Episode 145: Prostate Cancer Christmas Special

Silke Gillessen and Chris Sweeney give a year in review.

 

Tom:
This is the first Christmas podcast. Well, actually it’s the second year of the Christmas podcast, but it’s the first in this year’s series of the Christmas podcast. This hasn’t been the best start to the podcast.

Brian:
Which means everybody just listened to Christmas music, Tom, if Jamma did it correctly. Yes.

Tom:
If I was able to sort that out, that would be terrific, but we’re getting sidetracked. Brian, you’re getting sidetracked. We’re joined here by Chris Sweeney and Silke Gillessen, who are our fellow Uromigos and are our prostate cancer team. And we wanted to start off by… I’m going to ask Silke if I can, to start with. Listen, Silke, give me a quick rundown on the, let’s start with the Lutetium data, the radio-nucleotide data. That study came out at ASCO, Mike Morris, and then New England Journal of Medicine with a plenary session. It’s made a big splash and you talked very eloquently previously around why radium 223 was probably less impressive than this current data. One of the things I think would be really good to hear is where you think this is now going next?

Silke Gillessen:
Yeah, so thanks, Tom. I guess we all know that finally we have that drug not in all countries yet, so I don’t even know, Chris, in the States if you already can use it, we can use it in Switzerland. So right now I think the first step is that this should be really made also accessible to our patients. And then a lot of trials are ongoing in earlier DC setting, so that was a third line setting and more. So after at least docetaxel and one endocrine agent, kind of novel endocrine agent, but right now they want to go earlier in the CRPC state, but also plan studies in the hormone sensitive state. Don’t know, Chris, if you want to speak about that.

Chris Sweeney:
Absolutely. So I think it’s very clear the drug works, especially in patients who have PSMA positivity. The challenge is now to work out who it works best and what setting it works best, and how much of the target needs to be present when you are administering the agent. So as Silke said, the studies are now being launched of second line hormone switch versus Lutetium PSMA, and then crossover to Lutetium PSMA in a pre-docetaxel setting. It makes a lot of sense, many patients are not fit for chemotherapy where they would be fit for Lutetium PSMA, it’s the best of a controller, but as long as they can access it on the crossover, I think it’s a reasonable design if they have no other good options. So that’s called PSMA4 study and that’s just starting.

Brian:
And Chris, just putting the label aside-

Silke Gillessen:
And I guess one other thing is [inaudible 00:03:22] all of this also in mCRPC the sequencing, so what is the Optima sequencing? I guess we have a similar problem then in RCCC, that is a nice problem that we have now all these substances, but the Optima sequencing is really not really clear. So what are you doing if you have a patient with a BRCA mutation in the tumor? Would you, after let’s say one novel endocrine agent, first go for the BRCA inhibitor or for the Lutetium if he’s also positive from disseminated? I think this is now all these questions that we have to answer.

Tom:
Brian [inaudible 00:04:02] question.

Brian:
Yeah, I was going to ask Chris and Silke, where’s it going to fit? Let’s put the label aside, do you think it’ll tend to use it earlier or later, or in specific patients?

Chris Sweeney:
It also comes down to Silke’s issue of access, do we have to show when a patient has had docetaxel? I’m just going to say, I don’t know what I’ll be able to prescribe-

Silke Gillessen:
Chris, could you let me know what you don’t know? Because as you know, Brian is a ghost for me and I don’t understand the questions.

Chris Sweeney:
Yeah. Let me answer it where I would like to be able to prescribe it, I would like to prescribe it after progression on first line advanced hormonal therapy, ultimately, because I think it is very active, it’s better tolerated than chemotherapy and more able to be given to more patients. So that’s where I would like to be [inaudible 00:04:56]. Whether I will be able to, whether the FDA label in the United States will say that they have to have had prior chemotherapy is a question that we’re all wondering. But the PSMA4 study will hopefully be able to get that label extension to allow before docetaxel. But this is all up in the air. Now, as Silke said, we have to really thus categorize our patient, is a PARP inhibitor a good option for them? Is Lutetium PSMA a good option for them based on PSMA PET expression? Are they fit for chemotherapy? So it’s really going to be each patient is going to have to have the menu of options that are appropriate for them based on their clinical profiling and profiling the genomics of their tumor, as well as the imaging features.

