Targeting AML that’s not responding to treatment

Lead researcher - Professor Elaine Dzierzak, University of Edinburgh
Does GPR56 confer self-renewal properties on human hematopoietic stem cells and leukemic stem cells?
Amount awarded: £249,974
Award start date: 01 Aug 2018
Award duration: 3 years (36 months)

Young blood cells called ‘blood stem cells’ can make all the different types of blood cells found in our body. Acute myeloid leukaemia (AML) can develop when genetic errors occur to a blood stem cell, turning it into an AML stem cell. Instead of producing all the different types of blood cell, the AML stem cell only produces more AML cells.

One of the reasons that AML is difficult to treat is that there are many different genetic errors that cause and drive the disease. This means that each person’s AML is unique, and not everyone will respond in the same way to the same treatment.

Professor Dzierzak and her team are looking at a genetic error which makes AML harder to treat. This genetic error causes an increase in the level of a protein called GPR56. This protein is likely to play a part in healthy blood production by keeping blood stem cells in a state where they can easily renew themselves, but it’s role in AML is still unknown.

The researchers plan to examine in greater depth what GPR56 does in healthy blood stem cells and see what its role is in AML. If successful, the team could reveal new ways to tackle hard to treat  AML.