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Medscape Onsite: Prostate and Bladder Cancer Updates

  • Authors: Petros Grivas, MD, PhD; Alicia K. Morgans, MD, MPH
  • CME / ABIM MOC Released: 6/23/2023
  • Valid for credit through: 6/23/2024, 11:59 PM EST
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Target Audience and Goal Statement

This activity is intended for oncologists, urologists, and radiologists.

The goal of this activity is for learners to be better able to manage bladder and prostate cancer and provide recommendations for integrating emerging clinical trial data into clinical practice.

Upon completion of this activity, participants will:

  • Have increased knowledge regarding the
    • Key clinical trial data for the treatment of prostate and bladder cancer reported at a major oncology medical meeting
    • Incorporation of emerging data from a major oncology medical meeting into the treatment paradigms for patients with prostate or bladder cancer
  • Demonstrate greater confidence in their ability to
    • Stay abreast of evolving areas of interest for therapies from a major oncology medical meeting


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  • Petros Grivas, MD, PhD

    Professor, Division of Medical Oncology
    University of Washington School of Medicine
    Clinical Director, Genitourinary Cancers Program
    UW Medicine
    Professor, Clinical Research Division
    Fred Hutchinson Cancer Center
    Seattle, Washington


    Petros Grivas, MD, PhD, has the following relevant financial relationships:
    Consultant or advisor for: 4D Pharma PLC; Aadi Bioscience; Astellas Pharma, Inc.; AstraZeneca; Boston Gene; Bristol Myers Squibb Company; CG Oncology Inc.; Dyania Health; EMD Serono, Inc.; Exelixis, Inc.; Fresenius Kabi; Genentech/ Roche; Gilead Sciences, Inc.; Guardant Health, Inc.; Infinity Pharmaceuticals; Janssen Biotech, Inc.; Lucence Health; Merck Sharp & Dohme GmbH; Mirati Therapeutics; Pfizer, Inc.; PureTech Ventures; QED Therapeutics; Regeneron Pharmaceuticals, Inc.; Seagen, Inc. Inc.; Silverback Therapeutics; UroGen
    Research funding from: Bavarian Nordic; Bristol Myers Squibb Company; Clovis Oncology; Debiopharm; EMD Serono, Inc.; G1 Therapeutics; Gilead Sciences, Inc.; GlaxoSmithKline; Merck Sharp & Dohme GmbH; Mirati Therapeutics; Pfizer, Inc.; QED Therapeutics

  • Alicia K. Morgans, MD, MPH

    Associate Professor of Medicine
    Harvard Medical School
    Genitourinary Medical Oncologist
    Medical Director of the Survivorship Program
    Dana-Farber Cancer Institute
    Boston, Massachusetts


    Alicia K. Morgans, MD, MPH, has the following relevant financial relationships:
    Consultant or advisor for: Advanced Accelerator Applications; Astellas Pharma, Inc.; AstraZeneca; Bayer; Janssen Biotech, Inc.; Exelixis, Inc.; Lantheus Medical Imaging; Myovant Sciences Ltd.; Myriad Genetics; Novartis; Pfizer, Inc.; Sanofi; Telix
    Research funding from: Astellas Pharma, Inc.; Bayer; Lantheus Medical Imaging; Myovant Sciences Ltd.; Pfizer, Inc.; Sanofi


  • John Churchwell, MS, PhD

    Medical Education Director, Medscape, LLC


    John Churchwell, MS, PhD, has the following relevant financial relationships:
    Previously employed by Medtronic.

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  • Yaisanet Oyola, MD

    Associate Director, Accreditation and Compliance, Medscape, LLC


    Yaisanet Oyola, MD, has no relevant financial relationships.

Peer Reviewer

This activity has been peer reviewed and the reviewer has no relevant financial relationships.

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Medscape Onsite: Prostate and Bladder Cancer Updates

Authors: Petros Grivas, MD, PhD; Alicia K. Morgans, MD, MPHFaculty and Disclosures

CME / ABIM MOC Released: 6/23/2023

Valid for credit through: 6/23/2024, 11:59 PM EST


Activity Transcript

Alicia K. Morgans, MD, MPH: So excited to have you here. Welcome. My name is Alicia Morgans. I am a GU Medical Oncologist and an associate Professor of Medicine at Harvard Medical School and Dana Farber Cancer Institute. So excited to be here with my good friend and colleague, Dr Petros Grivas. Petros, can you introduce yourself please?

