Dr Noelia Che, University College London, is investigating the role of a protein called MYB to find ways to disrupt AML cells’ ability to use glucose, its primary source of energy.

The challenge

Acute myeloid leukaemia (AML) is the second most common type of leukaemia, affecting almost 3,100 people every year in the UK.

Whilst there has been some progress in treating this type of leukaemia, current standard therapies don’t work for everyone and just 13.6% of people survive longer than five years after their diagnosis. Dr Che’s research is focused on addressing the limited and harsh treatment options for childhood AML, aiming to improve outcomes for young patients. New, more effective treatments for the disease are vital to stop AML devastating lives.

The science behind the research

MYB is a protein that plays a crucial role in the survival of AML.  One role appears to include controlling how leukaemia cells use glucose – their primary source of energy.  Despite the clear importance of MYB in AML, the protein has so far been deemed ‘undruggable’, as finding ways to target it remain elusive.

Dr Che and her team have already discovered that MYB relies on a specific enzyme that plays a key role in glucose breakdown and could be important for survival. During her John Goldman Fellowship, Dr Che wants to know if targeting this enzyme could be a way of stopping AML in its tracks and opening routes to more effective treatments.

She will also explore whether MYB could be used as a prognostic biomarker – a way of stratifying those patients more likely to respond to treatments aimed at disrupting leukaemia metabolism, opening doors to more personalised medicine.