Phillip J. Koo, MD

At this point, we can ask some closing questions to each of our panelists. We’ll start with Phil. Could you summarize your thoughts on the use of lutetium-PSMA-617 in the metastatic castration-resistant prostate cancer setting? What do you think about patient selection and that treatment in general, when we think about this patient population?

 It was such an exciting day when you heard the announcement. Obviously, there was so much excitement around this, especially after the data were presented at ASCO [American Society of Clinical Oncology Annual Meeting] in 2021. Treatment and patient selection are still going to be determined and will continue to evolve. As our skill and ability to home in on certain questions improves, we’ll be able to answer that better. In the meantime, we need to be prepared and find ways to access this drug for our patients. Whether you’re in a purely private practice, an integrated health system, or an academic health system, there’s a path forward to make sure you can get your patients access to this through either nuclear medicine or radiation oncology. On the operational side, it’s easy. It requires a little work up front, but once you have it down, it can run like a well-oiled machine. In the end, you need champions. You need champions on the ordering side and on the administration side. I have no doubt that with those components, anyone can get this up and running.

That’s a very encouraging message, Dr Koo. Let’s hear from you, Tanya. What do you think?

 We still have some to learn about patient selection. We need to do the work because when we have multiple options, we want to have our patients access as many options as possible. But we also want to pick what’s going to be most effective earlier on and spare the health system the cost of choosing a treatment that’s going to be ineffective and spare the patient the potential adverse effects if it’s not going to work for them. With the 2 patient selection criteria from VISION and TheraP and from other work that’s being presented and ongoing, hopefully we’ll start to get some ability to individualize and say if this is a patient who’s better off with radium or with chemotherapy or this 1 is going to have a tremendous benefit from the lutetium-177. That’s what I’m looking for in further studies. Also, combinations will be really exciting. There’s interest in combining radiopharmaceuticals with immunotherapy. Hopefully, we can improve on this exciting new treatment option even further.

Ulka, what are your thoughts on lutetium-PSMA-617?

 Having treated patients on the VISION trial, I’ve been very excited about the efficacy of this agent and the tremendously tolerable toxicity profile. That makes me motivated to consider this therapy option up front in metastatic castration-resistant disease. Especially if we use triplet therapy or docetaxel increasingly in the frontline metastatic hormone-sensitive setting, it becomes even more important to immediately test patients with PSMA [prostate-specific membrane antigen] PET [positron emission tomography]scans when they turn castration-resistant and consider this therapy.

There are other advances you have to keep in mind. There are multiple exciting agents in the field that should be looked at, and clinical trials should be at the front of our minds when we consider treatment options for our patients. Then use second-line chemotherapy and genomic profiling, because if you find a targeted therapy that fits that patient’s genomic germline genetic profile, that’s another thing to consider up front in the metastatic castration-resistant setting.

Let’s go back to each of you. Think about what type of therapy you’re most looking forward to learning more about in this setting. Ulka, you’re leading a phase 1 program, so I’m sure you’ve gotten a lot of exciting molecules. What are you most excited about moving forward?

 Immunotherapy advances and cellular therapies are very exciting in the prostate cancer field, mainly because they hold the promise of long-term remissions with the treatment. On the flip side, there are AR [androgen receptor] degraders. We haven’t seen the last of tackling AR access in advanced prostate cancer, so that branch of treatment is also looking very promising.

 You’re probably aware that I’m a big fan of immunotherapy and, in particular, cellular therapeutics. Having a live treatment that can adapt as the immune system can as the cancer evolves is an advantage, and we believe it will get us to more durable remissions that patients are seeking. Of course, there are toxicities there that need to be managed and worked out, but there’s such a versatile platform. When we think about how some patients don’t express PSMA and wouldn’t have been included in the VISION trial, those patients are a real unmet need. Immunotherapy potentially could fill that gap by studying some novel targets.

I had a feeling you might say that. Phil, last but not least, and you’re welcome to focus on those options or the exciting new radiopharmaceuticals that are also coming down the line.

 It will come as no surprise that I’m a big fan of radiopharmaceuticals. It’s clearly been shown that radiopharmaceuticals can be safe and effective with the approval of radium-223 and now lutetium-177-PSMA. Obviously, there’s a lot of work being done with other radiopharmaceuticals, particularly alpha particles such as thorium or actinium. It will be very interesting to see what happens with that. Tanya talked about this earlier, but the combinations are where there’s a lot of potential as well. It will be exciting to see a lot of the work from you guys, who are so effective in this space, finding different ways to put things together and get that synergistic effect.

