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.
Our research aims to understand the epigenetic regulation of transposable elements and how their dysregulation contributes to the generation and development of cancer. In particular, we investigate their roles as gene regulators and triggers of anti-tumour immunity in blood cancers.
Our goal is to identify mechanisms that support haematopoietic stem cell function and understand how the leukaemic stem cells “play” with these mechanisms to thrive.
The central aim of our laboratory is to understand the biology of leukaemic stem cells and identify therapeutic targets to specifically eradicate them, thus discovering novel and efficient leukaemia therapies. We also focus on understanding haematopoietic stem cell biology with the hope to harness this knowledge for expanding them for therapeutic purposes.
My lab utilises state-of-art multi-omics methodologies to study how protein synthesis is dysregulated in cancer cells, and how this dysregulation contributes to various stages of cancer progression.
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.
The overarching goal of our laboratory is to understand the biology of normal haematopoietic and leukaemic stem cells in order to selectively kill cancer stem cells for better leukaemia treatment.
My laboratory research explores alternative pre-mRNA splicing in prostate cancer (PCa) biology, and liquid biopsy-derived molecular biomarkers of treatment outcomes.
My research focuses on kinase biology and how kinase signalling pathways are hijacked in cancer. We combine computational biology with proteomics and cell biology to uncover novel ways to target these dysregulated networks.
My group studies how RNA-mediated mechanisms, in particular long noncoding RNAs, regulate cell division and how dysregulation of these processes leads to genome instability and cancer.
I am a clinical collaborator in numerous laboratory-based studies particularly the localisation of Lipiodol in Hepatocellular carcinomas, inflammatory and immune responses to surgery, and tumour-stroma interactions in pancreatic carcinoma. Clinical areas of interest have been video consultations in tertiary care, surgery for pancreatic tumours (especially NETs) and liver tumours, and tissue banking.
The aim of my research project is to identify and functionally characterise candidate disease genes in familial leukaemia.
My research investigates the functional relevance of RNA-binding proteins (RBPS) in normal haematopoiesis and acute myeloid leukaemia (AML) pathogenesis.
My research focuses on understanding the role of RNA localisation in breast cancer progression. In particular, I am looking at how and why the cellular localization of some small nuclear RNAs (snoRNA) are altered during disease progression.
My research aims to understand the mechanisms through which long noncoding RNAs can control genome stability in cancer.
My research focuses on understanding how centrosome amplification impacts tumour angiogenesis and how this can be targeted to develop new cancer therapies.
My research project is focused on understanding the impact of centrosome amplification in cancer, in particular the role of extra centrosomes in tumour evolution.
My research is focused on studying the molecular mechanisms of integrin αvβ6-driven pancreatic ductal adenocarcinoma (PDAC) progression and metastasis.
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.
My project aims to explore the contribution of nuclear-cytoplasmic distribution and traffic of transcription factors that aid the aggressiveness of melanoma, and explore possible epigenetic aspects of melanoma initiation and progression.
My research focuses on understanding the relationship between chromosome instability mechanisms and tumour cells’ resistance to therapies.
My research is focused on investigating how the epitranscriptome regulates normal and malignant haematopoiesis.
My main research focuses on examining the immune landscape and identifying specific immune determinants that can predict the progression from actinic keratosis, a pre-malignant lesion, to cutaneous SCC. I am analysing single cell RNA-seq data and utilizing machine learning algorithms to evaluate potential diagnostic and prognostic markers that could aid in the identification of high-risk SCC patients. The identification of these markers is critical for early detection and intervention, which can significantly improve patient outcomes.
My research focuses on exploring why ASS1 is differently expressed in human cancers and how this information may be transferred for anticancer therapy.
My project focuses on the translation reprogramming in acute myeloid leukaemia upon stresses such as chemotherapy.
My research focuses on the perturbation of EMT-like pathways in follicular lymphoma and chronic lymphocytic leukaemia and how this promotes cancer propagation, transformation into a more aggressive form of disease and resistance to therapy.
Our research is focused in defining the cellular interactome of haematopoietic stem cells and leukaemic stem cells inside their niches during adulthood, ageing and disease. We are also interested in the cellular and molecular mechanisms that drive clonal selection and evolution in clonal haematopoiesis.
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.
My research focuses on exploiting cell cycle vulnerabilities and signalling rewiring in tumour cells, to find new approaches to treat cancer.
My research uses microscopy to examine how microtubule post-translational modifications affect DNA damage repair and how this could be exploited to enhance chemotherapy.
My project looks at the modelling of cancer for improved therapy development. I am carrying out in vivo cancer experiments, with and without modifications of the tumour microenvironment, to examine effects of such treatments on anti-cancer therapy efficacy.