Research programme 03
Stress adaptation, metastasis and therapy resistance
We investigate how altered RNA processing, translation, signalling and protein-state control help aggressive cancers adapt, disseminate and evade treatment.
Central question
Which adaptive molecular states let cancer cells survive genomic and metabolic stress long enough to become metastatic or drug resistant?
Cancer evolution is driven not only by the acquisition of mutations but also by the cellular systems that buffer their consequences. The laboratory examines how altered RNA splicing, translational control, DNA-repair responses, cell-surface signalling and protein aggregation create flexible states that support survival under therapeutic pressure.
A major theme is the p53 isoform network. Studies of Δ133p53β have connected isoform expression with invasion, inflammatory signalling, brain metastasis and context-dependent protein aggregation. These findings provide mechanistic routes through which tumour cells can move between proliferative, stress-tolerant and metastatic states.
Approaches
- RNA-sequencing and transcript-isoform analysis
- Proteomics and protein-interaction studies
- Three-dimensional and metastatic cancer models
- Cell-surface and signalling assays
- Functional genomics and perturbation screens
- In vitro and in vivo cancer models
Selected work
- Increased Expression of the Δ133p53β Isoform Enhances Brain Metastasis (2023)
- Δ133p53β isoform pro-invasive activity is regulated through an aggregation-dependent mechanism in cancer cells (2021)
- Adaptive homeostasis and the p53 isoform network (2021)