Thank you all for your thoughtful case presentations and 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 practical knowledge that can help you in your clinical practice.

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Oncologists share some final thoughts on lutetium-PSMA-617 and novel agents to look out for in prostate cancer treatment.

Lutetium-PSMA-617 and Novel Agents in Prostate Cancer

Let’s move on to our final patient case. This is another take on a case we talked about earlier but with a little twist. I’m going to review this case, and then Ulka will walk us through some data. Just to remind everyone, this is a 67-year-old gentleman who came into his primary care doctor with reduced urinary flow and some hematuria. He had pain on his left hip, and he had a past medical history that was relatively benign, just some hypertension that was quite well controlled. His PSA [prostate-specific antigen] was 7.4 ng/mL, and he had a prostate biopsy that showed Gleason score 8 and 4+4 prostate cancer and a bone scan that showed he had metastatic lesions in the left pelvis and the left lobe of the lung. He had an ECOG performance status of 0, with quite functional, well-controlled comorbidities. He started treatment with abiraterone ADT [

 and, of course, prednisone when he was taking the abiraterone. PSA decreased to 0.2 ng/mL, so he had a nice response, but 13 months later, he started to develop a rising PSA, suggestive of a progression. PSA peaked at 5.7 ng/mL when he underwent PET [positron emission tomography]–CT, which showed enhancing lesions in the lung and the ribs. At that time, he initiated treatment with docetaxel but stopped his treatment with docetaxel after 2 cycles because of intolerance, and this was at that time grade 2 neuropathy. 

Phil, I’d love to hear your thoughts. This is a patient who has metastatic disease. He has a progression of disease and was able to get a PET-CT. Perhaps that was on a clinical trial, but maybe it was for some clinical purpose. What are your thoughts? Does that change management as we talked about in terms of always having a purpose for a test as we’re ordering it?

 This is always the question that comes up over and over: why you did it, and all of a sudden you see more. What do you do then? We’d all agree that we want to follow the evidence as closely as possible. Unfortunately, or fortunately, the evidence we have is based a lot on conventional imaging. When you’re entering outside that space and making decisions based on new information you have on a PSMA PET, it might be the right decision, but you’re in a data-free zone. This is where a lot of times it’s a matter of building those teams and having those multidisciplinary discussions. That may not always give the right answer, but it’s backed by multiple perspectives that can hopefully lead to the best outcome for the patient.

As I think about patients in my clinic, and I’m trying to get prior authorizations to get some of these imaging modalities, I try to hold on to each of these until there’s a clinical reason to get this particular test, because I may only be able to get 1 or 2 in the course of this patient’s illness. Maybe I’ll be able to get more, but I don’t bank on that. Just make sure you’re judicious with the ordering of this particular modality, especially because it’s new. Hopefully in the future, we’ll be using PSMA PET scans to very easily follow disease progression and change over time, but it’s still in flux at this point. Ulka, from your perspective, how common is it for a patient to not really tolerate chemotherapy with docetaxel? Is that something you see regularly?

 No, but there are some odd patients who do have significant toxicity and intolerance, and a lot of it occasionally may be related to neuropathy, but frequently it’s related to systemic or cytopenias that lead to infection, hospitalization, etc.

Agreed. Thank you. If you weren’t able to use docetaxel for this patient because of intolerance and you’d already used abiraterone, Tanya, what are you thinking about in terms of treatment for this individual?

 One would like to have the option of cabazitaxel given the data showing the efficacy in the CARD study, as well as the FIRSTANA trial, which we’ll look at in a moment. It can be challenging because most of the time it’s restricted to the postdocetaxel setting. When I have a patient with neuropathy or poorly controlled diabetes, and I’m thinking that cabazitaxel would be a better fit for the patient, it can be hard to get that drug for them without going through the docetaxel. That’s a challenge.

That’s absolutely true. In this case, the patient has had a couple of cycles of docetaxel. To your point, it’s important for us to understand differences that might exist between docetaxel and cabazitaxel in the adverse effect profile. The first trial does provide some insight for us. Ulka, can you run us through FIRSTANA?

 FIRSTANA was a study that randomized patients to receive a docetaxel standard dosage of 75 mg/m²every 3 weeks along with prednisone 10 mg per day. The patients were randomized to 2 other arms of cabazitaxel, either cabazitaxel 20 mg/m²starting dose every 3 weeks or 25 mg/m². At the time this was standard dose evaluated in the TROPIC trial, which led to the FDA approval of cabazitaxel.

