Disrupting AML’s energy source to find better treatments
What if we could exploit one of the proteins driving AML? Could we cut-off leukaemia’s energy source and uncover new ways to treat the disease?
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.
Whilst there has been some progress in treating this type of leukaemia, current standard therapies don’t work for everyone and just 15% of people survive longer than five years after their diagnosis. 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.
What difference will this research make?
The ultimate goal of Dr Che’s research is to find ways to interrupt AML’s ability to use glucose efficiently, which could lead to the development of better, more precise treatment options for AML.
This research could offer hope to those AML patients who currently have limited treatment options or who don’t respond well to existing therapies.