My group is interested in epigenetic regulation of somatic mutagenesis in normal and malignant B cells. We aim to understand how alterations in the nuclear envelope influence B cell chromatin conformation, and what the epigenetic consequences of these alterations are.
My research group uses unique proteomics and computational approaches to understand how cell signalling pathways driven by the activity of protein kinases contribute to the development of cancer. Increasing this knowledge will be invaluable in advancing personalised cancer therapies.
We are interested in how cancer cells interact with each other and the microenvironment. We investigate how cancer cell communication with neighbouring stromal cells and the extracellular matrix can impact on invasion and response to targeted therapies, to try to block cancer progression, with a particular focus on breast and pancreatic cancer.
I am interested in studying the effects of the inflammatory microenvironment on disease progression and resistance to treatment in haematological malignancies with emphasis on survival and mechanisms of treatment resistance in chronic lymphocytic leukaemia and B cell lymphoma.
Our research is based on exploiting DNA repair defects in cancer for the identification of new personalised therapies. We use compound and siRNA screening to identify new therapeutics for tumours based on their specific DNA repair status.
My research is focused on describing the mechanisms underlying Lamin B1 nuclear disassembly in B-cell normal development and how a dis-regulated Lamin B1 removal pathway could lead to several haematological malignancies within the germinal centre in secondary lymph organs.
Our group has shown that internalised c-Met traffics through endomembranes positive for LC3B and Beclin1. Furthermore, c-Met sustains signalling from Autophagy Related Endomembranes, ARE. We hypothesised therefore that the AREs supporting c-Met trafficking and signalling belong to a novel non-canonical pathway.