The patient population was all patients with metastatic CRPC [castration-resistant prostate cancer], performance status 0 to 2 with no prior chemotherapy, no brain metastases, no immediate spinal cord compression, etc. Patients were treated until progressive disease or unacceptable toxicity. One thousand one hundred sixty-eight patients were randomized. If you look at the efficacy results, this study showed us that survival was fairly similar across each arm. The median survival, if you look at cabazitaxel 20 mg/m², is 24.5 months—25.2 months with the 25-mg cabazitaxel dose and 24.3 months with docetaxel 75 mg/m². You wouldn’t be compromising survival outcomes if you switch from docetaxel to cabazitaxel because of intolerable toxicity or certain reasons. Otherwise, progression-free survival was pretty similar, 4.4 months median, 5.1 months with cabazitaxel 25 mg, and 5.3 months with docetaxel.

The other thing that came out of this study is that cabazitaxel 20 mg/m² is a very standard, easier dose to use with the comparable efficacy and an improved toxicity profile. Looking at the response rates, PSA response rates also were fairly similar with no major differences between the 3 arms and similarly for pain progression-free survival. Also median was 8 months with cabazitaxel, 27.3 months with cabazitaxel 25 mg, and 10.1 months with docetaxel. In terms of other health-related quality-of-life markers, there was a pretty similar efficacy noted across the 3 arms and patients with pain progression, the median time to pain, as well as a pain response. There was no difference among the 3 arms. Based on this, switching from docetaxel to cabazitaxel, especially for patients who were intolerant of docetaxel, has been incorporated into the NCCN [National Comprehensive Cancer Network] Guidelines.

That makes sense if there are differences in tolerability, particularly when we use the similarly effective cabazitaxel 20 mg/m² dose.

Alicia Morgans, MD, MPH, presents the case of a 67-year-old man with metastatic castration-resistant prostate cancer.

Case 3: Metastatic Castrate-Resistant Prostate Cancer

Ulka, from your perspective, when you’re trying to sequence these agents, given the data as Tanya just pointed out, there are compelling data in this space for cabazitaxel and this interesting PFS [profession-free survival] benefit to treatment with lutetium compared with cabazitaxel. What do you think about sequencing these agents?

 A few of the points that came up from CARD are very important. The most important thing is not to use 2 hormonal agents back-to-back and interspersed chemotherapy or some other mechanism of action in between. Clearly, cabazitaxel showed an improvement compared with second hormonal therapy.

With the TheraP trial, we learned how to better select patients who would benefit the most from PSMA-lutetium in my opinion, as well as based on the FDG [fluorodeoxyglucose] findings. If there are only FDG findings and no PSMA [prostate-specific membrane antigen] uptake, that’s also critical information because it tells you that most likely, PSMA-lutetium may not be as effective. It may be time to go to chemotherapy or carboplatin-based if there are neuroendocrine features in this tumor, etc.

Both studies are very important, even though they’re smaller phase 2 studies—[they are] giving us much more insight into the scheduling as well as the better clinical application of these treatments. Then there’s the issue of genomic testing and germline testing to look at patients with DNA-repair mutations, where we have a fairly effective therapy option available with the PARP inhibitors.

Thank you for bringing in other options. We don’t have time to review every trial, but we shouldn’t forget that there are other agents, including PARP inhibitors and pembrolizumab, for patients who are MSI [miscrosatellite instability] high. These are also options for many of our patients, and we should absolutely keep them in the front of our minds as we’re trying to help patients choose.

Phil, I’d love to hear your perspective. We’ve talked about patient selection. Ulka just mentioned it again, but it’s important for things like lutetium-PSMA-617. It was done differently in the VISION trial vs TheraP. What are your thoughts on patient selection? Yes, we can give kudos to the team from Australia for putting together that nicely sensitive and specific assessment that led us to this population for TheraP. But is that something that’s going to be pragmatic when we’re trying to apply it in the clinic?