Petros Grivas, MD, PhD: Hello everybody. I'm Petros Grivas. I'm a medical oncologist in Seattle, Washington State. I am a professor of oncology and the clinical director of the Genitourinary Cancers Program at the University of Washington Fred Hutch, and I'm very excited to do this program together with Dr Morgans.

Dr. Morgans: Wonderful. Well, I am so excited to learn from Dr Grivas. This is the prostate and bladder cancer update from ASCO, and we are really excited to be able to present that to you. I will be presenting the prostate section and then Petros will be presenting the bladder section.

Now, this first study is so important and really interesting. It's called the Panther trial, and it's really looking at apalutamide and abiraterone plus prednisone in Black versus White men with metastatic castration-resistant prostate cancer. What's so important about this study from my perspective is that it is a follow-on study after Abi Race, which was a really interesting study of 50 men who were Black and 50 men who were self-reported Caucasian or White, and they were treated with abiraterone--and this was several years ago -- and followed for their disease control outcomes as well as their side effect profiles.

In that study, Abi Race, they found that there was similar disease control outcomes, though a trend toward perhaps the Black patients actually having a more robust PSA response to abiraterone. But they did have a higher rate of hypertension in the setting of abiraterone as compared to their White counterparts. Either way, all patients seem to have great PSA responses and great PSA control within that randomized trial. So this is really a follow-on to see, 'hey, can we do even better when we combine abiraterone with apalutamide in either of these races or for any of these patients?' Because at the time of the design of this trial, we were really thinking about using androgen receptor antagonist therapy, which is apalutamide, in combination with these androgen synthesis inhibitors, abiraterone.

So what we saw here in this study, which enrolled 43 Black and 50 White patients, was that when patients were treated prospectively, we could really compare their differences in terms of progression-free survival as well as side effect profile. What we see when we look at this is that we did, as I said, enroll 43 Black patients and 50 White patients in this study, and we did, we were able to treat them with apalutamide and abiraterone combination until disease progression, unacceptable toxicity, or that two-year time point. The primary endpoint here is radiographic progression-free survival. We also have these other really important endpoints, including overall survival, PSA response, and time to progression.

So digging into this data we can see--and just to remind everyone, there is a clear disparity, which is why we are trying to do this study, in terms of rates of developing prostate cancer, which is elevated in Black American patients. And we also know that there is an increased mortality, two-times mortality in Black patients when we compare those to White patients. So it's really important for us to make sure that this is not in any way related to our inability to get effective treatment to patients, and is really something that we are addressing at every level in terms of this particular disparity.

When we look at this, what I think is so fascinating in this table, and this is to the right, is that Black men had better radiographic progression-free survival at each of these time points than their White counterparts. We can see that at the 12-month and the 24-month time point.

We also see that the time to progression was prolonged among Black patients as compared to White patients when they were treated with apalutamide and abiraterone in combination for this MCRPC population. We also see that the 12-month and 24-month overall survival prolonged for Black men as compared to White men here.

There were relatively fewer patients, numerically at least, who had no PSA response in the Black patient cohort versus the White patient cohort. And then, PSA declined to less than 0.1 was higher among Black men than it was among White men. So really, really important here that we see extremely robust responses. And I spoke to Dan George, who is the primary or lead investigator here on this study, and he really feels like this suggests that there might be an important opportunity to use combination therapy potentially in Black men as compared to White men because of these robust responses. And this was when he looked at this data in comparison to Abi Race, which was abiraterone treatment alone in the MCRPC setting.

So obviously this is a non-randomized, this is a study where we are treating everyone the same way. And so, there are important things that we need to take from that in terms of limitations, but definitely hypothesis-generating. And perhaps this combination may not be effective or more effective than a single agent alone in a White population, but perhaps in a Black population we could get a synergistic or at least additive effect and have better disease control with a tolerable side effect profile. So really, really interesting and really important.

When we look at the side effect profile here, we see the toxicity rates. This is one of those really neat tornado plots that helps us try to understand side effects in terms of all grades. And then in the center, when we look at those darker blocks, the grade three to five events that are, of course, the more severe events, we can see that Black patients had increased hyperglycemia, hypokalemia, and some extremity pain that was a little bit greater than those White patients. However, White patients had greater fatigue.

