Research
The Cancer Evolution Laboratory investigates how genetic changes are translated into aggressive tumour behaviour. The group studies how TP53 mutations, p53 isoforms and dysregulated YB-1 reshape DNA repair, RNA splicing, translation, metabolism and cell division, allowing cancers to survive stress, resist therapy and metastasise. By combining experimental cancer biology with genomics, bioinformatics, CRISPR-based functional studies, microscopy, molecular modelling and preclinical drug testing, the laboratory aims to identify biomarkers and treatment vulnerabilities for genetically defined cancers.
We define how individual TP53 mutations and p53 isoforms produce distinct effects on genome stability, metabolism, invasion and patient outcome.
How do specific TP53 alleles and isoforms reprogramme cancer cells in ways that differ from simple loss of p53?Explore this programme →
We study how YB-1 controls cell division and enables TP53-mutant cancers to tolerate abnormal mitosis, genomic instability and treatment stress.
Which YB-1-dependent mechanisms allow genomically unstable cancer cells to complete—or survive—abnormal cell division?Explore this programme →
We investigate how altered RNA processing, translation, signalling and protein-state control help aggressive cancers adapt, disseminate and evade treatment.
Which adaptive molecular states let cancer cells survive genomic and metabolic stress long enough to become metastatic or drug resistant?Explore this programme →
We integrate genomic, molecular and clinical evidence to identify biomarkers and drug targets for genetically defined tumour subtypes.
Can multi-layered tumour data be converted into reliable biomarkers that predict prognosis and response to targeted or immune-based therapies?Explore this programme →