 That’s a great point. I’m a little less bullish, especially in the United States, with regard to all this additional imaging, though I’m an imager. You guys have all dealt with preoperatives and trying to get 1 PET [positron emission tomography]–CT approved from 1 patient. Imagine trying to get 2 in a 1-week period and then trying to access a PET-CT and get those 2 read in a timely fashion so you’re not delaying care. It’s challenging. No. 2, 13% of patients in VISION were only PSMA, so it’s a matter of perspective. Is 13 a lot? Is 13 a little? Who knows? There’s a trial, I believe through Alliance [Foundation], that doesn’t include PSMA imaging before you enroll in the trial. I don’t know the specific details, but that opens up this idea that maybe there are patients that will still benefit from this radiopharmaceutical that targets disease due to cross effect, cross talk, or whatnot without having all this imaging. Even with all this imaging, it’s still too early to be close to being able to say what the appropriate cutoffs are and how we define discordance. This shines a little light into this area, but it’s way too soon to come to any conclusions.

Thank you so much. That will conclude our patient case.

Experts share their thoughts on sequencing hormonal agents and patient selection for clinical trials.

Therapy Sequencing and Patient Selection in Prostate Cancer Treatment

Another study that informs this clinical space is the TheraP trial. Ulka, I’m going to ask you to walk us through this. As you’re talking through this, we’ll also ask Phil to comment on how patients were selected because that was a little different from VISION.

 TheraP was a randomized phase 2 trial of 177-lutetium-PSMA [prostate-specific membrane antigen]–617 as compared with cabazitaxel chemotherapy agent, taxane based, in progressive metastatic CRPC [castrate-resistant prostate cancer]. [To be eligible] patients had to have prior docetaxel and metastatic CRPC, and they had to be eligible for cabazitaxel. [They had to have] reasonable performance status, adequate marrow function, liver function, etc. I’ll ask Phil to comment on the PSMA testing done along with FDG [fluorodeoxyglucose] PET [positron emission tomography] to determine eligibility for this study.

 The Australian team deserves a lot of kudos for pushing the envelope and trying to investigate ways to do things better. No. 1, they introduced 2 radiotracers into this idea of patient selection, so PSMA PET determined whether it’s positive or negative, but also including FDG PET-CT into the work-up. We know prostate cancer is heterogeneous, and the data clearly showed that prostate cancer is very heterogeneous. In those patients who are PSMA positive, there’s discordance between PSMA expression and FDG utilization that maybe these patients wouldn’t benefit from PSMA. This speaks volumes about the heterogeneity and also speaks volumes about how aggressive disease can become in certain cell lines and how it will be different in the body. It also introduced the idea of quantitation. Rather than using just a binary visual approach to a lesion, it said, “Why don’t we use the tools that we have, and if the amount of SUV [standardized uptake value] matches above a certain threshold, then we’ll categorize that as positive. If it’s below a certain threshold, we’ll categorize it as negative.” It took us a step forward, but with this comes a lot of questions. How do we set the thresholds? How do we determine discordance? These are very interesting questions, and we’ll learn more over the years to come.

 Excellent points. Also, what this staging mechanism did is select much more stringently patients who are likely to have PSMA expression. Then they were randomized to get the lutetium-PSMA-617 as compared with cabazitaxel at a dose of 20mg /m2—the standard starting dose—and they were stratified. Patients were stratified with disease burden of 20 sites or more or less prior enzalutamide or abiraterone and then study site or location.

Here are the results of the TheraP trial showing that patients with the PSMA-lutetium therapy did significantly better as compared with cabazitaxel therapy. It’s a smaller study, but if you look at the PSA [prostate-specific antigen] response plot, clearly PSMA-lutetium had a much higher chance of PSA response: 66% of patients, compared with 37% with the cabazitaxel, had a PSA reduction of 50% or more.

The second graph shows the radiographic progression-free survival, and it also appears to be improved with the PSMA-lutetium. The hazard ratio is 0.63, and 

 value is statistically significant favoring the PSMA-lutetium therapy. In terms of adverse effects, not too many surprises there. Fatigue, pain, dry mouth, some diarrhea, and nausea were seen with PSMA-lutetium. Cabazitaxel showed its cytotoxicity with cytopenia as well as diarrhea incidents that were seen with the cabazitaxel. Neuropathy was fairly small: 10% with lutetium-PSMA and 26% with cabazitaxel. Otherwise, the dry mouth and renal dysfunction were seen with lutetium-PSMA.

Thank you for walking us through that. Tanya, thinking about both these studies, the CARD and TheraP trials, what’s your reaction? It’s a complex space. What are your thoughts in terms of treatment?

