Rate My Professor Margaret Currie

Currie's research focuses on the tumour microenvironment, exploring how its components—including tumour blood vessels, immune cells, fibroblasts, adipocytes, soluble growth factors, and signalling molecules—influence tumour growth, metastasis, and response to therapy. Tumour cells reciprocally affect the microenvironment, which varies with age and health due to systemic changes in metabolism, hormones, and immunity. The group's interests have expanded from initial studies on tumour blood vessel development and anti-angiogenic therapies to include tumour-infiltrating immune cells, breast cancer stem cell-like populations, and obesity-related factors. Her contributions are evidenced in highly cited publications such as 'The angiogenic switch for vascular endothelial growth factor (VEGF)-A, VEGF-B, VEGF-C, and VEGF-D in the adenoma–carcinoma sequence during colorectal cancer progression' (Hanrahan et al., 2003), 'Vitamin C and immune cell function in inflammation and cancer' (Ang et al., 2018), 'Low ascorbate levels are associated with increased hypoxia-inducible factor-1 activity and an aggressive tumor phenotype in endometrial cancer' (Kuiper et al., 2010), 'Intracellular ascorbate enhances hypoxia-inducible factor (HIF)-hydroxylase activity and preferentially suppresses the HIF-1 transcriptional response' (Kuiper et al., 2014), and 'Cytomegalovirus and Epstein-Barr virus in breast cancer' (Richardson et al., 2015). Recent works include 'The Role of Innate Priming in Modifying Tumor-associated Macrophage Phenotype' (Topham et al., 2024) and 'Gelatin-methacryloyl hydrogel stiffness influences epithelial-mesenchymal transition in MCF7 but not MDA-MB-231 breast cancer cells in 3D culture' (Wise et al., 2026).