When I look at this, what really stands out is the hyperglycemia, which looks higher in the Black men, but of course these are things that I think we can monitor, manage, and really be attuned to. What I think is interesting and one of the things that I'm very interested in is ensuring that we understand side effect differences, patient to patient. And over time, I'm really hopeful that our germline genetics are going to help us as a field understand which side effects to anticipate in our patients--not just their race, of course.

But it is really interesting that there might be some differences by race, that when we get down to the germline genetic level, will be really even more personalized so that we can say for this individual, we're going to watch you much more closely for hypertension, or for that individual, we're going to watch you for peripheral neuropathy.

So more to come here obviously. But this study is another of those studies that helps us understand how we might be able to personalize our approach to dealing with side effects and addressing side effects in our patient population. So really quite interesting, And I think again, a really important study in terms of addressing disparities that are very clear and very, very much know exist in prostate cancer and that we as a field, I think need to continue to address. And this study is one step towards that.

So, of course, TALAPRO -II was a study of interest at this year's ASCO. This is a phase 3 study of patients who have metastatic castration-resistant prostate cancer. This is first-line MCRPC. And TALAPRO -II is really a registration trial for the combination of enzalutamide and talazoparib. So, patients who had MCRPC first-line were randomized to treatment with enzalutamide with or without talazoparib. And they were followed for a primary endpoint, as you can see here, of radiographic progression-free survival by that blinded internal central review. And really, I think we are so interested in this particular story because there have been multiple studies of PARP inhibitors in combination with androgen receptor signaling inhibitors to try to understand if there's a synergistic effect here that might extend beyond those patients who have homologous recombination repair (HRR)-mutated cancers.

Importantly, this was an all-comers-inclusive study, and it was a little bit different from MAGNITUDE in that way, and a little more similar to Propel in that way. Well, we can see here (and again, this is something that was presented by Neeraj Agrawal, our good friend. Petros and I very much appreciate Neeraj, our good friend and colleague who is out of the University of Utah.) And he presented this at GU ASCO. And what I would say here is that we see the radiographic progression-free survival by HRR status, so those patients who had an HRR mutation, and those patients on the right who were HRR wild type or were unknown, and it was approximately 27% of patients who were unknown in terms of their HRR status at the time of analysis. So in the HRR deficient population, we can see a very clear improvement in radiographic progression-free survival with the combination of enzalutamide plus talazoparib versus enzalutamide alone.

And what I want to remind people of in this particular setting is that enzalutamide alone in the first-line MCRPC setting is a highly active agent. And this is in a patient population of that, for the most part, was never exposed to an androgen receptor signaling inhibitor. So first-line treatment with an ARSI in MCRPC really, really effective and is the standard of care. So this magnitude of difference is really, I think, quite compelling, that we might be interested in doing something like this in our clinics in the future. I would say that the combination of olaparib and abiraterone, a similar combination, was approved by the FDA on May 31, so just as ASCO was beginning. So this strategy is of high interest. What's interesting in TALAPRO -II, going to the right side of this slide, is that HRR non-deficient patients, and again, unknown as well, so a proportion of patients pretty large that we don't know here what their status is, there was clearly a benefit in those patients, too. I think we do need to see how this data is going to mature.

And when we get to know what those HRR unknown patients are, I think we'll have a lot more insight into whether these HRR non-deficient or wild-type patients, whether they're responding or not, to the combination. That's going to be really important. So we will see where that goes. What's important here, too, is that there were not really synergistic effects in terms of adverse events. We pretty much saw that each of these drugs, of course, has adverse events. They were not synergistic, but the adverse events were as if we just took each of these drugs and put them in combination with each other, and saw cytopenia, some hypertension, some fatigue--as we would expect when we combine a PARP inhibitor with enzalutamide. So no new safety signals here, and relatively low rates of MDS and AML.

I would also say that at ASCO, we did see an update that was a gene-by-gene kind of update that showed that there were nice responses in BRCA-2, BRCA-1 and CDK-12 patients, exploratory, of course, but very, very interesting. When we think about the patient-reported outcomes, I think what's important here is that we did not see additive detriment in terms of the detriment in quality of life for patients who were getting additional therapies. So essentially, patients who had combination therapy with talazoparib and enzalutamide did not have poorer quality of life than those patients who were treated with enzalutamide alone. And that was a new update from ASCO this year, really important.