Tom:
Chris, quick question for you and Silke, you talked about targeting and previously you talked about some of the shortcomings of the control arm, how convinced are you that this works in unselected patients?

Chris Sweeney:
Silke, you take that.

Silke Gillessen:
What do you mean was unselected? Not using PSMA PET/CT as a biomarker?

Tom:
Yes.

Silke Gillessen:
I don’t feel confident about that. One out of 10 who is not positive, so I personally think if we have a biomarker we should use it.

Tom:
Chris, what do you think is going to happen in the States?

Chris Sweeney:
I really don’t know the answer, what’s going to happen in the states. I do know what I think we should do, things we have an array of agents, we actually need to define the best biomarker for the Lutetium PSMA as well as the other agents that we have access to work out which is the agent to go to for a patient at any one time. I will just say, the drug is marketed as precision therapy, but at the same time we’re saying give it regardless of PSMA PET imaging, so I think we, the field, really need to get on the same page and work out what is the best profile for when to use Lutetium PSMA. So I personally would like to see some PSMA PET positivity to justify its use, at least as the amount as described by the VISION study.

Brian:
Chris, aside from PSMA PET positivity-

Silke Gillessen:
And I guess, can I still-

Tom:
Oh, just wait a second. Silke, so we’ve got something unique [inaudible 00:07:14], that Brian can’t hear Silke, and Silke can’t hear Brian.

Brian:
No, I can hear her, she can’t hear me.

Tom:
Okay, so Silke, what we’ll do for this is when Chris speaks we’ll assume Brian’s going to talk afterwards, is that reasonable?

Silke Gillessen:
That’s very reasonable, so tell me when I should talk.

Brian:
Never anything but high quality on Uromigos Podcast.

Tom:
Can’t beat it. You can’t beat it.

Brian:
Chris, I was going ask aside from PSMA-

Silke Gillessen:
Brian, go on, even if I don’t hear you.

Brian:
Aside from PSMA PET positivity, what clinical features are you going to use to select patients? Presumably we won’t have other biomarkers for a while to select patients, so in the clinic is there other features or no?

Chris Sweeney:
If a patient has really bad anaplastic neuroendocrine features or AR negative, a high burden of liver metastases and they are chemo fit, I think I may try to get a platinum taxane doublet in. Because they were patients who were excluded by and large, and if they had just a faint trace of some PSMA positivity, but PSMA PET negative liver metastases, I think I would need to go with the more broadly nonspecific cytotoxic agents in that setting.

Brian:
Got it.

Tom:
Let’s move on, unless there’s anything else, Silke, you want to say around radio-nucleotides? Could we move on to PEACE-1? We had some really interesting discussions this year about triplet versus doublet therapy, PEACE-1 was presented at ASCO and then ESMO with a really great PFS and then really quite impressive OS data. But the trial was complicated and Eric Small came on our podcast, and Eric was very, very eloquent, and he talked about some of the shortcomings of the control arm and that he wouldn’t be using triplet therapy. We didn’t speak to him after the survival signal. Do you think the world has changed when that survival signal came out? And do you think this is a treatment for all patients?

Chris Sweeney:
Silke, you go. Maybe not. Tom, can you hear me?

Tom:
Yeah, fire away Chris, why don’t you have go?

Chris Sweeney:
I’ll have a shot. So the answer is, I think it is a rapidly evolving field. I think the question is now going to come down to who with metastatic hormone sensitive prostate cancer, where we treat with hormonal therapy, ADT testosterone suppression plus abiraterone in this case, we add docetaxel to… I think that’s where we’re at because of the survival signal. It’s hard to say we shouldn’t do that when there is this clear survival signal. Now there are arguments against it saying, well, maybe if the control arm was testosterone suppression plus abiraterone alone, and we can come back to that, but what I would say is now that the ARASENS press release, as a Friday, says that there’s a survival benefit of adding darolutamide to ADT and docetaxel versus ADT and docetaxel, we now have two studies showing the survival benefit.

