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.
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.
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 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.
My focus is on investigating the epigenetic regulation of the PI3K pathway and identifying an effective combination therapy that will disable compensatory bypass routes, overcoming drug resistance.
My work is focused on exploiting cell cycle vulnerabilities in tumour cells, particularly the role of MASTL or Greatwall kinase in cell cycle control. My research will explore the role of MASTL in AML and whether it could be a new therapeutic target in this disease.
My research focuses on exploiting cell cycle vulnerabilities and signalling rewiring in tumour cells, to find new approaches to treat cancer.
My research focuses on developing novel methodology for in-cell monitoring of direct downstream kinase phosphorylation and phospho-isoform substrate specificity. This work will contribute towards enhancing our understanding of cell cycle protein signalling and elucidating the role of the activation loop in substrate switching.