Role of Conventional Imaging vs PSMA PET in mCNPC

EP: 1.Polling Questions: Advanced Prostate Cancer

EP: 2.Patient Case #1: Treatment Selection in mCNPC

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EP: 3.Role of Conventional Imaging vs PSMA PET in mCNPC

EP: 4.Treatment Options for High-Volume mCNPC

EP: 5.Patient Case #2: Choosing Optimal Therapy in mCRPC

EP: 6.Role of PSMA PET Imaging in mCRPC

EP: 7.Sequencing Therapy for mCRPC

EP: 8.Optimization of Genetic Testing for mCRPC

EP: 9.Recap: Recent Advances in the Treatment of Metastatic Prostate Cancer

Daniel P. Petrylak, MD: I have a castration-resistant case where all the lesions regressed except a new lesion, and we can’t find anything on conventional imaging in bone. The question is, for a patient who has all the metastatic—4 lesions, for example—and you find 20 on a PSMA [prostate-specific membrane antigen] PET [positron emission tomography], do you change their management? We use the conventional imaging as our way of determining whether they have extensive disease. A PSMA PET is nice. It’s a great thing, but at this stage, we need to understand how we’re going to use that in our management.

Oliver Sartor, MD: Dan, you’re making a great point because all our level 1 data are built around conventional imaging. As we introduce a PSMA PET—and it’s here—it raises a new series of questions to which our level 1 evidence does not apply. I mentioned the tests as directed therapy, but I may get a PSMA PET scan. This guy may not have 1 lesion to the bone, and he may have 14. Then it becomes a whole different scenario. As we gain new imaging insights, we also have to ask new imaging questions and address it with clinical trials to have the best answers.

Raoul S. Concepcion, MD, FACS: That’s great. Let’s go around the table. Oliver, you said you’d consider PSMA. Obviously, 69, ECOG 1 is in retention, which is fairly active. Jason, given that he’s got conventional imaging and low-volume disease, would you push for molecular imaging?

Jason M. Hafron, MD, CMO: Yes, I would. It’s coming, and we’re getting into a space that we don’t have data on. Based on the STAMPEDE data, which showed a significant improvement in overall survival, over 30%, I’d give localized therapy to this patient and then probably transition to novel hormone therapy. The issue with PSMA and finding more bone lesions is that, as Oliver said, it’s up for grabs. It’s hard to apply the old literature to this new imaging. But of what we presented, and the case that’s there, I’d offer them localized therapy based on STAMPEDE.

Also, I’d like to bring up for the audience SWOG S1802. You talk about historically treating advanced prostate cancer. There’s a major US trial looking at radiation therapy or even surgery. It’s crazy to think that we could potentially be operating on advanced disease and removing the prostate. The key is that we’re moving away from single modality therapy and clearly moving into multimodality therapy. How do we apply it with this new imaging? I guess we’ll have to wait for Oliver and Dan to create some great trials to make that connection to the past.

Raoul S. Concepcion, MD, FACS: Your point is well taken relative to this SWOG trial because we’re finally moving forward in these patients with high-risk, high-grade localized prostate cancer, or in this case, which seems to be an oligometastatic disease. To me, that is the way it’s moving, given that we do have better systemic therapies beyond ADT [androgen deprivation therapy]. Oliver’s point relative to how we incorporate hereditary germline and somatic testing isalso going to be key as we launch into this era of precision medicine.

Transcript Edited for Clarity