Chris Sweeney:
What I suspect is that the patients had accrued to the ARASENS study are very poor prognostic, and the survival signal, as my suspicion, will be driven by those with advanced disease, de novo high volume disease as was seen in the PEACE-1 study. So I think that’s the bare minimum of patients who I feel comfortable giving docetaxel to, and with an advanced hormone, be it darolutamide or abiraterone at this stage. Now, we need to see the ARASENS data, ENZAMET we’ll read out in the first quarter of 2022, we’re just waiting for the last few events to be able to report out the longer term study of ENZAMET where there is a cohort of patients who got ADT, doce, and enzalutamide.

Chris Sweeney:
Now let’s take the counter view, a lot of people say couldn’t it be just with abiraterone, darolutamide, [inaudible 00:11:16], enzalutamide alone. [inaudible 00:11:22] nicely showed that we crossed the 60 month barrier for the de novo high volume median oval survival for the first time with PEACE-1, which we haven’t seen with abiraterone in STAMPEDE or abiraterone in LATITUDE, so that’s encouraging. But the other thing I think what we’ll need to do is get all this data into a large individual patient database and match patients as best we can to do a propensity score to see if there is a group that actually gets a clear benefit in using network meta-analyses with very refined clinical characterization. And I think that is the way we’re going to identify which patients benefit from adding docetaxel to the advanced hormones. Other people would argue we need to do the study of ADT, doce, advanced hormone versus ADT, advanced hormone, but I suspect we won’t be able to do it and we’re going to have to rely on the meta-analysis approach.

Tom:
Silke, have you got a feel for this? Who would you be using triplets on as routine?

Silke Gillessen:
I don’t know, I think you didn’t hear me before. Do you hear me now?

Tom:
Yes, we can. We’re good to go. We’re good to go.

Silke Gillessen:
Oh, good, I went out and in again. I guess most of it I heard what also Chris said. So I guess right now, for me, it’s clearly the patient who are de novo, because all the patients in that trial were really synchronous metastatic patients, the same in our sense. So even if we haven’t seen that data yet, and the patients with a… I know that Chris doesn’t like it, but the high volume definition, so a lot of disease and obviously patients who are fit for chemotherapy, I guess you could always argue, there’s a lot of discussion if the PEACE-1 was not so perfectly designed because the question is docetaxel in both arms and then plus, minus abi. But I think the treatment was more effective and I agree with Chris that there will be some patients who really profit.

Tom:
So overall, that sounds to me like you’ve both come to a position over them year where you think this trial is practice changing, particularly for the high volume patients. Chris, do you accept that?

Chris Sweeney:
Yeah, I’ve been there since I saw PEACE-1 data overall survival. But again, that’s a provisional until we see all the data and put it all together. But if it were me with the best information I have right in front, I would like the triplet if I have the poor prognostic disease, which is deliver high volume.

Tom:
Chris, you’re going to use the triplet-

Silke Gillessen:
Agree.

Tom:
Until proven otherwise, I guess?

Silke Gillessen:
Change [crosstalk 00:14:06]

Chris Sweeney:
Correct. Exactly.

Tom:
Silke, fire away.

Silke Gillessen:
No, that’s fine, I just wanted to say I was skeptical with the rPFS data only, but the OS data really, I have to say surprised me first of all, but also convinced me.

Tom:
What are the outstanding issues with that PEACE-1 data? What do you still need to see?

Chris Sweeney:
I’ll double down on that. I think the question is how much of an rPFS benefit translates into an overall survival benefit? And it’s not just going to be the PEACE-1, Tom, it’s going to be seeing all the data sets from all the studies and seeing, okay, in different groups, how much of an rPFS benefit leads to a notable survival benefit? Because it was less in the de novo low-volume but it was more impressive in the de novo high-volume. So there are clearly some patients where you can give sequential therapy and they do really well, whereas, others they need the triplet upfront concurrently I think. So I think that’s the question we’re going to have to work out is who needs the intensification of all three agents upfront right at the beginning versus not?

Silke Gillessen:
And, Tom, also the other question that obviously PEACE-1 is then hopefully going to answer is, should you also add radiotherapy primary to it? Because that was a two times two design, but we haven’t the answer to that question. So this is really something that we’re all be very excited to see. Because obviously now especially for the low-volume patients maybe there is the question, should you also add radiotherapy to the primary? And I think that is a quite interesting question.

