For years, researchers have been attempting to target a gene called MYC that is known to drive tumour growth in multiple cancer types when it is mutated or over-expressed. However, this has been challenging.

Researchers in the Perelman School of Medicine of the University of Pennsylvania have just identified a new pathway that works as a partner to MYC. It involves a protein called ATF4, and when it’s blocked, it can cause cancer cells to produce excess protein and die. These findings could help to inform a new therapeutic approach as inhibitors that can block synthesis of ATF4 already exist.  Results were published in the journal Nature Cell Biology.

“What we’ve learned is that we need to go further downstream to block tumour growth in a way that cancer cells can’t easily escape, and our study identifies the target to do just that,” said Constantinos Koumenis, the Richard Chamberlain Professor of Radiation Oncology and vice chair and research division director of Radiation Oncology.

These results are hugely exciting for oncology and the team are keen to take their work forward. “We’re also working to confirm this approach will not cause any serious off-target effects,” said lead author Feven Tameire, who conducted the research while she was a doctoral candidate at Penn. Scientists say future studies will continue to investigate how ATF4 works, which may help to uncover other potential targets in the chain.