This research investigates macrophages, immune cells that regulate infection, tissue repair, and cancer responses. Through laboratory experiments and machine-learning models, it aims to predict macrophage function across different diseases and patients. The work could improve prognosis, guide treatments, evaluate drug safety, and forecast recovery following major illnesses and injuries.

This research uses spatial transcriptomics to map interactions between T cells, cancer cells, and immunosuppressive cells in tumours. Findings suggest cancer suppresses immune responses by surrounding and weakening T cells. The work aims to improve immunotherapy and enable personalised cancer treatment through detailed tumour mapping.

This research investigates how melanoma switches between two gene states—one fast-growing and treatable, the other slow but highly invasive and responsible for brain metastases. By identifying genes that control this transition, the study aims to force melanoma into a more treatable form, improving therapeutic options and patient outcomes.

This research uses yeast to study conserved molecular machinery that ensures safe chromosome division. Focusing on a key cohesin-regulating protein, the work reveals how DNA is accurately separated during cell division and how failures in this system can lead to chromosomal errors, developmental disorders, and cancer.

Mitochondria power cells and communicate with the nucleus to control gene expression. This research builds minimal artificial cells containing only mitochondria and nuclei to isolate this signaling pathway. The system reveals how mitochondrial dysfunction alters gene expression, offering new insight into mechanisms underlying cancer and neurological diseases.

This research investigates how cells repair dangerous DNA double-strand breaks through the non-homologous end joining pathway. By identifying key proteins involved in this error-prone repair process, the work reveals new opportunities to sensitise cancer cells to radiation and chemotherapy, potentially improving treatment outcomes for aggressive cancers.

Breast cancer most often kills by spreading to the brain, where hormone therapies fail. This research reveals a signaling pathway that drives tumor growth in both pre- and postmenopausal settings. Identifying alternative activators of this pathway opens new therapeutic opportunities for deadly brain metastases.

Cancer cells survive extreme oxidative stress by importing lipoproteins that deliver vitamin E, a powerful antioxidant. This creates a fire-resistant shield that prevents ferroptotic cell death. Blocking vitamin E delivery or lipoprotein uptake removes this protection, revealing a new vulnerability that could influence tumor growth and treatment response.