Chris Sweeney:
I’m going to throw out a thought experiment on that.

Tom:
Go on then.

Chris Sweeney:
So we see that adding hormonal therapy to patients who have had their primary treated, so ADT and enzalutamide, and I think apalutamide as well in the metachronous setting, they have a survival benefit and we don’t see that with docetaxel.

Silke Gillessen:
Exactly.

Chris Sweeney:
So my thinking is if you got the primary controlled with either radiation in the de novo low-volume or in the metachronous setting, your systemic therapy is augmented by adding the hormones to it. Whereas what we don’t see is adding docetaxel in that setting, which is a different disease, so just trying to piece it all together, when we see a clear survival signal for the systemic control with docetaxel added to testosterone suppression, and we see it with the hormones with testosterone suppression, it’s when we see the clear signal with both that we’ll see the clear signal with the combinations, the triplets. And I think that’s the same with radiation to the prostate, where we see a survival signal with that, with de novo low-volume and with the hormones. So I think where we go back to the classics, if we see a survival signal with a single agent and then you combine the single agents, you get the synergy in the increase survival when you do the combination. So that’s how I’m thinking about this.

Silke Gillessen:
The interesting thing, maybe also that we see from STAMPEDE is that it seems really that a combination hormonal treatment plus radiotherapy, the combination is more effective than adding docetaxel to radiotherapy. So I think these are all a lot of interesting questions and I hope the answers are coming up soon.

Tom:
Brian, what about a Christmas question from you?

Brian:
A Christmas question, like about Christmas?

Tom:
No, prostate-

Chris Sweeney:
Let me give everyone’s Christmas wish about prostate cancer that they don’t get it in 2020.

Brian:
Right.

Tom:
That’s very reasonable. That’s a very reasonable Christmas wish.

Brian:
So we’ve talked about-

Silke Gillessen:
I haven’t also a wish please.

Brian:
We’ve talked about PEACE-1 and the radio-nucleotides, what maybe the third biggest clinically impactful data in 2021, for either of you?

Chris Sweeney:
Yeah, go Silke. Silke, biggest none-

Silke Gillessen:
Look, I still can’t hear Brian. I can now hear you-

Chris Sweeney:
I will [crosstalk 00:18:19] you.

Tom:
Why don’t you answer it, Chris? You go, Chris. If you repeat the question-

Chris Sweeney:
Yeah. Silke, the question is, other than PEACE-1 and the radionuclides, what’s the breakthrough in 2021? And I think clearly the answer is adding an advanced hormonal therapy, in this case abiraterone, to testosterone suppression and radiation to patients with high-risk localized disease. And the STAMPEDE abiraterone zero arm, where they looked to see if there was an MFS benefit and they saw a hazard ratio of a MFS of 0.53, 47% reduction in mets and death, which translated into about a 38%, I think, decreased chance of death as well.

Chris Sweeney:
So an improvement in overall survival. So the big finding to me was that the ice-cap of MFS endpoint was utilized and found to be helpful, and that then stands as a great step to be able to say, we do increase the survival with adding the advanced hormones to radiation. And that will allow us to actually also get readouts from Atlas, with apalutamide in the same design and with enzalutamide with ENZARAD in the same design in high-risk localized and with DASL-HiCaP with darolutamide, hoping that we can get darolutamide which is probably the best tolerated agent in an adjuvant setting in the long term.

Tom:
Silke, this seemed to be just a race to go as early as you possibly can with the most powerful hormone treatment you can imagine, is that basically the rule of prostate cancer now as it transpired really early heavy therapy works? Is there any evidence that what I’ve said is not true?

Silke Gillessen:
No. I think that is very good. I think we have to just remind ourselves that STAMPEDE was really high-risk patients, it wasn’t a low-risk patient who got some radiotherapy. So it was selected for the really high-risk patients with nodal disease or T3, 4, PSA over 40, a Gleason eight or more. So this is really now something that I think we should do in these high-risk patients. And no, yeah, it’s exactly what you say, we take them as early as possible and we… And again, I think the important thing is that they have only two years of abiraterone and after that you can stop the therapy. So that’s obviously the nice thing about it.

