Transcript:
Alan Bryce, MD: Dr Lowentritt, what about patient and disease factors that lead to this treatment selection? We have an embarrassment of riches, we have a lot of choices now, so how do you decide who gets what regimen in the first-line [of] metastatic hormone-sensitive [prostate cancer]?

Benjamin Lowentritt, MD, FACS: I don’t know if there’s a straightforward answer because not only do we have an embarrassment of riches and options, we also have a lot of different criteria that we’re using to stratify patients, and they don’t always line up clearly in a way that makes a choice easy. Everything Dr [Elisabeth] Heath was saying, I completely agree with. [You must have] the ability to understand what’s out there and be able to cater this to the patients but understand that there are a lot of different pieces to this. For instance, going back to the CHAARTED study [NCT00309985]—which now, what is it, 7, 8, 9 years ago? It’s not that old, but that’s ancient history at this point—there was the low-volume, high-volume discussion, and there seemed to be a better response in the higher volume of metastases for patients receiving ADT [androgen deprivation therapy] plus docetaxel. The low-volume patients maybe weren’t getting the same response but then, of course, there’s this question, was it de novo disease or was it recurrent disease? I think that is a big part of this. We know that de novo disease is a more aggressive profile. Maybe that’s a more appropriate patient base to consider intensification with chemo, etc. There’s data that suggested that even in the CHAARTED and STAMPEDE [NCT00268476] subsets that there was a component to what we were seeing in the high-volume, low-volume discussion; that still plays in the back of the mind. If there are visceral metastases vs bone metastases vs just lymph node metastases, those all have different survival profiles. I think fit to your discussion, if a patient is showing up, we don’t want them to progress to have ureteral obstruction from their lymph node [metastases], but maybe we don’t have to throw everything at them at once. I think there’s room there to cater treatment based off that vs a patient with visceral disease who should be getting more intensified therapy. Now we’re layering on all the genomic information, whether it’s prognostic, genomic factors, and there’s certainly increasingly genomic testing that suggests not even looking at HRR [homologous recombination repair] mutations but just prognostic tests that may allow us to decide what patients may benefit from intensification or not. You talked about comorbidities as sort of overriding all of that, and I think that’s critical, but I also think that what we’re coming back to is that is there going to be a way to identify patients who we cannot intensify up front, maybe incorporate radiation along with some of these others to allow them to have holidays down the road, and is that really a possibility? We’ve talked about that a little bit in the nmCRPC [nonmetastatic castration-resistant prostate cancer] space as well, but maybe they’re patients who, after a certain amount of time, we can give them a window, not thinking we’ve cured them, but just allowing them to recover and maybe not have some of the cumulative exposure and difficulties that we know can happen. All these things factor in. As you said earlier, I agree that we should be getting at least 2 therapies to these patients in almost all cases, and, increasingly, 3 is an up-front type of therapy. We’ll talk through these more as we go through. It’s never going to be a one-size-fits-all approach, so I think you must layer all these things in.

Transcript edited for clarity.