Funded by The Little Princess Trust and administered by CCLG
Lead investigator: Professor Katrin Ottersbach, University of Edinburgh
Award: £35,775.60
Awarded March 2023
Leukaemia in infants under one years old is a rare and severe type of blood cancer, which is often hard to treat and frequently comes back after treatment. The disease starts before the child is born, unlike leukaemia in older patients, which makes it challenging to study and to understand how it starts and progresses.
In infant leukaemia, just one genetic error can cause two different subtypes of leukaemia: myeloid leukaemia and lymphoblastic leukaemia. Unusually, infant leukaemia can change from one subtype to the other following treatment. This means that treatment no longer works and often leads to the cancer coming back and there being no further options.
In infant leukaemia, researchers don’t know what exact type of cell the disease starts in. Mature blood cells, like red blood cells and white blood cells, come from blood stem cells. These mature blood cells all have tiny molecules on their surface which show the exact type of cell and decide how the cell will behave. Together, these markers make up the ‘phenotype’ of the blood cell.
Studying the different phenotypes and cell surface markers would help researchers to understand how leukaemia cells decide what each cell will do. We also need further research into how leukaemia cells can change from one subtype to another. Understanding these mechanisms would help to improve treatment options for this young group of patients.
In this project, Professor Katrin Ottersbach at the University of Edinburgh will focus on one the cell surface markers, called CSF1R, and look at how it changes the behaviour of infant leukaemia cells. Using expert techniques to look at what genes are active in cells with CSF1R, and what happens when it is removed, her team will be able to find out what CSF1R does and how it affects cancer cell behaviour. Their next step will be to look at whether there are any chemicals which can stop CSF1R activity, and whether these could form part of a new and better treatment.