Research

Ionising radiation creates DNA damage that can lead to death, durable arrest or recovery. The laboratory investigates p21 as a central regulator of this decision and examines how its cell-cycle, DNA-repair and stress-response functions contribute to radioresistance.

By comparing cancer and normal-cell systems across radiation qualities and schedules, the group seeks molecular signatures that distinguish protective arrest from irreversible loss of proliferative capacity and identify rational routes to radiosensitisation.

Radiotherapy can influence tumour biology outside the irradiated field. The laboratory investigates the molecular and cellular mechanisms underlying the abscopal effect and develops frameworks for evaluating combined immunoradiotherapy.

Particular attention is given to particle radiation, treatment fractionation and the balance between immune activation, tumour-cell death and normal-tissue effects.

Flat monolayer cultures cannot fully reproduce gradients of oxygen and nutrients, cell–cell contact or extracellular matrix found in tissues. The laboratory therefore develops three-dimensional spheroid and scaffold-based cultures.

These systems are characterised for growth, viability, molecular response and radiosensitivity, providing experimentally tractable platforms for comparing tumour and healthy-tissue effects and testing new treatment combinations.

Charged-particle therapy can reduce dose to surrounding healthy tissue, while FLASH radiotherapy introduces ultra-high dose rates that may produce distinct biological effects. The laboratory studies how these modalities influence DNA damage, stress signalling, cell survival and immune responses.

Collaborations with physics, accelerator and biomaterials groups connect beam characteristics and dosimetry with biological endpoints in cancer and normal-cell systems.