Alan Bryce, MD

 I'm going to go over the PROfound Study data and then we're going to go over [the] TRITON2 [study]. The PROfound Study was a phase 3 study looking at olaparib versus physician's choice of therapy in a mixed population of patients with mCRPC [metastatic castration-resistant prostate cancer]. And I'll explain that a bit here. Everyone had to qualify as having 1 of the qualifying 

[homologous recombination repair] gene mutations. In cohort A was 

. In cohort B were all of the other qualifying aberrations which you see listed on the bottom of the slide in blue. And then, within each cohort, patients were randomized to olaparib versus physician's choice in a 2-to-1 randomization, and the physician's choice was either abiraterone or enzalutamide—whichever drug the patient hadn't previously received. Looking at the efficacy for PFS [progression-free survival] and OS [overall survival] in both cases, in cohort A, it strongly favored the olaparib arm. Thus, rPFS [radiographic PFS], the hazard ratio was 0.34. It doesn't get much better than that, right? That's beautiful. And then the OS. Here again, the hazard ratio is 0.69; 19 months versus 14.7 months—strongly positive for both primary end points. You can see the overall response rate was 33% with olaparib versus 2% in the control group. Here again, when you use ABI [abiraterone] or ENZA [enzalutamide] after ENZA or ABI, you don't get a lot of response. Median time to pain progression—course, it's a secondary end point [and] goes right along with the PFS and OS end points, thus strongly favoring olaparib. When we look at the safety, you do see some increased adverse events of Grade 3 or higher in olaparib. It has some myelosuppression. But you can see [that] these are fairly modest numbers. Nothing too dramatic. [It is] very manageable for an oncologist.

Ultimately, olaparib was approved by the FDA [Food and Drug Administration] in May 2020 specifically for men with mCRPC with a deleterious or suspected deleterious 

 gene mutation. And in fact, it's really the whole list that you saw there on the first slide who had been previously treated with enzalutamide or abiraterone. [There was] no requirement for a prior taxane. Then, in November 2020, the FDA approved the companion diagnostic, which is the FoundationOne Liquid CDx assay. For rucaparib, we have the TRITON2 study so far. TRITON3 is not yet reported. TRITON2 was the phase 2 single-arm study of rucaparib in men who had a qualifying deleterious 

 gene alteration, had been treated with 1 to 2 prior lines of an androgen receptor pathway inhibitor, and had received 1 prior line of taxane-based chemotherapy. These are later patients than we saw in the PROfound Study, for the most part. Patients were treated; everyone received rucaparib at the standard dosing until radiographic or unequivocal clinical progression or toxicity. The primary end point was in cohort A, looking at patients with measurable disease. They were looking at the overall response rate. This is really the outcome the FDA wanted to see for initial approval. And then, for patients without measurable disease, it's the confirmed PSA [prostate-specific antigen] response rate, the PSA-50 rate. When you look at the characteristics of patients with a 

 mutation, so 1781 patients screened, 209 enrolled, 115 had a 

alteration at screening. You can see here germline was approximately 38%. Somatic was approximately 61%. Again, the germline is only capturing less than 40%, so we want to look at the somatic. 

 by about 8 to 1, and that's consistent with other data sets. It's usually 5 to 10 times higher—something in that ballpark.

Early on, we were asking a lot of questions about zygosity; biallelic loss versus monoallelic loss and where the data was available, because it wasn't available in all patients, but you see biallelic loss happening more commonly in the 

 patients. About 33% of the patients versus 6% [who were] monoallelic. [There’s] a little bit of a different distribution in 

, but the numbers were so small, I'm not sure you'd draw any conclusions there. In looking at the radiographic response to the primary end point, the complete response [CR]—the overall response rate was over 50%: 50.8% of patients, so 33 out of 65. Complete response of 6.2, which really means they only had soft tissue disease—not bone disease, because there's no CR in the bone metastases patients. Partial response is 45%: 44.6%. An additional 38.5% with stable disease. And then, looking at the safety summary, again, you see a fairly safe drug, but nevertheless, the Grade 3 treatment immersion [for] adverse events was 52.9%. Treatment interruption, 48.2%. Just under 30% of patients would get a dose reduction. Only 6% had discontinuation due to toxicity. Ultimately, rucaparib was approved by the FDA. Also, in May 2020, a couple of days before the olaparib for deleterious 

mutated metastatic CRPC in patients who had received at least one AR [androgen receptor]-directed therapy and 1 taxane-based chemotherapy. Thus, a different label than we see with olaparib, right? More restricted in the mutation and more prior lines of therapy required. And then, here again, FoundationOne Liquid CDx was eventually approved as a companion diagnostic.

