Expert panelists review risk stratification strategies for patients with prostate cancer and summarize the evolving use of conventional versus newer imaging modalities for diagnosis, treatment selection, and monitoring of these patients.
David Albala, MD: Hello, and welcome to this Urology Times® [discussion titled] “Advances in PSMA-Targeted PET Imaging for Prostate Cancer.” I’m Dr David Albala, the chief of urology at Crouse Health in Syracuse [New York] and a member of Associated Medical Professionals. Joining me in this virtual discussion are 3 of my colleagues and friends, Dr Gerry Andriole from Johns Hopkins University, Dr Ashley Ross from Northwestern [University], and Dr Gary Ulaner from USC [University of Southern California]. We’re going to discuss the emerging roles of PSMA [prostate-specific membrane antigen]–targeted PET [positron emission tomography] imaging vs conventional imaging in patients with prostate cancer. Let’s get started [on our first topic].
We’re going to talk about the background on prostate cancer and conventional imaging modalities. I’d like to start with Dr Ross. Can you give us insight on how you talk to patients with clinically localized prostate cancer and stratify them based on risk using the NCCN [National Comprehensive Cancer Network] criteria?
Ashley Ross, MD, PhD: Thank you very much, Dr Albala. When we think about risk groups for presumptively clinically localized prostate cancer, the NCCN puts people into different buckets. They go from very low-risk prostate cancer to very high-risk prostate cancer. The favorable-risk groups are: your very low risk, low risk, and favorable intermediate risk. These are men who have low-grade prostate cancer, meaning a Gleason score of 1 or 2 and a lower PSA [prostate-specific antigen], which is usually under 10 ng/mL; they have less than half of their prostate involved by prostate cancer. It’s people with lower-grade disease under the microscope—old Gleason scores were 3+3=6, 3+4=7. It’s people with a lower PSA. Usually [their PSA is] under 10 ng/mL, although in some rare cases 10 to 20 ng/mL is considered. [If you’re] not feeling much with your finger, the T-stage is lower. Usually in T1c, I can’t feel anything with my finger but prostate. In T2a or T2b, I feel a little bit or half of the prostate. These guys have low metastatic potential. Usually when you’ve diagnosed them with clinically localized prostate cancer, they’re clinically localized. You’re thinking about watching them on surveillance or treating them with definitive therapy.
The other NCCN risk groups are your unfavorable intermediate-risk, your high-risk, and your very high-risk with virus features. Those individuals have their risk based on their T-stage, where you can feel with your finger; their Gleason score, or what it looks like under the microscope; their PSA; and how many cores are involved. If their Gleason score is 3 to 5—that’s 4+3=7 and higher—or if you can feel cancer with your finger throughout their prostate or even coming out of their prostate, or their PSA is more elevated, greater than 20 ng/mL, then that automatically makes you high-risk. If you have multiple high-risk features, then you’re very high risk. That’s important for this discussion because once you get to that unfavorable intermediate-risk group and above, you’ve got metastatic potential. We’re presuming your disease is clinically localized, but there’s a chance you have metastatic spread of disease. Staging, to the best of our ability, to make sure you’re clinically localized is going to be crucial to determine your next step in treatment.
David Albala, MD: Thanks, Ashley. We can always learn something from the past. Gary, can you give us an idea on that historical perspective for imaging for prostate cancer? What have we used in the past? How do you see this landscape changing as we move forward with advances in prostate cancer imaging?
Gary Ulaner, MD, PhD, FACNM: Thank you, Dave. I divide imaging for patients with prostate cancer into local disease and nodal and distant metastases, as well as by whether you’re doing initial staging or have a follow-up treatment response to biochemical recurrence staging. For local disease, prostate MRI is the gold standard for the evaluation of the prostate gland in the initial staging and often in follow-up. For nodal and distant metastases, we’ve utilized CT scans and bone scans, in initial staging and follow-up, as well as a whole host of nuclear imaging studies. There were the original indium-targeted agents, which I don’t think any of us liked. Those were replaced by choline and fluciclovine agents, which demonstrated some great potential, particularly in the era of biochemical recurrence.
These days, PSMA-targeted PET imaging has superseded virtually everything that we’ve used before for initial staging, biochemical recurrence, and evaluating patients who are going to go on to PSMA-targeted therapy. The only area for which PSMA imaging hasn’t superseded has been in evaluation of treatment response, with NCCN Guidelines and the Society of Nuclear Medicine and Molecular Imaging Appropriate Use Criteria still debating whether PSMA imaging will be used for evaluating treatment response. So other modalities such as FDG [fluorodeoxyglucose] PET are still utilized. But in most cases of initial diagnosis with unfavorable intermediate-high and very high-risk disease, and in the cases of biochemical recurrence, PSMA PET is the standard of care.
Gerald Andriole, MD: One thing that’s impressive is that we used to have a category of disease called nonmetastatic castration-resistant prostate cancer. That was in the pre-PET era. That basically doesn’t exist anymore because virtually 100% of those patients will have something on a contemporary PET scan. That shows the power that these modalities have in changing how we look at and treat men with prostate cancer.
Transcript edited for clarity.