We study how cancer cells adapt, survive, and change over time, and how these processes shape and are shaped by evolution, leading to treatment resistance and progression/relapse.
Cancer is not static. Under treatment, cancer cells can switch identity without changes in the genome (phenotypic plasticity), and/or select for (epi)-genetic states that enable survival.
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Our lab investigates how phenotypic plasticity and genetic evolution interplay to drive treatment resistance, with a particular focus on paediatric cancers.
For children with cancer, treatment resistance leading to relapse remains one of the biggest clinical challenges.
Understanding how cancer cells adapt and evolve to treatment is essential to predicting disease progression and designing more effective therapies.
We aim to uncover the principles that govern these cancer evolutionary processes, so that clinical practise can be designed to anticipate and block adaptation, rather than react to it.
We develop and apply single-cell and lineage-recording approaches to quantify how individual cancer cells change state under stress and treatment.
We build quantitative and mechanistic models that link cell-state dynamics to genetic evolution, selection, and long-term tumour behaviour.
We focus on paediatric solid tumours, where lower mutational burden and strong selective pressures make plasticity-driven adaptation especially visible and clinically relevant.