معرفی
Dr. Alexandra Davis is a Senior Lecturer in Biomedical Science at De Montfort University, affiliated with the School of Allied Health Sciences and the Leicester Institute for Pharmaceutical & Health Innovations (LIPHI). Her work bridges virology and cancer biology, focusing on tumour-stroma interactions and fibroblast-mediated drug resistance in breast cancer.
- BSc in Biomedical Science
- PhD in Viral Oncology, De Montfort University
Her research investigates how Epstein-Barr virus (EBV) Latent Membrane Protein 1 (LMP1) influences the tumour microenvironment by inducing epithelial-mesenchymal transition (EMT) and fibroblast-to-myofibroblast differentiation. She developed innovative 3D co-culture models to study these interactions in a more physiologically relevant context. Her findings highlight key signaling pathways such as TGFβ and ERK/MAPK as critical mediators in stromal transformation and tumour progression.
The recent publications reflect a strong focus on viral oncology, cellular transformation, and 3D modeling of tumour-stroma dynamics. Her work consistently explores mechanisms of invasion, paracrine signaling, and therapeutic resistance, particularly in epithelial cancers. These studies contribute to understanding how viral proteins manipulate host microenvironments to promote metastasis.
Scientific recognition includes:
- Fellow of the Higher Education Academy (FHEA)
Dr. Davis is actively involved in pedagogic research and teaches across multiple programs, including the BSc Biomedical Science, BSc Medical Science, and MSc Advanced Biomedical Science. She supervises research projects and contributes to curriculum development. While no formal advisees are listed, her role in research training is evident through student engagement in her lab work. She is also associated with LIPHI, contributing to collaborative pharmaceutical and health innovation projects.
Her laboratory focuses on developing and applying 3D culture systems to model breast cancer stroma interactions, aiming to uncover mechanisms of fibroblast-driven drug resistance and identify novel therapeutic targets.
