Daniel J. George, MD:When I have a patient who I’m following for castrate-resistant prostate cancer but they’re not yet metastatic, it’s variable as to how often I’ll image those patients. Part of that depends on what their PSA [prostate specific antigen] level is, and part of it depends on their PSA doubling time. For patients with really long PSA doubling times, say 10 months or longer, I’m pretty comfortable imaging them once a year, or even less if their PSA is down in the low single digits. As that PSA gets up into the range of 5 to 10, I’m going to start imaging them every time there’s a doublet. So if it’s 10 months, it’s every 10 months. If it’s 3 months, it’s every 3 months. If it’s 6 months, it’s every 6 months. That doubling becomes a marker for me on how to image.
What I use for imaging may vary. Right now, I still use a traditional CT [computed tomography] and bone scan. We’re open to understanding when the optimal time is for using molecular imaging, in terms of understanding the prognosis and implicationswhere to look for metastatic disease to show up by CT and bone scan in the future and prepare them for what they might be available for in terms of molecularly targeted therapies.
Once patients become metastatic castrate-resistant, I typically image them every 3 months while they’re on treatment. The reason for that is because PSA alone may not tell us the whole story. There are patients who had disease progression on both the PREVAIL and COUGAR-AA-302 studies that didn’t have PSA progression but had new radiographic disease. You’re only going to find that if you continue to monitor and check for that. Yes, there are cases in which we’ll cut this back after a year or 2, but at least for that first year or so I like to image every 3 months on therapy.
When I think of a drug like radium-223, I typically like to image at 3 months. That wasn’t done in ALSYMPCA, and you don’t have to do that, but I want to look to make sure that I’m not missing some disease biology. Have I stressed the tumor in the bone so much that now we’re going to see biologic disease growing elsewhere? Has this disease changed? Is there a new biology afoot that radium-223’s not tackling, that is progressing elsewhere now that I’ve stopped, or are we seeing progression on their prior hormonal therapy? Are there other complications that these patients are developing that I’m not aware of, like fractures? To pick those kinds of things up, we need to do imaging. We want to know about that because it can impact how we support and manage these patients. In some patients, I’ll stop radium-223 therapy and switch if they’ve got new visceral disease. It would be good to know that, but that’s a relatively rare complication. The majority of my patients, even if they show signs of new or progressive disease on bone, are not necessarily progressing. That can be a flare effect, and I’ll follow that and complete their radium-223 course.
Transcript edited for clarity.
mCRPC Treated With Radium-223 Therapy