I am a cancer cell biologist focused on tumor suppression with a strong interest in cellular plasticity and selective transcription. My research aims to advance early cancer detection, prevent cancer progression and develop strategies for selective cancer cell killing.

I earned my BSc from Sichuan University and MSc from Pekin Union Medical College, Chinese Academy of Medical Sciences in China. I moved to the UK with a competitive fellowship from the World Health Organization’s International Agency for Research on Cancer. Following my PhD at University College London (UCL) and the former Imperial Cancer Research Fund, and postdoctoral training at Dundee University, I established my independent research group at the Ludwig Institute for Cancer Research. I was appointed as the Director of the Ludwig Institute in London at UCL in 2004. I moved the Ludwig research activities to the University of Oxford and established Ludwig Oxford in 2007.

My research group studies tumor suppression with long-standing interests in the regulation of the most mutated tumor suppressor, p53. We were one of the first groups to show how to selectively regulate p53’s tumor suppressive function through our identification of the ASPP family of proteins (ASPP1, ASPP2 and iASPP) as key cellular regulators of p53 and its family members, p63 and p73.

Our current research focuses on the identification of molecular switches of cellular plasticity. In particular, we study how a given cell can sense external signals, such as infection or mechanical stress, and relay these to the nucleus to achieve target selective transcription and cell fate determination.

By applying our knowledge of cellular plasticity regulation to clinical settings, we aim to identify 1) the cancer-initiating cell of origin and 2) the molecular switches that control the conversion from the benign to an early cancer state. As cellular plasticity is a programmed biological process in development and dysfunction of this program will cause cancer, we also have strong interests in developmental disorders, particularly following our recent identification of the involvement of the ASPPs in two developmental disorders: 1q41-42 microdeletion syndrome, a neurological disorder involving ASPP2 deletion; and cardiac sudden death and cardio-cutaneous syndrome caused by iASPP deletion.