The same was true for the Propel study, which was, of course, patients in first-line MCRPC who were treated with abiraterone, with or without olaparib. Again, as I just said, this olaparib abiraterone combination prolonged radiographic progression-free survival, particularly impressive among patients with BRCA-1, BRCA-2, and an approval came out for the combination in BRCA-1 and BRCA-2 patients on 531.

So what's really important here is that those patients did not have a clinically meaningful difference in terms of health-related quality of life over the course of the trial. And that was reported out at ASCO just this year. And then to dig into MAGNITUDE, which was also a combination ARSI plus PARP study in first-line MCRPC, this included, as you can see here, all those HRR-positive patients in that center block with multiple different alterations. Patients were randomized here in that first-line MCRPC setting to abiraterone with or without niraparib. Importantly, in MAGNITUDE, there were two cohorts: one cohort with HRR-positive, and that's what we're really focusing on. The HRR-negative cohort was stopped for futility because there was no clear indication that there was benefit to the combination of niraparib and abiraterone versus abiraterone alone. In that HRR-positive cohort, which is what we're going to dig into, some of the analyses looked at the duration of exposure to abiraterone and whether that would affect their responsiveness to the addition of niraparib.

And what's so interesting here is that we see, when patients were exposed to abiraterone for less than or equal to two months, or had no prior exposure to abiraterone, they had a really robust response to the addition of niraparib to abiraterone in this HRR-positive population. When they had exposure to abiraterone for greater than two months-so up to four months--they did not seem to maintain necessarily that really robust positive influence of the addition of niraparib. Numbers are really small here. I think this is hypothesis-generating at most, and really interesting to think about from a biologic perspective. But if you're going to try to add niraparib to abiraterone in a biomarker-selected population per the MAGNITUDE protocol, I would say try to do it before two months.

And that, I think, was the investigator and the reporting doc's recommendation as well. So just to kind of finish out our prostate cancer section here, I want to just also mention the starter protocol and phase 2 salvage trial. This is another friend of ours. Petros and I love Tian Zhang, who is at UT Southwestern, and we're very, very proud of her and her recent move. This work was done when she was at Duke, and this was a study of patients with biochemical recurrence who had had a prior prostatectomy. They were getting salvage radiation. And in this study, they had ADT apalutamide radiation, and they also then had that follow-up with docetaxel, and this is for biochemical recurrent. So we're really aggressive protocol here. And you can see this schema where patients got that apalutamide, ADT apalutamide, and then docetaxel for six cycles. Really, really, as I said, aggressive for those highest-risk patients that they were trying to salvage.

And what we can see in these curves here is that PSA, progression- free survival, was improved with the addition of all of this therapy: ADT, apalutamide, and docetaxel, as well as radiation. And this was compared actually to their previous study, the STREAM study, which was not necessarily so intense. So really quite a benefit on a benefit is what I would say.

Time to testosterone recovery was for most patients at least a year, as you can see on the curve on the right. And what I think is so interesting is that there was a 40% historical progression-free survival, and here in the STREAM trial, they had a 53% progression-free survival here at that time point. So really, really important. And the primary endpoint was three-year PFS rate improved to 72%, and that really does suggest that there might be some durable disease control.

What we see in the AEs is that they were AEs as we would expect--anemia, some thrombocytopenia, neutropenia. I think that in general we expect this with chemotherapy, as well as seeing, of course, hot flashes, fatigue, alopecia. These are any grade that I just mentioned, those last few. But the hematologic are the ones that might have been of most interest because of course we're adding docetaxel in a biochemical recurrent setting. In any event, really provocative data. Can we be more aggressive? We certainly can. Patients will take it and they might even do better. And I just want to pass off to Petros.

Dr. Grivas: Thank you so much, Alicia. What a wonderful way to cover so much data in an efficient amount of time. Thank you for doing that. Really, really interesting data we saw at ASCO, and I will try to go quickly here for the updates for urothelial carcinoma. There were many interesting posters and discussions. I will focus on the theme of FGFR3 receptor, which I think is a very important targeting urothelial cancer. And targeting that receptor was the topic in three different presentations at ASCO of this year.

I will start with the adjuvant setting patients who were enrolled on the PROOF 302 adjuvant trial. Just to be remind for context, this trial that took place over the last few years in patients that had already resected urothelial carcinoma high risk with high risk of recurrence. Those patients had either upper tract urothelial cancer--renal, pelvis, or ureter--and a small proportion, about 15% of this trial, were patients with bladder cancer.

