Genetic and Epigenetic Drivers of CMML/MDS

We aim to comprehensively characterise genetic and epigenetic abnormalities that drive CMML | MDS pathogenesis and leukaemic progression. By employing advanced techniques such as single-cell RNA sequencing, genomic profiling and CRISPR-based functional screens, we seek to uncover critical mutations and epigenetic changes responsible for disease initiation and progression.

Translational Models and Novel Therapeutic Approaches

Our research prioritises developing translational models that accurately reflect the biological complexity of CMML and MDS – including genetically modified murine models and patient-derived xenografts (PDXs). These models provide critical tools for investigating disease mechanisms and evaluating novel therapeutic interventions. By employing these pre-clinical systems, we will rigorously test treatment strategies – targeting signalling pathways, epigenetic regulators and immune checkpoints – to facilitate rapid clinical translation and improve patient outcomes.

Immune Surveillance and Tolerance of Myeloid Clones

Here, we focus our efforts on understanding the basis by which abnormal myeloid clones subvert immune surveillance often for years at a time. Using CRISPR-based functional screens and mass spectrometry – we seek to identify vulnerabilities that can ‘reboot’ host immunity. Our goal is to seed next-generation immunotherapies that eradicate pre-leukaemic clones before malignant transformation and improve patient survival outcomes.