BackTable Urology
Ep. 210 Personalizing ADT Across the Prostate Cancer Spectrum with Dr. Rana McKay
Tue, 21 Jan 2025
What is the role of androgen deprivation therapy (ADT) in prostate cancer treatment? In this episode of the BackTable Urology Podcast, Dr. Rana McKay, a medical oncologist from UC San Diego, joins host Dr. Aditya Bagrodia to discuss the administration of ADT and other management strategies for prostate cancer. --- This podcast is supported by: Photocure https://www.photocure.com/ --- SYNPOSIS The doctors offer a historical perspective into the evolution of ADT over time and discuss the variety of different ADT treatment options available. They compare management strategies for localized and metastatic prostate cancer and discuss how to align therapy with patient goals, focusing on the side effects. The conversation also explores the impact of prostate-specific membrane antigen (PSMA) PET imaging on management and the future directions of hormonal therapies in urologic oncology. --- TIMESTAMPS 00:00 - Introduction 05:25 - ADT Options 10:36 - Choosing an Agent and Managing Side Effects 26:42 - Continuous Versus Intermittent Therapy 30:30 - Closing Remarks --- RESOURCES Photocure https://www.photocure.com/
We know that TURBT procedure is critical in the care of patients with non-muscle invasive bladder cancer. With data that shows that CIS was missed by TURBT in more than 45% of radical cystectomy cases and 86% of residual tumors have been found at the original resection site, it's clear that enhanced visualization could be a significant benefit during TURBT's.
Further, with only 23% of patients coming back for re-resection, it's all the more important to do a complete TURBT right from the start.
everybody does it different, every doc doesn't different, there isn't sort of like a system. So I think like kind of being a little bit more systematic about, you know, these are the options that you have.
And these are the side effects, you know, at our institution, a DTF kind of we piloted together kind of like an ADT order set, you know, like when you're going to start ADT, these are the things to think of, these are the labs to think of, this is the imaging, here's the teaching. And I think that that really kind of takes out a lot of bias from the process.
So I think standardization is important and also kind of seeing what the goals are for the patient and aligning with them is really key.
This is Aditya Bagrodia as your host this week. And I'm very excited to introduce our guest today, Raina McKay, who's one of my partners here at UC San Diego. Welcome back to the show, Raina. How are you doing today?
I'm doing great. Thanks for having me.
Oh, it's a pleasure, Raina. I literally think every time I interact with you, I get inspired and I get smarter. And, you know, what you're able to do for our team and for the GU community is amazing. And I've got to take this opportunity to throw a little plug in. Raina is on the ballot for the nominating committee for ASCO elections this year.
There's literally I don't think anybody who's out there currently that's contributed so much to our field and oncology in general. So if you're a member, get out there and vote for Raina. She's amazing. You don't need me to tell you that. All right, Raina. So this is actually an episode that is kind of backed by request and popular demand.
You know, as prostate cancer, both in the localized and advanced contexts, gets more and more complicated, ADT, androgen deprivation therapy, still just holds such a central role. And maybe I'll ask you to just take a little walk down memory lane over the course of your career, how you've thought about ADT, how it maybe it's come more within your wheelhouse than other places.
Can you share a little bit on that?
Yeah, I mean, absolutely. I think, you know, androgen deprivation therapy has been the backbone of systemic treatment for patients with prostate cancer for decades, has been and will likely continue to be just given the addiction of prostate cancer to the androgen receptor and androgen receptor signaling pathway.
And I think there's been definitely an evolution over the last several decades in how we facilitate a medical decline in testosterone levels with a therapeutic intent to treat prostate cancer. Historically, before we had GnRH analogs, we just used good old bilateral orchiectomy to treat patients.
And, you know, there's still a role for that even in the modern era, if you will, if we think about the cost of care and in people who are going to be on indefinite ADT without any reason to discontinue therapy, it still plays a role in the modern era for a select number of patients.
