My lab aims to understand the basic mechanisms controlling DNA replication in mammalian cells and how disruption of this process leads to genomic instability and cancer.
My group aims to discover the epigenetic changes taking place during cancer initiation and develop potential drugs that can prevent these changes which may be abnormal but reversible, before many damaging mutations occur.
My research group works on molecular pathology, genetics and progression of leukaemia and lymphomas, aiming to improve on current diagnostic, prognostic and treatment strategies.
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 group is involved in investigating nuclear and mitochondrial DNA repair as a therapeutic target in cancer. In particular, we have focused on the DNA mismatch repair (MMR) pathway, the system for recognising and repairing mistakes in DNA replication and so preventing genetic mutations.
My lab aims to understand the mechanisms that underlie numerical and structural chromosome aberrations in cancer at a molecular level, which also involves understanding how normal cells replicate and segregate their genomes.
My research focuses on understanding the genetic and molecular mechanisms that underlie the initiation and progression of B-cell non-Hodgkin’s lymphomas in order to define clinically-relevant biomarkers.
My laboratory research explores alternative pre-mRNA splicing in prostate cancer (PCa) biology, and liquid biopsy-derived molecular biomarkers of treatment outcomes.
I have broad research interests and experience in bioinformatics, cancer genomics and data analytics. These research areas mainly involve developing and applying bioinformatics and computational approaches to analyse large-scale cancer datasets to uncover novel diagnostic and prognostic biomarkers. I also lead the Cancer Research UK Barts Centre Bioinformatics Core Facility.
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.
We are interested in understanding the cellular and molecular mechanisms responsible for relapses in acute lymphoblastic leukaemia and progressing these insights into translational diagnostics and clinical trials.
My work is currently focused on lymphoma, working on variant calling and gene expression analysis of NGS data.
My research aims to understand the mechanisms through which long noncoding RNAs can control genome stability in cancer.
My research focuses on novel strategies to enrich, isolate and characterise a chemo-resistant population in patients with follicular lymphoma.
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 work focuses on the global analysis of miRNA in pancreatic cancer and developing miRNA biomarkers for early detection of this malignancy.
My research activity aims to characterise lncRNAs involved in the maintenance of genomic stability and to understand how their dysregulation can lead to cancer development.
I am developing SNPnexus, a software dedicated to improving our understanding of the functional role of genetic variations to prioritise clinically relevant ones facilitating the promise of precision medicine.
The aim of my work is to develop clinically-relevant biomarkers that could aid in earlier disease detection, predict treatment response, and inform clinical management of patients.
I am interested in understanding whether epigenetics can play a driving role in the transition from normal to transformed cells in the breast.
Using the fruit fly, Drosophila melanogaster, I aim to dissect the role played by protein phosphatases in regulating the tissue growth controlling Hippo signalling pathway, which has commonly been implicated in cancer development, progression and metastasis.
We are using a variety of molecular and cytological techniques to study the mechanisms underlying chromosomal instability (CIN) in high grade serous ovarian cancer (HGSOC) that allow these highly adaptable tumours to become drug resistant.