DR Marie-Liesse Asselin-Labat

DR Marie-Liesse Asselin-Labat


  • Epigenetic regulator of lung morphogenesis
  • Lung stem cells in normal development and in lung disease
  • Role of DNA repair mechanisms in adult lung stem cells and disease



  • www.wehi.edu.au/people/marie-liesse-asselin-labat

    My laboratory is investigating lung development and lung cancer.

    We are studying how lung development is controlled. This is a precise process that is essential for breathing. Defects in this process can result in respiratory failure at birth. The goal of our research is to understand how lung developmental disorders occur.

    Our research is also revealing how lung cancer forms. We are developing new laboratory models of lung cancer that allow us to assess new treatments. We hope in the long term to improve the outcomes for people with lung cancer.   


Selected publications


Additional Grant Information

  • 2016-2020 Viertel Foundation Senior Medical Researcher Fellowship
    2017-2020 NHMRC Project Grant
    2015-2017 NHMRC Project Grant
    2014-2016 WCR (formerly AICR) Project Grant,
    2013-2015 NHMRC Project Grant (x2)
    2012-2014 NHMRC Development Grant    


Education and training

  • PhD, Universite Paris Sud (Paris XI)


Available for supervision

  • Y

Supervision Statement

  • We are interested in studying the cellular and molecular mechanisms underlying lung development and lung cancer formation.

    We are interested in evaluating the contribution of epigenetic mechanisms in modulating the plasticity and specificity of early lung progenitor cells. We are specifically interested in understanding how chromatin remodelling factors control cell fate maintenance. We aim to define the contribution of epigenetic modifiers in the transcriptional and structural changes required for embryonic lung formation. This will provide insights into how lung diseases develop, and will identify potential new therapeutic targets.

    We study molecular and cellular events driving lung cancer formation. We have shown that different lung cell types possess different DNA repair capacities. We are now interested in determining how perturbation in DNA damage responses can participate in lung cancer formation. Additionnally, we have developed preclinical models of lung cancer that are used to study the mechanisms of drug response and resistance to therapy. We use these models to identify novel biomarkers predictive of drug response and to evaluate novel therapeutic approaches.