Research

We investigate the role of functional p53 in the acute cellular and tissue responses to anthracycline chemotherapy using AML cell lines and in vivo models. Our work dissects signalling events that determine whether DNA damage leads to repair and recovery or to apoptotic cell death and therapy resistance.

Experiments integrate pathway analysis, genetic perturbation of p53 and upstream regulators, and timed chemotherapy exposures to map critical nodes that could be targeted pharmacologically to improve anthracycline efficacy while limiting harm to normal tissue.

We develop PEGylated, ligand‑targeted liposomes co‑encapsulating daunorubicin and agents such as emetine or prodrug derivatives to circumvent pump- and non‑pump-mediated resistance. Formulations are characterised for drug loading, stability, targeting moieties and release kinetics.

Biological evaluation uses AML cell panels (including p53-deficient models), primary patient samples and in vivo xenograft models to assess efficacy, biodistribution and toxicity relative to free drug. Results guide optimisation towards translationally relevant formulations.

This programme bridges formulation science and pharmacology in order to translate repurposed drugs into effective anti‑leukaemic therapies. We combine formulation strategies with pharmacokinetic and pharmacodynamic evaluation to understand how carrier composition, surface chemistry and size affect circulation, uptake and therapeutic index.

Parallel work addresses challenges in clinical translation — manufacturing, stability and regulatory considerations — and explores how priming strategies (for example metabolic or folate‑mediated priming) can increase selective uptake by AML cells.

We screen extracts and purified compounds from marine microalgae, cyanobacteria and epiphytes for cytotoxic activity against AML cells. Hits are progressed through fractionation, structure elucidation and target-deconvolution using biochemical and cell-based assays.

Mechanistic studies focus on modulation of protein phosphatases, kinases and apoptotic regulators to place natural hits into signalling contexts that enable rational combination with existing chemotherapies or nanoparticle delivery approaches.