Chris Sweeney:
For sure. But let me clarify one thing. Yes, when we’ve advanced the hormones forward, we’ve seen marked improvements in overall survival at every step of the way, non-metastatic castration resistant, M1 hormone sensitive and now adjuvant, but we do not see that with docetaxel. So we don’t have a clear survival signal out of the three or four studies of adjuvant docetaxel, but we have seen it with abiraterone. We do not see a survival benefit with docetaxel in the rising PSA biochemical recurrence only setting when added to testosterone suppression. So yes, we are seeing moving forward the hormones at every step of the way we get a benefit, but not with the taxanes.

Tom:
Brian, why don’t you ask Chris a quick question, in view of our IT issues, I think I might start sharing this [crosstalk 00:21:43].

Brian:
Chris, I was just going to follow up and say, do you think that’s because, I don’t know, the taxanes if you will, require more disease to work? If you know what I’m saying, like it requires the visceral disease, the M1 disease, et cetera, versus an earlier setting, does that make sense?

Chris Sweeney:
Are you setting me up? Yeah, I do. I do think there’s-

Brian:
Am I? No. Not intentionally.

Chris Sweeney:
No, this is my argument all along, where there’s a subset of patients who benefit from the taxanes and the more higher burden of disease, the more rapidly progressive we do see a benefit. And we’re hopefully going to get biomarkers that can characterize that at a biological level and not be reliant on imaging and timing of presentation with metastatic disease. So, yes, I think there’s a set group of patients and that’s here this conversation about why I say, I don’t think the taxanes benefit metachronous low-volume more of an indolent disease, we don’t see any benefit what we do see with the hormones. Hopefully we get to biomarkers in that [crosstalk 00:22:36]

Tom:
Can I ask you a question? Silke, where are you in terms of biomarkers? I know that there’s a DDR HRD part biomarker, which is pretty questionable in my opinion, with the exception perhaps of BRCA2, where are you in terms of biomarkers in predicting patients who need chemotherapy? And where are you in circulating biomarkers in prostate cancer?

Silke Gillessen:
So I guess for me, some really important work is going to come out from good [inaudible 00:23:10] lab who really is looking for a lot of STAMPEDE samples. I guess, I can’t remember Chris, he’s also working together with you on the chartered samples?

Chris Sweeney:
Yeah, so I’ll just pick up. The one data set that we have right now is the Luminal B from the PAM50 from the chartered samples, had a very strong benefit with docetaxel, but we saw no evidence of benefit in those who had the basal of the PAM50. So Ged has now send the docetaxel arm samples to the same platform with Decipher to see if we can validate that. Right now, Ged is looking at the abiraterone using the same platform to see if there’s a signature for the hormone benefit. And we’ll be sending ENZAMET specimens as well. So hopefully the answer is in 2022, Tom, we may have some clarity on that. But there’s no clarity from circulating tumor to DNA, exome profiling, or gene expression profiling from the primary, but hopefully in the next 12 to 18 months, we will have data.

Tom:
Brian, do you want to ask Chris question?

Brian:
I was just going to ask, sort of looking forward to big… You alluded to this, big data sets in 2022, what’s the clinically impactful data that’s going to come out? I guess, ARASENS we got the press release for, but what else?

Chris Sweeney:
For sure. So going from castration resistant to hormone sensitive to adjuvant, I think the answer is we will get greater clarity on the triplet therapy from ENZAMET and ARASENS, for metastatic hormone sensitive. We will get some longer term pull up data from the role of [inaudible 00:24:52] with abiraterone and metastatic castration resistant prostate cancer. It is very possible if we see a very big signal, we may see data for adjuvant apalutamide in high-risk disease, localized adjuvant in the ATLAS study and ENZARAD, if there’s a really big signal, if we have enough events in the next 12 to 18 months. So will we be potentially seeing more patients cured with more advanced hormones with those agents in 2022? Possibly, but it could sneak into 2023. So I think they’re the big ones. Who should we treat with triplet therapy and who should we add the advanced hormones to in high-risk localized disease and getting the agents approved and decreasing death rates from prostate cancer? Is very foreseeable in the 12 to 18 months.