Those patients may or not have received neoadjuvant suspend-based chemotherapy, and based on the pathologic stage and the recurrence risk, they were randomized to either infigratinib, an FGFR inhibitor, versus placebo as a pure adjuvant therapy in order to prolong disease-free survival. It was a primary endpoint. Patients, as you see, to be enrolled had to have an activating alteration, either a mutation or fusion or rearrangement on FGFR3. As I mentioned before, this receptor is relevant in driving carcinogenesis in urothelial carcinoma and seems to be a relevant therapeutic target. That trial closed early. Only 39 patients were enrolled, and it was much shorter than the end goal of 218. Patients was accrual goal.

We're going to have some updates from the clinical data in the future meeting by Dr. Pal, who is the PI of the study, along with Dr. Daneshmand. However, the purpose of our poster at ASCO this year was to evaluate the frequency of FGFR3 alterations, how common this alteration type is in urothelial cancer in the context of the screening that took place for this clinical trial, because there is some variability in the estimate of the frequency of these alterations across different prior studies.

Just to hone down on the results, overall we had about 882 unique patients were screened. From those, 617 had a genomic sequencing report that we can evaluate. And overall we saw that only 19% of all screened patients had the activating alteration in FGFR3. And if you break it down, it's about 30% of patients with upper tract urothelial cancer, and only 13% of patients with bladder cancer, so the frequency of FGFR3 alterations seems to be a little bit lower than expected. And obviously this also results in a little bit lower than fast as expected accrual, slower than expected, I would say. However, the trial was stopped because of infigratinib. Development was halted by the sponsor.

I think it's important to still follow up and report any clinical data from the limited dataset. And, as I mentioned, the implication of this study is just to get the sense of the frequency of these alterations a little bit lower than expected, still is very, very important, and we'll see that in the next few slides. It's very important that we need to screen all patients with metastatic urothelial cancer with genomic sequencing, and do genomic sequencing analysis because we can identify an FGFR2 or 3 genomic alteration, mutation, or fusion that can be relevant for erdafitinib, that is actually approved in metastatic disease. I'll show you the data in a second supporting use of erdafitinib. This trial that I show you here is not practice-changing, but relevant in the field. And this is the breakdown, the mutation types between upper tract and lower tract, as you see. And we also look at other FGFR genes, FGFR1, 2, 3 and 4, and we try to break down the frequency of those alterations based on the location of the tumor, uppers versus lower tract, and by age of the patient. And there was no significant association between the frequency of FGFR3 alterations and the age of the patients.

Now, before we talk about the third trial, I want to briefly mention that as we now move from adjuvant setting to metastatic disease, and as I mentioned the adjuvant setting, there is no use of FGFR inhibition. This was just a clinical trial. In metastatic disease, we have data with erdafitinib; however, the data is in patients with prior platinum-based chemotherapy.

And before I talk about the third trial, I want to mention that there was a separate trial called NORSE, N-O-R-S-E. That trial was in the first-line setting, cisplatin-eligible patients who did not receive any prior systemic therapy for advanced urothelial cancer. Those patients were randomized to either erdafitinib by itself or erdafitinib plus cetrelimab, a checkpoint inhibitor inhibiting, I think, a PD-L1 pathway. And that's important because we want to evaluate the potential combination of a target therapy with immunotherapy.

In that first line trial, we saw the data for Dr. Siefker-Radtke. And we saw that the combination of the PD-1 inhibitor and cetrelimab plus erdafitinib result in a response rate of 55%, while erdafitinib by itself was about 44%. This is, again, first-line cisplatin-eligible patients. There was actually a signal that there was a doubling of the median progression-free survival favoring the combination of cetrelimab and erdafitinib in the frontline setting, and also promising signal for overall survival.

However, the data from the NORSE trial are not practice-changing. I think they're interesting and favor further evaluation of cetrelimab and erdafitinib. However, I have not seen any future trials with that combination. I think people are waiting to see what will happen in the frontline setting with the other combination of pembrolizumab plus enfortumab vedotin, and the results of that trial are pending from the randomized Phase 3 EV-302. Until that trial reports out, I do not see any activity in developing further the combination of cetrelimab and erdafitinib, but it was definitely an interesting signal there with a combination. And also, erdafitinib as a single agent had a response rate of 44%, which is comparable with the response rate we see in later lines of therapy. So again, such interesting data from the NORSE trial. Even if it's not practice-changing, something that you can read at your leisure time.