And certainly as we think about underserved, you know, regions of the world where there's a lack of access to drugs and treatments. I think as we think about the GnRH analogs, I think there's been an evolution. Classically, we think of GnRH agonists that have been kind of the backbone of treatment. And if we go back to normal physiology, typically the LH and FSH are released in a
let's say, pulsatile fashion, if you will, when there's a continuous stimulation of the pituitary hypothalamus access, it results in complete kind of shutdown of the access, you know, pulsatile therapy versus continuous therapy. And that's basically how we achieve suppressed T levels with the GnRH agonist.
And then the antagonists have come around, which instead of, you know, working first to turn on the access before they turn it off, immediately suppress. And then, you know, now we've got androgen receptor pathway inhibitors. I mean, there's many of them out there that further suppress or block androgen signaling that have really entered into the landscape.
So I think we've seen an evolution from surgery to the injectable analogs to now next generation potent oral agents.
Totally. And you know, I think as fortunately, in my opinion, as advanced prostate cancer management has gotten more complex, really digging into side effects, mitigating those side effects, explaining those side effects. You know, early on as a urology trainee, it was like, all right, we're gonna start you on Lupron. And the counseling might've been, you know, you might have some hot flashes.
Okay, we'll see you in six months with a PSA and a testosterone. And I'd like to think that, you know, it's a bit more advanced than that. So maybe you kind of alluded to it, you know, obviously this is prostate cancer. It is addicted to testosterone. We've got to get those testosterone level down to castrate.
Can you just talk a little bit about, maybe we start with disease states, early disease states, all the way to advanced disease states. When you think about this, how do you kind of think about when ADT might be appropriate? Yeah.
Yeah, absolutely. So very good question. You know, I think in the localized setting for individuals that are undergoing surgery, at the present time, there's no role for perioperative therapy, though there are clinical trials that are looking at investigating that, but currently no role.
I think for people that have, that are undergoing radiation, there absolutely is a role for ADT and the duration and intensity varies dependent on the risk of the patient. And so in the context of intermediate risk disease, six months of a GnRH analog would be sufficient for patients with high risk disease, two years of therapy.
And for patients with very high risk disease defined as a PSA of greater than 40, at least an 8, 9, 10 disease or T3 disease, having two out of three of those factors, they're getting the addition of abiraterone to ADT. So that's treatment in the definitive setting with a curative intent. And we know that there are some patients that go on to relapse following definitive treatment.
for those individuals that relapse post-surgery, there certainly is a role for ADT combined with radiation. And particularly, it's largely dependent on what's the PSA level at the time of radiation, and also what's the patient's risk factors coming in to the radiation therapy, whether they should or shouldn't undergo ADT. And then for those individuals that have a relapse
post definitive treatment, post salvage radiation, post definitive radiation. They're not really a candidate for any more pelvic directed therapy. We're treating with intermittent ADT in the BCR setting. And again, the potency, of treatment is largely dependent on risk of disease.
For patients with a rapid PSA doubling time, we're generally now leaning towards doublet therapy with ADT plus an ARSI, particularly enzalutamide, which has been tested in this setting for intermittent duration. So one year of therapy and then off treatment.
And then in the metastatic disease setting, you know, that's where we're really thinking about more continuous therapy with more lifelong hormonal therapy, though I think that many are beginning to challenge that paradigm a little bit. But more lifelong therapy and particularly for those individuals with high risk disease or de novo metastatic disease, adding an additional RSI.
And I think, you know, the one caveat to everything that I've just stated is like PSMA PET imaging has really kind of wreaked havoc in our defining of different stages of prostate cancer. And so we're identifying disease earlier, we're identifying low volume metastatic disease,
And sort of some thought around, you know, intermittent therapy for people with metastatic disease by PSMA PET imaging, but conventional imaging negative and not wetting those patients to lifelong ADT. So that's still sort of also being tested.
But that's sort of the spectrum, I think, across the way, the intensity and the potency and the duration is really largely been driven by the risk, the patient risk factors.
Yeah, and I think that really kind of perfectly captures that ADT kind of has a role potentially across the disease spectrum. And maybe just one question, primary ADT, is there a unique patient these days that that might still be an option?
For just ADT alone without an ARSI, just straight up by itself?
localized prostate cancer, really not a candidate for surgery, radiation. Are there patients that you might be considering primary agency for?