Tom:
Silke, if you were looking for one-

Silke Gillessen:
Can I ask you something quick? Sorry, Tom. But what I’m really interested in is that I just heard from [inaudible 00:25:50] that EMA may not even kind of approve that abi in that situation, because obviously you as a company have to make a new approval in a new indication. And if no one is interested because abi’s now generic, it could be that in Europe it will be difficult to give these drugs that are very efficient in the [crosstalk 00:26:17] State. What happened to the state?

Chris Sweeney:
So the answer is a week we’ll be able to prescribe it, I think based on guidelines and insurance companies will cover it. But having said that, there’s a reason why we’ve designed enzalutamide even as a cooperative group with Enza and the related groups with ENZARAD, we’ve actually got it at industry level and had conversations with the FDA along the way so that it actually could be on the labels in Europe and the United States and Australia eventually. So it’s how the study’s been conducted an conversations with the regulatory agents along the way, and we are doing that with both ENZARAD and DASL for that very reason. But in the United States, we’ll be able to write and our writing for abiraterone in the adjuvant setting based on the STAMPEDE abiraterone data.

Silke Gillessen:
Okay.

Tom:
Okay. Quick question for you both. What are you getting for Christmas this year, and in prostate cancer, what would you think would be a terrific Christmas present? What would be the best case scenario in 2022 that would make a big difference? One answer. Silke, you go first?

Silke Gillessen:
So I don’t know what I’m getting for Christmas, so I can tell that in January, that should be a surprise. So what will be the best? I mean, that’s a very good question. Can I say something maybe a bit not very interesting, but I think if we would have finally treatment against hot flashes for men, that would be really helpful. I just don’t see any kind of trials ongoing in that setting, and that’s really something that’s very bothersome for our patients.

Tom:
Chris, what are you getting for Christmas, number one? And number two, what would big breakthrough that’s reasonable do you think might happen this year if you had to pick one?

Chris Sweeney:
So the first answer is my cellphone connection to Santa Clause is like the cellphone connection to Uromigos podcast, it’s busted at times and not working.

Tom:
It’s flawless. It works really flawless.

Chris Sweeney:
But what I do wish is that we actually-

Chris Sweeney:
Actually this is the holiday present I hope for everyone, is that this COVID thing goes away. That’s what I’m wishing for 2022 for everyone’s holiday season and beyond. The next thing though, is what I’m hopeful is that we can all get on the same page about clinical and patient characterizations about how best to treat patients with which agents, and get as much of the data into one database so that we can really get high level data to say, “This patient with these features clinically and genomically can benefit from this class of therapy.” And then also say, “Okay, now we’ve got these new agents showing some benefit with AKT inhibition, potentially CDK4/6 inhibition, Lutetium PSMA, that we can actually then now start design the next generation of trials for the right patients and be well on the way to further decreasing the death rate from prostate cancer.

Tom:
Brian, a final word from you.

Silke Gillessen:
Tom, can I ask one last thing?

Tom:
Yes, of course.

Silke Gillessen:
Because we were just like a lot of [inaudible 00:29:23] about that, so as you have seen in the States, but also [inaudible 00:29:27] in Belgium, there is still a very high percentage of men with metastatic prostate cancer hormones sensitive that gets only ADT, so I think here we are making progress and progress and progress, we are already speaking the third time about the triplet therapy, but there are still lots of men still only treated with ADT in the metastatic setting. So there is really the question, why is that? What are the hurdles? Is that really only access? But probably not because it was also in Belgium. Is that education? So maybe how can we get our new results to the physicians who treating these patients?

Tom:
There’re more than three things here.

Chris Sweeney:
I’ll pick up on that. Silke, that’s why I think if we can all globally get on the same page and say, “These patients should get this treatment,” and it’s clear-cut for everyone such that there’s not this versus that option, it’s this is what we think and then have that as a clear education mission.

Tom:
Brian, a final-

Brian:
Yeah, no, I think this has been great. I think we’re up against time, we should probably cut our audio losses at this point. Thank you guys, [inaudible 00:30:39], I know Silke can’t hear me.

Tom:
I missed that.

Chris Sweeney:
Cheers guys.

Brian:
Hey, look, thank you very much everybody. Going to see you very soon.

Chris Sweeney:
Look forward to it.

Silke Gillessen:
Ciao.

Brian:
Cheers, happy holidays.

Chris Sweeney:
And to Brian, bye-bye.

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