO Conference, Barcelona 2016
2015 First prize, Scientific Image competition, The Institute of Cancer Research, London, UK
2015 Dean Award, Pathway of Independence, The Institute of Cancer Research, London, UK
2012 Runner-up, Postdoctoral Fellow Poster competition, Cancer Institute Annual meeting, UCL, London
2011 Kitty Cookson Foundation Travel Award for 102nd AACR Annual Meeting in Orlando, Florida, USA

Publications

  • The importance of murine phospho-MLKL-S345 in situ detection for necroptosis assessment in vivo

    Necroptosis is a caspase-independent modality of cell death implicated in many inflammatory pathologies. The execution of this pathway requires the formation of a cytosolic platform that comprises RIPK1 and RIPK3 which, in turn, mediates the phosphorylation of the pseudokinase MLKL (S345 in mouse).…

    Link to the publication

  • CDK9 inhibition as an effective therapy for small cell lung cancer

    Treatment-naïve small cell lung cancer (SCLC) is typically susceptible to standard-of-care chemotherapy consisting of cisplatin andetoposide recently combined with PD-L1 inhibitors. Yet, in most cases, SCLC patients develop resistance to first-line therapy andalternative therapies are urgently…

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  • RIPK1‐mediated immunogenic cell death promotes anti‐tumour immunity against soft‐tissue sarcoma

    Drugs that mobilise the immune system against cancer are dramatically improving care for many people. Dying cancer cells play an active role in inducing anti‐tumour immunity but not every form of death can elicit an immune response. Moreover, resistance to apoptosis is a major problem in cancer…

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  • RIPK1 and Caspase-8 Ensure Chromosome Stability Independently of Their Role in Cell Death and Inflammation

    Receptor-interacting protein kinase (RIPK) 1 functions as a key mediator of tissue homeostasis via formation of Caspase-8 activating ripoptosome complexes, positively and negatively regulating apoptosis, necroptosis, and inflammation. Here, we report an unanticipated cell-death- and…

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  • LUBAC determines chemotherapy resistance in squamous cell lung cancer

    Lung squamous cell carcinoma (LSCC) and adenocarcinoma (LADC) are the most common lung cancer subtypes. Molecular targeted treatments have improved LADC patient survival but are largely ineffective in LSCC. The tumor suppressor FBW7 is commonly mutated or down-regulated in human LSCC, and oncogenic…

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  • RIPK1 prevents TRADD-driven, but TNFR1 independent, apoptosis during development

    RIPK1 is an essential downstream component of many pattern recognition and death receptors. RIPK1 can promote the activation of caspase-8 induced apoptosis and RIPK3-MLKL-mediated necroptosis, however, during development RIPK1 limits both forms of cell death. Accordingly, Ripk1-/- mice present with…

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  • Potent pro-apoptotic combination therapy is highly effective in a broad range of cancers

    Primary or acquired therapy resistance is a major obstacle to the effective treatment of cancer. Resistance to apoptosis has long been thought to contribute to therapy resistance. We show here that recombinant TRAIL and CDK9 inhibition cooperate in killing cells derived from a broad range of…

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  • MLKL post-translational modifications: road signs to infection, inflammation and unknown destinations

    Necroptosis is a caspase-independent modality of cell death that requires the activation of the executioner MLKL. In the last ten years the field gained a substantial amount of evidence regarding its involvement in host response to pathogens, TNF-induced inflammatory diseases as well as pathogen…

    Link to the publication
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