Laboratory of Molecular Cancer Genetics
Research
We define how ETV7 rewires interferon and stress-response networks to create breast-cancer states that survive chemotherapy and retain stem-like plasticity.
ETV7 is a transcriptional repressor whose elevated activity can reshape cancer-cell identity. The laboratory studies how ETV7 suppresses interferon-response and mitochondrial stress pathways, alters inflammatory signalling and promotes survival under chemotherapy.
We investigate how shorter p53 and p73 isoforms change localisation, transcriptional output and aggressive behaviour in melanoma and other cancers.
The TP53 family produces multiple protein isoforms with distinct domains and activities. The laboratory measures isoform expression and localisation and tests how altered ratios affect canonical p53-family responses.
We study how MYC, inflammatory signalling and stromal cues coordinate epithelial–mesenchymal transition, angiogenesis, invasion and metastatic colonisation.
Metastasis is not produced by a single oncogene but by coordinated changes across cancer cells and their environment. The group investigates how MYC and other transcriptional networks alter secreted factors, extracellular signalling and angiogenic programmes.
We translate mechanistic findings into expression signatures that classify breast and colon cancers and may predict prognosis or treatment response.
The laboratory analyses gene expression in biopsies from cancer patients alongside cell-line and model-system data. This design helps distinguish mechanisms that are experimentally tractable from associations that remain relevant in human tumours.
