My undergraduate research focused on the molecular mechanism by which a mutant form of β-catenin, Batface (Bfc), drives elevated Wnt signalling levels. Despite finding the intricacies of protein function fascinating, I was eager to expand my investigation of disrupted signalling pathways into the context of cancer models. This desire to translate my research in a broader, more clinical sense led me to the Leedham lab.
Our research focuses on the exquisitely balanced signalling pathways and morphogen gradients that define intestinal stem cell homeostasis and the subsequent disruption of these pathways in carcinogenesis and disease.
My current project utilises human tissue and cancer cell lines along with genetically modified mouse models to investigate somatic mutation as a window to underlying disease pathogenesis.