Videos

Expert perspectives on the PROfound and TRITON2 studies of olaparib and rucaparib, respectively, in metastatic castration-resistant prostate cancer.

PARP Inhibition in Metastatic CRPC: The PROfound and TRITON2 Studies

 We’re down to our last couple of questions. Eleni, I’ll start with you. What other advances are you excited for in the prostate cancer field?

Even though we’ve been through this horrid pandemic, it’s been a couple of good years for therapy development in prostate cancer. We mentioned earlier how to harness the value of sequencing the tumor and improve those methodologies and access to them. That’s what I’m truly excited about—a pragmatic deliverable in our clinic. But I also have a soft spot and a lot of hope for development in even earlier disease—high risk, localized—which is arguably our biggest unmet need. These are my 2 tangibles. We’ve got patients who we need to treat. We need to look ahead because they’re young, they’ve got aggressive disease, they should have a longer life span, and we need to give it to them.

 Absolutely. Well said. Dan, what are you looking forward to for further advances?

 I’ll echo everything we just heard. I’ve used the words “the future is bright” a few times throughout this presentation. I very much feel that way. I tell my patients sometimes that 1 of our goals is to maintain where we are now until that next big development comes out. You’re going to have more options, better options. In years past, that sounded like a pipe dream. It sounded like a nice thing to say. But that’s happening now. I’m very excited about where a number of things are heading. We have to keep our patients alive, and we’ll get there.

 Fair enough. I agree with both of you. The future is incredibly bright in prostate cancer when you think about the pace of change. From 1941 to 2010, we had something like 7 drugs approved. From 2010 to now, we’ve had more than a drug a year getting approved. The pace of change is absolutely gangbusters. How many ASCO [American Society of Clinical Oncology Annual Meeting] Plenary Series presentations on prostate cancer were there in the 1990s? There was nothing. Now, at every ASCO, there’s a prostate plenary because the pace of change is fantastic. I hope everyone will stay tuned and stay up to date. There’s so much happening, and it’s getting better every year.

When I’m treating patients for mHSPC [metastatic hormone-sensitive prostate cancer] with first-line therapy, they say, “What would you do next?” I say, “I have no idea. Because with what I’m doing, you’re going to respond for at least 2 years. And what I’m doing today is nothing like what I did 2 years ago. Two years from now, it will be even better.” I tell them, “Let us do the research. We’re going to get something better. Hang in there.” I try to give them a hopeful message.

That’s the end of our presentation. I want to thank the panel. Eleni and Dan, it’s always a pleasure to work with you. Thank you for your thoughtful case presentations and the informative discussion. To our viewing audience, thank you for joining us for this 

® presentation. We hope today’s discussion was a valuable use of your time and that you acquired some practical knowledge that can help you in your clinical practice. Thank you very much. Have a good night.

Closing out their discussion on novel treatment approaches in prostate cancer, experts consider future strategies and remaining unmet needs in this setting. 

Looking Toward Future Management Strategies in Prostate Cancer  

 Let’s go back to Eleni here. Number 1, do you repeat genetic testing in patients at progression? What are the guidelines around testing for germline/somatic mutations? We've touched on some of this, but how do you approach it?

 As I mentioned earlier, I do repeat genetic testing in patients at progression, especially if we're talking about these cases that have a long history and their biopsy or radical prostatectomy is more than 3 or 4 years old, which hopefully is the case. We have enough information to include even a potential change in MS [multiple sclerosis] status. It is worthy. I used to have a huge fight with [the] pathology [department] when I would ask for MS status to be reassessed, and they would block it until the paper was published that showed that this can [happen]. And we have wonderful papers from several groups now showing that with the advent of the progression of the disease, we have accumulation of mutational events, so we don't really know at the end of the day which 1 will be the driver. What we do know, based on the data that came from the PROfound Study and the analysis that was done in somatic testing, is that usually if you have a 

 mutation, this is a driver event still in the far advanced disease, whether it is something that is an archival tissue and of course, always in germline. But my preference is also to repeat, not just for MS status or other events such as you mentioned, that could be found later on, or selected later on. And importantly, to actually look at the TMB [tumor mutational burden]. And TMB does change, as well. Now we're not there yet when it comes to IO [immuno-oncology], but I think there are enough exciting data that it's not far from where we're going to be able to have some more certainty in patient selection groups.

