Professor of Cancer Biology
- Director, Ludwig Institute for Cancer Research, Oxford Branch
- Theme Lead, Multimodal Cancer Therapies Theme, NIHR Oxford Biomedical Research Centre
- Director, Oxford Centre for Early Cancer Detection
The main goal of our research is to identify molecular mechanisms that control cellular plasticity and suppress tumour growth. Cells are able to change their characteristics and cell fate in response to external signals. This ability to change – cellular plasticity – underlies cancer initiation, metastasis and resistance to therapy. We are particularly interested in ‘guardians’ of plasticity in epithelial cells, from which over 80% of human tumours originate. We have a long-standing interest in the tumour suppressor p53 and the ASPP family of proteins (Apoptosis-Stimulating Protein of p53; Ankyrin repeats, SH3 domain and Proline rich sequence containing proteins), which have several roles including regulation of p53.
Our current areas of interest include: understanding how selective transcription is controls cell fate; identifying regulators of cellular plasticity in upper gastrointestinal cancer initiation and metastasis (particularly oesophageal cancer and gastric cancer); and understanding the influence of infection on cell plasticity and cancer (particularly Helicobacter pylori and Epstein Barr Virus (EBV) infection).
iASPP oncoprotein is a key inhibitor of p53 conserved from worm to human.
Bergamaschi D. et al, (2003), Nat Genet, 33, 162 - 167
ASPP2 controls epithelial plasticity and inhibits metastasis through β-catenin-dependent regulation of ZEB1.
Wang Y. et al, (2014), Nature cell biology, 16, 1092 - 1104
Single cell RNA-seq reveals profound transcriptional similarity between Barrett’s oesophagus and oesophageal submucosal glands
LU X. et al, Nature Communications
ASPP2 maintains the integrity of mechanically stressed pseudostratified epithelia during morphogenesis
Royer C. et al, (2022), Nature Communications, 13
Human ZBP1 induces cell death-independent inflammatory signaling via RIPK3 and RIPK1.
Peng R. et al, (2022), EMBO reports