We aim to identify genetic alterations that influence cancer development, progression and therapeutic responses, in particular prostate cancer, and further develop them into biomarkers for cancer diagnosis and therapeutic stratification, with a current focus on circulating biomarkers.
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 group combines mathematics, computer simulations and genomic information to study evolutionary processes. We aim to understand how a tumour’s evolutionary history is reflected in its genome, how evolution can be quantified in individual tumours and how this information predicts future evolution.
My research focuses on the fundamental aspects of leukaemia initiating cell (LIC) biology in adult acute lymphoblastic leukaemia, with the aim of gaining fundamental insight into the underlying biology of LICs to reveal dependencies that are tractable targets for therapy.
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.
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.
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.