 Dan, let let's wrap the second and third questions together. What percentage of your patients test positive for a deleterious germline and/or somatic 

 mutation? And then, what are the treatment options we should talk about for patients with 

 Sure. And to sort of echo on the previous points, I think as the ease of testing has gone up, especially with liquid biopsies, we are testing more often in our practice. And coinciding with that, we are finding more patients – often, surprising patients – who are testing positive for mutations that either did not have it before or we weren't expecting it, and it can have direct impact on treatment-making decisions. As far as what to do with the 

, we're becoming more and more lucky in having more options in this space. We've participated very extensively with the development of rucaparib. We have olaparib, which is approved for a wider gene expression profile. Thus, the options are going up here. And [there are] very positive results, especially in that population with 

 The controversial population is the population with 

[mutations], and you get different answers. I've been on the podium and had this debate with my colleagues. I'm of the opinion that 

-mutant prostate cancer does not respond to PARP inhibition based on the clinical trials, but those are subsets. There is a label indication for olaparib, but the hazard ratio in the PROfound Study trial for patients with 

 mutations was 1.04. There's no signal. In my practice, I would say [concerning] 

 mutations, I want to take you to clinical trials. I want to look at ATR [ataxia telangiectasia and Rad3-related] inhibitors. Eleni, where do you land on that?

 I land on what are we going to do now that we have data that says it doesn't matter? I'm still struggling. I'm having meltdowns here looking at the PROfound data. But it's pretty strong data. I keep going back and looking at those hazard ratios. And in the population with 

 [DNA damage repair]—which, hopefully, we're going to get more clarity on—it looks like it's just an amazing response in the combination with abiraterone, so it speaks to earlier introduction. I am with you when it comes to the 

 genes. However, I give the benefit of the doubt because it looked, if you remember that gene-by-gene description, that the hazard ratio was a huge range. It needs to be a little bit more specific. What I would like to refer to is a beautiful trial that I think is from a European group, the PROREPAIR one. I don't know if they’ve a published the paper yet, but they presented it at an ESMO [European Society for Medical Oncology meeting] a year or 2 ago, and they showed that it is not enough to just look at the presence of a 

 event, but to also look at the presence of other events that are happening simultaneously; that maybe thinking over the leads such as NIK amplification and the like, if I remember correctly. And you mentioned a couple of others. This is not a linear presence of 1 event. Going back to what you said, you need to have the whole picture.

 I think we've seen in some reports that ATM expression by IHC [immunohistochemical diagnostic assay] is more predictive and ultimately—and probably to your point—has to do with some of the comutations that are occurring. It's really not the ATM at the heart of it, right? But we'll see. We'll see. There is more to come, for sure.

A brief discussion on the importance of germline/somatic BRCA1 and BRCA2 mutations in metastatic CRPC, accompanied by practical advice on genetic testing.

Testing for Germline/Somatic BRCA Mutations in Metastatic CRPC 

 Lutetium is based on the phase 3 VISION study. Everybody has heard of this by now. It was a slightly complicated study design. I’ll try to walk through it step by step. The patients were required to have at least 1 next-generation androgen receptor pathway inhibitor and at least 1 line of taxane chemotherapy. This was a randomized study vs protocol-permitted standard of care. The control arm was not an absence of therapy, and even the treatment arm was lutetium plus that same standard of care. Based on the exclusions, that meant either abiraterone or enzalutamide, 1 of the oral androgen pathway inhibitors. Patients were required to have a good performance status, a life expectancy of greater than 6 months, and a PSMA [prostate-specific membrane antigen]–positive PET [positron emission tomography] CT using gallium-68 PSMA 11. That was 85% or 90% of patients, so most patients do. Patients were stratified by very standard criteria: metastases, ECOG performance status, etc. There were alternative primary end points of radiographic PFS [progression-free survival] or OS [overall survival]. Of 1179 patients screened, 1003 were positive, so 86.6% have the PSMA expression, so that’s the vast majority of patients. Ultimately, 831 patients were randomized of the 1003 who met criteria.