Now, since we just talked about erdafitinib in the frontline setting, now let's talk about the third trial. You can see the schema in this slide. This is a phase III trial called THOR presented by Dr. Yohann Loriot at ASCO. What you see here is a phase 3 trial in patients with prior checkpoint inhibition. These patients may have received platinum-based chemotherapy. However, the eligibility criteria was specifically for prior immunotherapy. You see that these patients have up to two prior lines of therapy, and they had to have an activating alteration on FGFR2 or FGFR3, specifically an activating mutation or fusion. ECOG PS was 0, 1, or 2. Patients were randomized to erdafitinib 8 milligrams daily as a starting dose, versus salvage chemotherapy, docetaxel in the U.S., or vinflunine in Europe. Primary endpoint was overall survival.

As you see, this was a positive trial. This trial saw this overall survival benefit with erdafitinib, the FGFR inhibitor, in these selected patients versus salvage chemotherapy, hazard ratio 0.64. There was also a significant improvement in progression-free survival. You see median PFS 5.6 versus 2.7, a doubling of the median PFS, hazard ratio 0.58. The response rate, 46% versus 12%. So definitely a clear, I would say, practice-informing trial here. For context, erdafitinib has already accelerated approval by the FDA in patients with prior platinum-based chemotherapy. I think this data I'm just showing you, it's very likely that we're going to, it is going to result in a regular approval, full approval of erdafitinib, but in selected patients. Patients with FGFR2 or 3 activating mutation or fusion, not amplification.

That actually corroborates my previous comment. We need to do genomic sequencing in all patients at the time of diagnosis of metastatic disease to have the data and results ready, because these patients may need erdafitinib at some point after prior therapy and we'll have to see what the label of the FDA will be.

Toxicity is important to note, and here are the tables looking at hyperphosphatemia, diarrhea, stomatitis, dry mouth, hand-foot syndrome and nail changes, onycholysis, and also some lower rates of bone marrow suppression. You see the chemotherapy side effects are mostly bone marrow suppression. We do not see more bone marrow suppression with erdafitinib. However, we see, as I mentioned, these skin changes, nail changes, dry mouth, mouth sores sometimes, diarrhea, and hyperphosphatemia. This drug requires close follow-up and ophthalmology evaluation at baseline and during therapy, laboratory monitoring, and potential dose titration based on the labs and toxicity evaluation.

I think we already covered the very interesting data from prostate. I will finish my talk just talking about antibody-drug conjugates. There are two of them that are now approved from metastatic urothelial cancer, enfortumab vedotin against Nectin-4, and such as sacituzumab govitecan, SG, against TROP-2. Those antibody-drug conjugates have approval for previously treated patients. However, enfortumab vedotin is also approved by the FDA, together with pembrolizumab combination, in cisplatin-ineligible patients in the frontline setting.

Now, we have sacituzumab govitecan, SG, accelerate approval for patients after chemotherapy and after checkpoint inhibitor like third and fourth and beyond lines of therapy, so the question here is, can we potentially bring sacituzumab govitecan earlier? And the cohort 4 is evaluating the trial in progress, evaluating the combination of sacituzumab govitecan antibody-drug conjugate against TROP-2 plus cisplatin. Also, there is a maintenance part of the treatment here evaluating sacituzumab plus check inhibition.

So, stay tuned, and this is a more detailed schema of the study. If you have this trial open, keep it in mind and we'll try hard to enroll patients in cohort 4, 5, and 6 of this TROPHY U-01 trial. We're also waiting for the phase 3 tropic TROPiCS-04 trial and will result in a future meeting. Alicia, I will stop here.

Dr. Morgans: Yeah, wonderful. I would just say that lots and lots of developments here. In terms of promising biomarkers, I would say that keep an eye on the AI, artificial intelligence, space. That is something that is definitely just like powering through prostate, and through many conversations that I had at ASCO, I am hoping to push that into urothelial. And I am sure that Petros would be very excited for that, too.

I just want to say thank you so much, Dr. Grivas, for participating in this with me today, and certainly all of the folks who are online.

Dr. Grivas: Thank you, Dr. Morgans. It's great to see you.

This transcript has not been copyedited.

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