Chronic Lymphoid Leukaemia (CLL)

Chronic Lymphocytic Leukaemia (CLL) is the most common type of adult leukaemia, yet it remains one of the least understood when it comes to why some patients live for decades without symptoms while others progress quickly to serious illness.

Professor George Kannourakis, who leads this project has been studying CLL for over 26 years, and 2024 has been a turning point. With one of the world’s most unique collections of patient tissue samples, some dating back decades, we are now closer than ever to identifying the molecular and protein-level changes that drive disease progression.

Our research is focused on both the cancer cells themselves and the immune cells that surround them. Dr Monirul Islam has been working to isolate pure CLL cells using advanced cell-sorting techniques, allowing us to study the subtle genetic and molecular differences between progressive and non-progressive cases.

We’ve now completed whole genome sequencing on 20 patient samples with long-standing, non-progressive disease to see whether harmful mutations are present, and if so, why they haven’t led to active illness.

Importantly, we are now combining these genetic studies with protein analysis. Using flow-sorted CLL cells, our team is examining changes in the proteins found on the outer membrane of cancer cells, a powerful tool for identifying what changes as the disease becomes more aggressive.

One of our most exciting developments has come from a specialised phage-display screening program. So far, we’ve identified 48 phage clones that bind specifically to proteins found only on diseased CLL cells, not on healthy or asymptomatic ones. This work, by Dr Sharon Olsen, could pave the way for targeted antibody therapies that help the immune system recognise and destroy cancer cells before they progress. Dr Olsen has taken over this program following the departure of Dr Dilys Leung, who has moved on to Cabrini Medical Research.

We’re now sequencing those phage clones and preparing to test whether those same disease-specific proteins appear in other aggressive cancers. If they do, this discovery could go well beyond CLL and unlock new treatment pathways for multiple cancer types.

The ultimate goal? To develop targeted, antibody-based therapies that stop CLL from progressing, or prevent it from starting in the first place.

With every new insight, we move closer to transforming how CLL is managed and offering patients a future free from progression, fear, and uncertainty.