Practice Updates in Prostate Cancer Imaging - Episode 11
A look at how PSMA PET imaging fits into the monitoring of a patient with prostate cancer.
Neal Shore, MD, FACS: This is a hot topic: the role for PSMA [prostate-specific membrane antigen] PET [positron emission tomography] in monitoring. Let’s assume cost isn’t an issue. What’s the role for PSMA PET in monitoring, particularly for this patient, who presumably received a course of ADT [androgen deprivation therapy] radiation for a period of time, whether it was 12 months, 18 months, or 2 years. He ultimately becomes eugonadal, and we start to see some slow but concerning PSA [prostate specific antigen] rise from the nadir. What’s the role of PSMA PET, and how are you addressing and thinking about it as a monitoring imaging modality?
Lawrence Saperstein, MD: Great question. How I’m thinking of it and how it’s going to be in practice right now are very different things. I believe it will have an important role in monitoring patients, but we don’t have the ability to do that at this point because we don’t have the data, the large-scale study to support that. But that brings up a very important point. We continue to do bone scans daily in patients who have metastatic prostate cancer who have been treated. That’s the way we’re following them. But you can put 1 and 1 together there. We need to address this problem because our patients will likely be better served with follow-up PSMA scans.
Steven Finkelstein, MD, DABR, FACRO: If I did radiation therapy and what I described, and I told patient that we’re going to follow you—whether you did well or not—[by giving you] a blood test, a PSA blood test and watching it go down. As opposed to saying to the patient that we’re going to get this picture beforehand. We’re going to build your entire treatment planning based on that. Now we can get it again. We probably would give it enough time for radiation to do its thing. We say in the textbook that it may take up to a year for radiation to have its full effect. But is it unreasonable to get a PET a year from when you do the definitive treatment, to show [see if] all those sites of disease have gone away? Do you need to do 100 PETs in that patient? Probably not, but in my mind, you should do 1, and that’s not the standard. As this becomes more available, patients are going to see, as we do in other disease sites, a picture that’s done before treatment and a picture that’s done after treatment. As I said, in radiation therapy, this is the undiscovered country, which is extremely exciting going forward.
Lawrence Saperstein, MD: Those are great points. What you’re saying is reasonable. Whether we can get those scans covered is maybe the rate-limiting factor. Mike, I don’t know if you’ve encountered this. We’ve been using these agents for several months. We’re doing them quite frequently, but this is going to come up, and it has to be reckoned with.
Neal Shore, MD, FACS: Mike, it would be great to have your thoughts because you’ve been with Marty Pomper and Steve Rowe at [Johns] Hopkins, 1 of the early pioneering institutions. What’s been your experience at Hopkins? How has that translated into the community in terms of PSMA PET monitoring?
Michael Gorin, MD: I take a slightly divergent view from was offered earlier. PSA monitoring remains the standard once you’ve established that a patient has distant disease and you’re going to initiate systemic therapy to follow them and, based on inflections in the PSA level, determine whether to switch to the next therapy. The caveat to that statement is what was Dr Finkelstein was speaking about: if you foresee taking a metastasis site-directed approach in a patient’s care, at that point in time it’s reasonable to order this test to direct the radiation therapy, which is most commonly delivered with SPRT [stereotactic prostate radiation therapy]. But outside the intention of delivering that, if the scan shows oligometastatic metastatic disease, I’m not convinced of the utility of ordering these scans in a serial fashion.
Remember, there are some concerns about how androgen deprivation therapy impacts sites of disease in patients undergoing PSMA scanning. Early scanning after induction of androgen deprivation therapy causes an increase in SUVs [standard uptake values] in patients who are imaged with PSMA PET. That’s because of the inverse regulation of PSA and PSMA in response to therapy. But we know that if you image a patient who’s been stably on therapy for several months, the SUVs start to come down and many lesions disappear when you image on a PSMA PET. But we’re not exactly sure when it changes from an increase to a decrease. The timing of that isn’t quite clear.
The other thing to keep in mind is that as patients advance through lines of therapy and develop more of a neuroendocrine dedifferentiation, that size of disease will start to lose PSMA expression. We know from work that’s been done in Australia, where patients have been imaged with PSMA PET and FDG [fluorodeoxyglucose]–PET before initiation of PSMA-targeted therapy or radiotherapy, that there could be substantial discordance in the sites of disease that one sees on PSMA PET and FDG-PET. Potentially, we can make incorrect treatment decisions if we’re basing on imaging in these later stages of disease, where there’s been selective pressure for neuroendocrine dedifferentiation. For all those reasons, I take a slightly divergent view from what was offered.
Neal Shore, MD, FACS: Those are good points. Larry, can you comment on some of the nice work that’s been done by Michael Hofman and others in Australia regarding this concomitant use of FDG-PET, and which Michael brings up in conjunction with PSMA PET?
Lawrence Saperstein, MD: I want to add 1 more thing to that discussion. Those are great points. We must be mindful that we have the CT when we do the PET CT. They’re technically nondiagnostic CTs, but we get a lot of diagnostic information from them. It’s too soon to say. We may be dealing with a heterogeneous population of tumor. It’s a very interesting topic, and it has yet to evolve. But historically, we didn’t use FDG for prostate cancer because the tumors weren’t taking up fluorodeoxyglucose. As we know, that’s based on metabolic rate. I’ll defer to the other speakers about the data, but that was our experience.
Transcript edited for clarity.