When these data were presented, they knocked my socks off. Coming on the heels of CARD, which already elevated how we viewed cabazitaxel as being a really effective agent, you have this trial—somewhat smaller but well designed and clearly showing that lutetium-177-PSMA is even more effective than cabazitaxel, which is already effective. There’s some criticism of the VISION trial in terms of how active the control arm was. Therapy answers that question, that it’s truly a very active treatment. We’re so glad that we can start offering it to our patients relatively soon now that it’s FDA approved.

A review of recent data from the TheraP trial.

mCRPC: The TheraP Trial

Why don't we dive into another study that helps us understand what we can do after progression on 2 lines of therapy? This is the CARD trial. Tanya, can you walk us through that, please?

: The CARD study looked at cabazitaxel vs a second AR [androgen receptor]-targeted drug in men with metastatic castrate-resistant prostate cancer which had progressed on an AR-targeted agent, and they could have had docetaxel or not. They were randomized to receive either cabazitaxel at the 25 mg per meter-squared [25 mg/m²] dose or the alternative AR agent, either ABI [abiraterone] if they had been on enzalutamide previously, or enzalutamide if they had been on ABI previously. The primary end point was radiographic progression-free survival, with key secondary end points, including overall survival as well as objective responses, pain response, skeletal events, and quality of life. This was a unique patient population in my view, because if you look at how they were progressing at the time of study entry, the bulk of the patients that get put on are progressing based on prostate-specific antigen [PSA] alone, and here about two-thirds were progressing in terms of pain. I would just put a caveat that this is not every prostate cancer patient. In terms of visceral metastases, it was below 20%, so in that way, it is quite representative. There was a good balance from the randomization in terms of how long the previous treatment had been effective. The radiographic progression-free survival was significantly better with cabazitaxel compared with the second AR-targeted agent. It was 8 months compared with 3.7 months, so it was a big difference—statistically significant—and a hazard ratio of 0.54. Looking at the subgroups, some subgroups were a little bit small—like the visceral subgroup—but generally speaking, the forest plot shows that cabazitaxel was really better for the various types of patients who were included. In terms of progression-free survival for cabazitaxel, it was 4.4 months median, and for the ABI or ENZA [enzalutamide] second AR-agent, it was 2.7 months. Again, very statistically significant. Overall survival was 13.6 months compared with 11 months, with a hazard ratio of 0.64. Although this was not as large a trial as VISION, I think this really did change practice, and hopefully, raised awareness that a second AR-targeted agent may not be the most effective strategy. This doesn't mean it's never a choice, but for someone who's a cabazitaxel candidate, this is really more effective. Now, one thing that people worry about when they're looking at cabazitaxel is tolerability. I think this trial was reassuring. There was a significant population of patients who were over 70 years old included in the trial, and yet the serious adverse events were really similar between the 2 arms. It was about 39%, whether you were on cabazitaxel or the second AR-targeted agent. Maybe we have to rethink how we view tolerability. Again, this was with the 25 mg/m² dosing. Of course, for patients who had up-front docetaxel and then maybe were just on castration maintenance, and then maybe got an AR targeted agent, you could reach for docetaxel as a rechallenge but I think the CARD data just really provide compelling evidence of the efficacy of this agent in this particular population.

Thank you for walking us through that and for thinking through the tolerability, particularly in our older patients, even at this 25 mg/m² dose. I think that's really, really important.

Tanya Dorff, MD, explains safety and efficacy data from the CARD trial.

Reviewing Data from the CARD Trial

Let's move on to case 2. Case 2 is another patient. This time we'll have you introduce that patient. Would you mind taking it away, Tanya?

: This patient is a 72-year-old gentleman who presented with an initial prostate-specific antigen [PSA] of 47.5, with potential symptoms of nocturia and low back pain. A bone scan was done due to the high PSA level, [and the scan detected] 3 bone metastases in the spine and 2 bone metastases in the pelvis. Treatment was started with androgen deprivation therapy as well as up-front docetaxel. He had a good response. His PSA dropped down to 0.3. However, 22 months later, the PSA began to rise again, and there was a progression of his disease noted, so he's now metastatic castrate-resistant and enzalutamide is initiated.

Now, Ulka, from your perspective, what do you think about the way the treatments have progressed to this point?

: I think the treatment done so far is perfectly appropriate. Given the PEACE1 trial data, as well as ARASENS, I think something to consider—especially in patients with high-volume disease and patients with up-front de novo metastatic disease—is to have a discussion about triplet therapy, where you do an androgen receptor inhibitor in addition to docetaxel and ADT [androgen deprivation therapy]. That is definitely a new finding in the field that can improve overall survival. I think so far the treatment plan is perfectly appropriate and it is now time to look at other treatment options.