As we see, there was relatively low enrollment of Black African, African American, and Asian patients. Most patients received 1 prior androgen receptor pathway inhibitor and 1 prior taxane, so presumably just dosing. About 40% to 50% of patients received more than 1 of either the AR [androgen receptor] pathway inhibitor or taxane. One of the alternative primary end points was rPFS [radiographic PFS], which favored the lutetium 8.8 vs 3.6 months. There was a positive hazard ratio of 0.43. There are 2 points here: 1 is that lutetium works nicely, and the other is that when you use abiraterone, or after prior abiraterone or enzalutamide-docetaxel, it does nothing. It’s placebo. The rPFS benefit was preserved across most of the prespecified subgroups, not in the Black or African American or Asian populations, but in very small populations. The overall survival end point favors lutetium PSMA. There are 2 points: there’s a survival advantage, a good hazard ratio of 0.63, but if you’re not giving the lutetium, then survival is then less than a year in this population. These men are very far down the road. That’s always important to keep in mind as a data point.

When we look at the adverse events, you see a higher rate with the lutetium. The serious adverse events were a little under 10%; grade 3 to 5, about 8%; grade 5—that is, death—in just under 1%. In the treatment-emergent adverse events, what you see with lutetium is some myelosuppression, because so much of this will be taken up into the marrow and the bone, where there’s presumably prostate cancer metastases. Then you see dry mouth nausea, vomiting, and dry eyes because of the expression of PSMA and the salivary glands and the lacrimal glands. Then you see some excretion of lutetium into the GI [gastrointestinal] tract. There’s also excretion into the urinary tract. You see some renal effects and some potential cystitis impact on renal function. You don’t see a big signal in terms of secondary malignancies and no excess intracranial hemorrhage.

Shared insight on the VISION trial, which analyzed 177 Lu-PSMA-617 in previously treated PSMA-positive metastatic castration-resistant prostate cancer. 

VISION Trial: 177 Lu-PSMA-617 in Metastatic CRPC 

 Now, we’re going to talk about metastatic castration-resistant prostate cancer [mCRPC]. This patient is a 70-year-old man who came in with urinary obstruction, hematuria, and some low-back pain. He did have a history of hypertension. On initial work-up, his PSA [prostate-specific antigen] was 39.8 ng/mL, and he had 4 bone metastases in the pelvis. He was asymptomatic with a good performance status, aside from that low-back pain. Genetic testing showed no detectable alterations in his HRR [homologous recombination repair] genes. He started on ADT [androgen deprivation therapy] and docetaxel and had a nice PSA decline down to 0.6 ng/mL. Twenty-two months later, he’s having increasing fatigue. His PSA is rising to 25 ng/mL, and imaging shows lung metastases. He’s more symptomatic, as already described. Of course, he has castration-resistant prostate cancer, so abiraterone is added to his regimen. The first question—Eleni, I’ll start with you—is how has the evolution of the treatment of mCSPC changed the treatment landscape for mCRPC in your mind? What are we doing now?

 This is a great question. You can’t help but think what of we’re going to be doing given the new data we just saw. The profile data that came through and the whole controversy there, what are we going to be doing in a year? The concern I have is that I don’t even see what you just showed us. If we’re going to be compiling everything in castration-sensitive disease, we may even have the enhanced antigen signal inhibition early on. It’s not a bad concern, because I agree that it increases the life span. We just need to start thinking more along the lines of what you proposed: let’s do that sequencing early on, potentially develop more of the liquid biopsies with ctDNA [circulating tumor DNA], and monitor the changes and the mutational events and alterations that may guide our practice. We heard great news last year when we got the data on the first targeted diagnostic-driven radiopharmaceutical, and it gave us a breather. Every day in the clinic, when you speak about this data, it gives the patients a breather too because we have something in CRPC. The landscape is changing rapidly. You described it as way into CRPC. I see it the question of what do we do after docetaxel and enhanced antigen signal inhibit coming up even earlier.

 It’s definitely a challenge. I’ve grown up with a belief of not necessarily keeping the best option in my back pocket, believing that I don’t know what’s going to happen by the time patients are ready for second- and third-line [therapy]. I want to give them what I believe to be the best early on, and that’s going to be a triplet while it could theoretically exhaust various options later. I still want to give the patient the benefit of the doubt and treat them the best way I can off the bat. For some of these patients who had prior docetaxel exposure, if it was awhile ago, there are times I go back to chemotherapy or cabazitaxel. We have some data about the benefits of switching from 1 oral to another vs introducing cabazitaxel in the right setting. It appears that there’s more benefit toward secondary chemotherapies than there are toward alternative oral agents.

