Research

Germinal-centre B cells undergo rapid proliferation, mutation and stringent selection. The lab studies how mutations such as those affecting BTG1 alter competitive fitness, allowing abnormal clones to dominate otherwise regulated immune reactions.

Multi-allelic mouse models, patient-derived systems and primary human samples are used to connect altered competition with aggressive diffuse large B-cell lymphoma and to distinguish adaptive immune selection from malignant evolution.

Competitive B cells and lymphomas must match rapid cell division with increased nutrient uptake, mitochondrial activity and macromolecular synthesis. The programme maps metabolic states associated with superior fitness and aggressive disease.

Metabolic flux measurements are integrated with genetic perturbation and functional assays to identify dependencies that are dispensable in normal B cells but essential in clinically unfavourable lymphomas.

The laboratory examines how normal germinal-centre plasticity is co-opted during lymphomagenesis. Changes in chromatin regulators such as ARID1A can alter sequential transcription-factor binding and push cells towards high-risk precursor states.

By combining genomics, imaging and functional models, the programme traces how transient immune states become stable malignant identities and how those states influence disease subtype and clinical behaviour.

Aggressive DLBCL cells must survive outside their original lymphoid niche and adapt to new microenvironments. The group investigates extracellular signals, cell-cell communication and biochemical adaptations that support dissemination.

Mechanistic findings are tested in patient-relevant models to identify vulnerabilities for rational combination therapies, with emphasis on relapsed or refractory disease.