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.
We are updating the bioinformatics data management system, expanding the analytical modules and functionalities, developing purpose-built graphical pug-ins and designing the bioinformatics infrastructure to allow the querying and analysis of data returned from projects using BCNTB tissues.
My research is focussed on the disturbed epigenomic landscape within pancreatic tumours.
In particular, I investigate the bi-directional epigenetic reprogramming between the tumour microenvironment and pancreatic cancer stem cells that leads to cooperative tumour outgrowth.
The Receptor Tyrosine Kinase c-Met continues its signalling life cycle post-endocytosis. 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 .
High-grade serous ovarian cancer (HGSOC) represents the major subtype of ovarian cancer and displays high levels of chromosomal instability.
We are collaborating with the Balkwill and Lockley laboratories to investigate mechanisms driving chromosomal instability in gynaecological cancers.
I apply mathematical and computational approaches to understanding cancer evolution. A lot of my work is inspired by population genetics and evolutionary biology and I have been developing ways to adapt methods and theories from these fields to the study of cancer as an evolutionary system.