The earlier treatments definitely play a role in what we’re going to do later. We’ve mentioned the testing a few times. If I have a setting to introduce something devoted toward 

 mutations, I’m certainly thinking about that by the time patients are progressing. We’ll see how things work with Pluvicto, with lutetium. We’re very excited about the approval. The future is going to be very bright in that agent as well.

 Eleni, what about PSMA [prostate-specific membrane antigen] PET [positron emission tomography] imaging? When would you bring it in? Do you think providers need to worry about gallium 68 vs F-18?

 I don’t get why we worry. For the time being, I’m worried about what can I get my hands on. But honestly, this is resolved. I agree with some data that the germline may be more specific, even though with the Pylarify option we’ve explored recently, I’ve been quite satisfied. I’m more concerned about our relying solely on molecular imaging and forgetting anatomic imaging. Also, to switch it a little, if we want to forget anatomic imaging, should we at least explore the opportunity to look at discordance in molecular imaging, PSMA expression vs straight FDG [fluorodeoxyglucose] expression that would speak to a more aggressive disease? If we combine nuclear medicine with good anatomic imaging, we might have a solution. The VISION trial had that point of looking at that discordance with anatomic imaging, but not a lot of that is discussed. It’s in the footnotes. My point is that I’m very concerned about relying solely on molecular imaging.

 No. 1, you can only order your PSMA scan when it’s approved by insurance. It ought to be approved if you’re trying to qualify a patient for lutetium. That’s clear enough. But we still live in this world, and it’s going to be uncertain for a while. One thing I struggle with a little—I’m not sure how much payers have picked up on this or if we’re going to have to deal with it—is that if you strictly read the FDA label for lutetium-177, it says that patients have to have PSMA expression using a PSMA 11 agent. Now, Pylarify is not PSMA 11. Gallium-68 isn’t necessarily PSMA 11. It could be PSMA 617, 1007. I don’t think most providers are thinking about this at all. But what are we going to do if they come down and say, “You have to have a PSMA 11 agent and it’s only available 2 hours away”? Because cross to half-life of all these gallium agents is shorter. The availability is different from F-18. F-18 has an advantage. I don’t know if that language in the label is going to be a problem for us, but in the back of my mind, it’s causing me a little worry.

 I absolutely agree. It’s concerning for a lot of the practices, but we’re still finding our way in the dark. Do you have it available already, Alan?

 At Mayo [Clinic], we have it at our Rochester campus because we had an NDA [new drug application] in flight. We have an NDA in flight at the Arizona campus as well. I expect we’ll have PSMA 11 gallium-68 available fairly soon. But for a long time, I told patients, “If you can get a PSMA scan, I don’t care which 1 you get.” Don’t get on a plane to get 1 over the other, just get the 1 that’s available locally. I’m not sure that’s going to hold if the payers are strict about the label.

 I was referring to if you have lutetium set up running right now?

 I’m sorry. We’re not giving lutetium yet because there’s no coverage determination.

Moving on to their last patient case, expert panelists review the diagnosis and management of a patient with metastatic castration-resistant prostate cancer. 

Case 3: A 70-Year-Old Man With Metastatic CRPC 

 I think maybe we can ask the first 2 questions together. Eleni, how do you counsel your patients about the role of chemotherapy in this setting?

 It's usually one of those very long first meetings where you go through all the potential options— leaving out ADT [androgen deprivation therapy] alone, and you present the different agents and the pros and cons. The question about chemotherapy—it's the dreaded word—but what helps is, once the patient has the understanding that this is a 6-cycle-and-out process, [then] we're done. And if it happens early on, we also always comfort the patient when we have this discussion; we are going to go to full dose. It's very likely you will have no problem, but we will be there if need be. Let's say [they are of] Asian descent, and the like, to cut down on that. You have to babysit these men. I know we're speaking to oncologists who are not necessarily the only practicing GU [genitourinary] oncologist. Prostate patients are a completely different breed. They're vulnerable even when they look like they're doing CrossFit and running around more than we are. It just the nature of the beast. The fact that they’re losing their testosterone makes them very vulnerable. And that is where a lot of time is spent: describing that, yes, we saw it with the CHAARTED [Chemohormonal therapy versus androgen ablation randomized trial for extensive disease in prostate cancer trial] data. We saw that dip in quality of life and they literally tell them, “Life will suck for 3 months, we will be there for you after that; we'll be fine.” But now with the addition of darolutamide, I had a man who I was struggling trying to start. He was falling apart. He had been admitted. I met him in inpatient because he had gone into diabetic ketoacidosis. And at the same time, [he had] high volume, highly symptomatic constitutional symptoms. The guy is on docetaxel and darolutamide—which I started just when the press release came through—and he's doing great. But at first, I give them the worst-case scenario and we take it from there. That's kind of my approach: no sugar coating. It's chemo. You're older men – let's do this. Again, it might be a little bit of a tougher approach to life, but it usually works.

