Professor Sue Burchill
University of Leeds
Awarded: £116,374
Completed
The challenge
There are some genes and molecules in normal cells which are inactive. But in Ewing sarcoma some of these cells become activated, causing the Ewing cells to grow and divide out of control. One molecule, called c-MYC, is important in regulating these processes. It is important for cancer cell survival as it switches on lots of genes, which makes cells grow. For this reason, it is sometimes referred to as a ‘cancer supercontroller’.
If c-MYC could be switched off, this would reverse progression and relapse of cancer in patients. But at present, there are no clinically useful drugs that directly switch off c-MYC.
How will this project tackle this challenge?
For the first time in Ewing sarcoma, the team discovered that c-MYC interacts with another molecule called Aurora Kinase A.
Prof Burchill and her team, including PhD student Molly McNae, found that blocking Aurora Kinase A with drugs known as Aurora Kinase inhibitors can prevent this interaction. This stopped the cells from growing and caused the cells to die.
What this means for people affected by sarcoma
We need to find ways of stopping Ewing sarcoma from developing and growing. The team hope that the results of this research will help develop treatments in the future – in particular, being able to predict which drugs will be most effective for each patient and develop personalised treatments for Ewing sarcoma.
If c-MYC could be switched off, this would reverse progression and relapse of cancer in patients.
