Researchers at the Garvan Institute of Medical Research have discovered that the activity of a protein called CDK1 in breast cancers is linked to how they respond to a common therapy – an insight that could inform more personalised treatment approaches for patients.
The study, published in Advanced Science , looked at estrogen receptor-positive (ER+) breast cancer – the most common type, fuelled by the hormone estrogen. Many people with this cancer now receive drugs called CDK4/6 inhibitors alongside hormone therapy. These drugs stop cancer cells from multiplying, but they don't work for everyone, and in advanced cancer eventually stop working for most patients.
"CDK4/6 inhibitors have made a real difference for people with breast cancer, but right now we can't tell who will get the most out of them, or whether they've stopped working," says Associate Professor Liz Caldon, Lab Head at Garvan and co-senior author of the study. "We wanted to find a signal in the tumour itself that tells us who is most likely to benefit and whether the therapy is doing its job."
Is the engine on?
CDK1 belongs to the same family of proteins as CDK4 and CDK6, which control when cells divide. CDK4 and CDK6 set the process in motion, while CDK1 is needed for the final stage, when the cell splits in two. Healthy cells divide this way – cancer is what happens when that process runs out of control.
Associate Professor Caldon explains: "CDK1 is like the 'engine' that has to start for a cell to divide. CDK4/6 inhibitors work by jamming the cell's ignition, but some cancer cells find a way to 'hotwire' around it. Even then, the cell can only divide if the CDK1 engine is running – so checking whether it's switched on shows whether the drugs are still holding the cancer back."