 You started out talking about how they need to be babied, and then you ended up so tough. That was a transition.

 Kind of like, “We're here for you. That's how we babysit you. We'll see you every week. We'll be on the phone with all of that, we will hand-hold you, but it's not going to be pretty.” They know. The younger guys do well, but when our older patients come on, it's harder. We agree on that.

 Dan, what about unmet needs in this space?

 Well, we're getting better, thank goodness. Just a few years ago when I told everybody I was going to be a GU oncologist, they looked at me and said, “Why? You guys don't have anything that you can offer patients.” Thank goodness, we've made quite a few strides in this setting, but making strides come with certain challenges. One is understanding sequencing, understanding the exact value of chemotherapy as we're debating, hopefully, [whether] it's going to be less and less as time goes on. But 1 thing you mentioned is that still the best survival data does come from combination therapy. We're still stuck in the chemotherapy world, for now; hopefully moving away from this, but there are a number of other exciting things, hopefully, on the horizon, whether that's going to be more PSMA [prostate-specific membrane antigen]-directed therapy, whether it's going to be other combinations on the horizon. I think the future is very bright as opposed to what my colleagues told me just a few years ago.

 What I like to tell patients when I give these talks about mCSPC [metastatic castration-sensitive prostate cancer] is this concept of treatment intensification recognizes that since 2015, we're on an unbroken winning streak of 9 straight studies. Intensification works, and we're late to this game. Look – intensification with multidrug therapy was proven with MERCK back in the seventies. Come on. And it takes 45 years for prostate cancer to start to do the same thing. The research in this space is going to be gangbusters for the foreseeable future because every drug that is yet to be tested in first line is going to be tested in first line. We're going to be doing various combinations; obviously PARP inhibitors are coming into the first line. Lutetium-177 is coming into the first line in clinical trials. And I don't think we're about to slow down. We've gone to 2 drugs, we’ve gone to 3, we’re going to try various combinations. I think part of the message in this space is please think about the clinical trials, because there are a lot of great questions to be asked and answered in this space. And if we take it 1 step further, my real hope—and I alluded to this with the way I practice—we're going to be somatic testing every patient and defining the different genotypes with different treatment pathways per genotype. Just like up-front breast cancer where it's ER [estrogen receptor]-positive, HER2 [human epidermal growth factor receptor 2]-positive, triple-negative. That's what prostate cancer has to look like. To me, that's where I hope we are 5 years from now.

 And actually, institutions like where I'm at, when I proposed exactly that they embraced it like up-front, let's just throw the whole sequencing and put it in a cloud and have it to further explore it. That's the way to go and not butterfly-collect those tissues for some use at some point, which is what is the traditional. I really liked your point, Alan, about how late we are in the game. I think that I'm seeing the light being you're in this amazing institution and I'm now back into a great general hospital, and I'm seeing all these 90-year-old men who now are looking into life with still a lifespan. Back in the eighties and nineties, you'd say: 65- and 70-year-old, and you would say, well, there's no expectation. These have changed thanks to the advent of modern medicine. And this is helping us just to joke a little bit about it. Today, I had three 90-year-old patients. One of them was ready to go to his South-of-France escapade, another one on a Kenya visit to see the elephants. It is like they're living the life and they have the expectation to live well and longer. That is what has changed, literally.

Before closing out their discussion on metastatic CSPC, expert oncologists consider how best to educate patients and address the remaining unmet needs in this setting.

Alan Bryce, MD | Authors

Articles

PARP Inhibition in Metastatic CRPC: The PROfound and TRITON2 Studies

Looking Toward Future Management Strategies in Prostate Cancer

Testing for Germline/Somatic BRCA Mutations in Metastatic CRPC

VISION Trial: 177 Lu-PSMA-617 in Metastatic CRPC

Case 3: A 70-Year-Old Man With Metastatic CRPC

Metastatic CSPC: Educating Patients and Addressing Unmet Needs