Professor Sue Burchill
University of Leeds
Awarded: £116,374
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?
However, the answer may lie in another molecule, called Aurora-A. We know that Aurora-A and c-MYC are produced together in Ewing’s sarcoma cells, so if you can stop Aurora-A from working, you can also reduce the amount of c-MYC produced. This means you can kill the cancer cells.
In this project, Prof Burchill and her team, including PhD student Molly McNae, will explore different chemicals which stop Aurora-A from working, to find those which kill Ewing sarcoma cells most effectively. They will also explore the underlying biology of how Aurora-A and c-MYC work together to help develop new treatments.
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. But at present, there are no clinically useful drugs that directly switch off c-MYC.
