Cancer is driven by genetic alterations that accumulate in our cells over a lifetime. Large-scale sequencing has catalogued the mutations found in human cancers, yet we still lack a comprehensive understanding of how these alterations shape cancer biology.​ Our lab aims to bridge this gap by connecting cancer genotypes to molecular mechanisms, cellular phenotypes and therapeutic response. Our research has three interconnected components:

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Technology development. We develop CRISPR-based functional genomics tools, including Perturb-seq approaches [1], combinatorial CRISPR screens [2] and prime editing screens [3], to systematically investigate gene function, genetic interactions and the functional consequences of specific genetic variants.​​

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Mechanisms of cancer and therapy resistance. We use these tools, together with single-cell transcriptomics and computational analysis of genetic interaction networks, to uncover the molecular mechanisms underlying cancer development, therapeutic vulnerabilities and drug resistance.​​

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Patient-derived tumor models. We establish and use patient-derived tumour organoids from patients with pancreatic cancer and advanced colorectal cancer to study genetic dependencies and treatment responses in models that reflect individual patients' tumours.

 

By combining these complementary approaches, we aim to identify actionable vulnerabilities and translate our insights into improved treatment strategies for patients.