Thank you for bringing up the triplet. I think that's really such a new aspect of our treatment paradigm, but for patients who are fit for chemotherapy—and we're proceeding with that—it seems like it's really such a low burden—as long as there's not an issue with financials and copays—to just do the simultaneous treatment with the AR [androgen receptor]-targeted agent and then that maintenance phase.

From your perspective, Tanya, particularly if you were to do a treatment that was a triplet, but even in this sort of sequenced approach that has been done for this patient, what kind of patterns of progression do you commonly see for patients who develop a metastatic CRPC [castration-resistant prostate cancer]?

: I think it's very variable. Patients often ask me that question, and I sort of walk them through that. One common scenario is just a slowly rising PSA that can rise for many months or even years before there is a radiographic change or, certainly, before symptoms. In those kinds of patients, one thing to think about is sipuleucel-T. Although it was studied a long time ago—before we had all this up-front intensification—so of course this kind of a patient wouldn't have been represented, but I think there's still enough real-world evidence of ongoing utility in a patient who is asymptomatic or minimally symptomatic and has a sort of slower progression. Of course, we know that using it earlier is better than using it later. Sipuleucel-T is one thing I think about in those slow progressors. Another approach could be if there's just 1 area that's becoming more active, especially if it's symptomatic, giving radiation, and seeing how that impacts the PSA. I use that primarily in patients on 1 of the AR-targeted agents as a way of extending the duration, because you sometimes find that the resistant clones are really located in 1 or 2 areas and not the whole body and there's ongoing good disease control. Of course, in the registrational trials for those agents, we did not react to PSA alone. Treatment was only changed when there was radiographic progression. Occasionally, there is more rampant progression, and in those cases, you have to move more quickly. You have to think about a biopsy to see if there's neuroendocrine differentiation, but I think the majority is going to be a little bit more on that slow side.

I agree and I hope that it's a large majority, though. We don't always get what we wish for but thank you for walking us through that. Please continue through this patient’s case.

: In this case, it was about 10 months later that the patient started to have some new shoulder pain, and the PSA was rising.

Given that, Ulka, what testing and imaging would you order at this point?

: This is a patient who's had docetaxel as well as an androgen receptor inhibitor. I think it is time to consider lutetium-PSMA [prostate-specific membrane antigen], and probably, given the PSA progression, I would look at doing a PSMA-PET [positron emission tomography] scan in this patient.

: This is where I think it's so important to talk about what Ulka was talking about earlier about communication because I think nuclear medicine can really be a strong partner and friend as these cases come up. I think in patients who are nearly castration-resistant, oftentimes conventional imaging is your friend and it is the standard of care. But clearly, if your referring physician is thinking about PSMA and they know that lutetium-177-PSMA is something they're thinking about, you could use it as a tool to diagnose disease and see where they are. Then you'll also have it on board in case you do want to proceed with lutetium-177-PSMA. I think there are multiple benefits you can get with this test but it's really about making sure you're on board with all the team members and doing it efficiently as well.

Thank you for that because I think that we generally tend to restage using conventional imaging, but you absolutely need a PSMA PET scan if your goal is to use lutetium. If you're thinking about the options for this patient, Ulka, lutetium and beyond, what are you thinking about? What testing do you need to do? I think we heard some mention of biopsy as well. What are you thinking about?

: I think it is a time also to look at the genomic characteristics of the tumor so both next-generation sequencing, if possible, or even liquid biopsy testing would be critical to do at this point. In addition, you need germline testing also, because both of these could define some therapeutic options that you are not aware of at this time for the patient. It would be good to know because then you can sequence the patient accordingly and discuss each of these treatment options with the patient and make a sort of shared decision about which way to proceed first.

Dr Tanya Dorff presents the case of a 72-year-old man with metastatic hormone-sensitive prostate cancer.

Phillip J. Koo, MD | Authors

Articles

Lutetium-PSMA-617 and Novel Agents in Prostate Cancer

Case 3: Metastatic Castrate-Resistant Prostate Cancer

Therapy Sequencing and Patient Selection in Prostate Cancer Treatment

mCRPC: The TheraP Trial

Reviewing Data from the CARD Trial

Case 2: Metastatic Hormone-Sensitive Prostate Cancer