Inhibitors of CDK4 and 6 have shown really very substantial activity in metastatic ER positive breast cancer. The question now in the field is how do we work out which individual patients get the most benefit from CDK4/6 inhibitors.
Could you give an overview of your current research?
We’ve been trying to work out how cancers become resistant to CDK4/6 inhibitors, partly to help us treat patients whose cancers progress on them but also we’re doing a lot of work to understand why individual cancers respond to CDK4/6 inhibitors that we hope in the future will allow us to develop biomarkers to pick out which patients respond.
Why do you feel that CDK4/6 is a good molecular target in breast cancer?
ER positive breast cancers are really exquisitely dependent on CDK4 and 6 for their growth. So both oestrogen receptor and CDK4/6 work together to promote the growth of these cancers so targeting CDK4/6 makes a great deal of sense biologically to treat these women.
What are the potential clinical implications of your findings?
There’s a lot of interest with CDK4/6 inhibitors at the moment in addressing whether they have activity in the adjuvant setting. So there’s a large number of studies currently recruiting with CDK4/6 inhibitors to address whether they can improve survival in the adjuvant setting. It’s going to take a lot of years for these studies to report out but that’s the next big question we need to address with these inhibitors.
What is your take home message?
The take home messages are that CDK4/6 inhibitors have substantial activity in women with metastatic breast cancer but importantly they’re also really quite well tolerated. There are a lot of blood test abnormalities but many patients feel pretty normal while they’re taking the drugs. This is then reflected in the data that shows they also have very good quality of life when they’re taking them. They look like they’re tolerated very well and therefore they are drugs that we hope will have that potential to move into the early breast cancer setting.
