• Benign Prostatic Hyperplasia
  • Hormone Therapy
  • Genomic Testing
  • Next-Generation Imaging
  • UTUC
  • OAB and Incontinence
  • Genitourinary Cancers
  • Kidney Cancer
  • Men's Health
  • Pediatrics
  • Female Urology
  • Sexual Dysfunction
  • Kidney Stones
  • Urologic Surgery
  • Bladder Cancer
  • Benign Conditions
  • Prostate Cancer

Rapid Advances in Prostate Cancer Imaging


A background on the available options and recent advances in prostate cancer imaging.

Neal Shore, MD, FACS: Hi, everybody. Welcome to this Virtual Tumor Board®. What a great pleasure to talk with you today. I’m Neal Shore. I’m the chief medical officer of surgical oncology and urology at GenesisCare [in Myrtle Beach, South Carolina], and it’s been my great pleasure to be the medical director of Carolina Urologic Research Center for the last 20 years. We have a fabulous panel, and we’re going to talk to you about practice updates in prostate cancer imaging. We’ve traditionally called conventional imaging CT scan and technetium bone scan, but we’re into this fascinating and important area of next-generation imaging. That’s what we’re going to focus on, and we’re going to do a lot of case-based presentations.

I’m honored that we have a multidisciplinary faculty. We have Dr Michael Gorin, who is a urologist and a prolific researcher who is with Urology Associates at UPMC Western Maryland [in Cumberland, Maryland]. And Dr Steven Finkelstein. Dr Finkelstein and I have done many projects together: symposia, papers, and publications. Dr Finkelstein is a nationally renowned radiation-oncologist, and he is with US Oncology in Florida Cancer Affiliates in [Panama City] Florida. What a great pleasure to have Dr Lawrence Saperstein, who has done pioneering work in nuclear medicine radiology. He’s at the Yale School of Medicine [in New Haven, Connecticut]. We’re going to go through cases, and we’re going to have a full-throated discussion regarding all the potential ways of thinking about imaging. How does that imaging inform us? How does it teach us about our decision-making? That’s very important.

I want to thank everybody for joining. We’re going to go through a multitude of cases. At the end of the day, it’s important that we figure out the right treatment, right diagnostic, right imaging for the right patient and at the right time. We’re all ultimately trying to optimize our patient care. With this, I’d love to hand it over to you, Larry. The background here, what a great time for nuclear medicine radiology, not just in the United States but also globally. If you could, review some of these advances that are happening at breakneck speed.

Lawrence Saperstein, MD: I’m excited to participate in this discussion. As you can see, several modalities are displayed on the screen. The first is bone scan. We’re all familiar with that. As you said, historically it’s part of the conventional work-up for patients with prostate cancer. It’s a bone-seeking agent. It was good when we had it. Notoriously, it’s not as sensitive as we need it to be. Bone scan had its place, and we’ll talk about some of the things that have improved. Plain films are probably not as relevant to the discussion: x-rays, MRI, PET [positron emission tomography]–CT, PET–MRI, F-18 sodium fluoride. We can talk about that for a minute. That was used for quite some time. It’s a bone-seeking agent as well. We call it the super bone skin because the activity is similar to what we might see on a bone scan. What’s relevant to the discussion is that sodium fluoride PET–CT is not available at this point. It’s not covered by insurers or care or Medicare. It’s not available, and we have things that are better.

C-11 choline an interesting agent that’s been around for a while. It was helpful in imaging patients with prostate cancer. One challenge is the short half-life of C11. You must use it quickly. You need a cyclotron on-site, and that was a limiting factor that faded away. Of course, fluciclovine, which is a fluorinated compound. F-18 has a more usable half-life, 110 minutes and fluciclovine was and is a decent agent. Has a reasonable sensitivity, is able to detect prostate lesions at relatively low PSA [prostate-specific antigen] levels; the 2-ng/mL range, give or take. That’s what we used for a while, but the exciting development, as you said, are these PSMA [prostate-specific membrane antigen]–targeting agents. I’m sure we’re going to get into more detail, but those are where we are and a great place to be.

Neal Shore, MD, FACS: That’s a great summary. We’re going to talk a lot more about how to interpret PSMA PET scans. There are some key trials that you and Michael were coauthors on, specifically the CONDOR and the OSPREY trials, so it’s great to get your insights. I certainly want to talk about how we access these PSMA PETs. There are various PSMA PETs. Larry, you can talk more about PSMA PET and how PSMA differs from PSA. But I couldn’t help but thinking that it’s fascinating to look at the overview in this bullet about conventional imaging and some of the newer PET technologies, MRI, etc. All our phase 3 trials for the therapeutics that have survival prolongation for advanced prostate cancer, whether it’s hormone sensitive or hormone resistant—better said as castration sensitive, castration resistant—they’ve all followed the old conventional use of technetium bone scan and multislice CT scan. And now we’re on this marked inflection point: how do we make heads or tails? How do we interpret the greater accuracy, the greater sensitivity of picking up microscopic lesions that we haven’t seen with conventional imaging? That’s the basis for all our therapeutic approvals. Any thoughts on that, Steven or Michael?

Michael Gorin, MD: This is definitely a significant challenge, especially as we start to think about the directing therapy on the basis of either a low-volume or high-volume disease, for instance. As we do based on the results from CHAARTED, perhaps giving docetaxel to patients who have high-volume disease. High-volume disease using bone scan and CT means something different from high-volume disease with PSMA PET, which is much more sensitive. Those definitions, the number of lesions, and so forth were based on conventional imaging, and at this point we don’t know how to define high vs low volume on the basis of these scans. Additionally, we almost eliminated the category of nonmetastatic castration resistance because we know that if you do PSMA or even fluciclovine scans on these patients, for upward of 90% of them, you’re going to find sites of metastatic disease. This entity almost disappears in the new era. What do we do about all those medications that have labeling? Specifically for that disease state when the definition of the disease state was based on something completely different. It’s definitely a challenge and something I don’t think the field has reconciled.

Transcript edited for clarity.

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