Yeah, you know, I think that's a very good question. You know, I think at the end of the day, it depends on the patient's symptoms, their goals of care, their quality of life. I think if there's somebody that is maybe has high risk localized disease, the treatment's going to be resultant in a lot of morbidity from surgery or morbidity from radiation.
but they're high risk enough that you really don't want them to develop metastases. And there could be the potential that they would develop metastases in their lifetime. You can certainly think about doing ADT in that context, but I think it's very personalized depending on the patient's comorbidities and also what their goals of care are.
Totally. Couldn't agree more. And not to overgeneralize, many times it's the elder, sicker, infirm patients where they've still maybe got some gas left in the tank. You don't want to say good luck and good night, but surgery or radiation, you know, maybe due to their underlying urinary symptoms, et cetera, aren't going to be great options. Okay, fantastic.
So, you know, I love the way you mentioned that it's the duration, the intensity, and the kind of intent of therapy that are largely modulating this. And maybe we can start out with, you know, four to six months ADT for generally unfavorable intermediate risk prostate cancer. What agents, any kind of major preference? And maybe I'll just throw this out there.
You know, once upon a time when I was prescribing a lot of ADT, I was like, let's give you a six month shot of Lupron. Let's be done with it. It's cost effective, rock and roll. And there's baked in compliance. Now, I'm not saying that that's the best route, but let's just talk about an intermediate risk patient that's getting ADT coming into your office. And what does that conversation look like?
Yeah, no, very good question. You know, I think that, you know, a lot of times we're talking about one, what's the intent of treatment, but we're going through a lot of the side effects, you know, a lot of times, the bulk of the clinic visit is spent around, well, this is all the risks that are associated with ADT.
And these are all the things we need to guard against when you go on hormonal therapy. So I think it's an overview of sort of the risk and the toxicity. But I think with regards to the different agents, there's a ton of different agents that are out there. And
There are certain things that I think we do in clinical practice because they're just very practical and feasible to orchestrate in the clinic. But, you know, technically at the end of the day, there's like Degarelix that can be given as a one month subcutaneous injection. There's, you know, Luprolide or Trelstar that are given as
Once a month, three months, four months, six month injections, you know, and now there's also an oral agent called Relagolix that can be utilized. What we've seen with the GnRH antagonist is that there does seem to be a little bit more faster time to T recovery post discontinuation of the treatment. And I think there's very controversial data about GnRH.
the potential cardiovascular, not to say risk, but mitigated risk with antagonist versus agonist. But I think there's a choice in the matter. Some patients may have a strong preference one way or another, and in which case they do, there's options, which is a good thing. Some patients are very
fearful of side effects where you may not necessarily want to give them a six-month injection and the way to actually help encourage that they get evidence-based you know treatment is by saying you know what let's just do one month at a time or let's just do the pills and then if you have any side effects we'll just stop so I think that can be very appealing to some individuals yeah totally couldn't agree more I think you know that idea like a bit of a of a trial and
You know, while I think we like to get those durations of ADT in for the intermediate risk patients and for the high risk patients, it's kind of a little bit of a conversation, right? If they're completely miserable and life is not worth living, then it's not like we're going to strap you down and get you two years in.
It might be, all right, you know, you're high risk, let's really try to get a year in and, you know, we can horse trade after that. Okay. So, yeah, you kind of mentioned, you know, there's injections, there's Degrelix, Erigolix, there's good old-fashioned ADT. Antiandrogens, do those have much of a role anymore?
You know, very good question. I think there's probably a lot more, you know, hand-waving around the testosterone flare when people first start on an agonist than anything else. You know, I think when it's absolutely necessary are in individuals who have symptoms, urinary
symptoms that you're worried about obstruction, metastatic disease, pain, cord compression, that's where it's like absolutely critical to, you know, ensure that you kind of guard against the testosterone flare that can happen. You know, certainly an antagonist avoids that completely.
you know, I think it has gotten complicated because of the ARSI and the fact that we use ARSI a lot in multiple settings. And, you know, are you going to put somebody on Lupron or biclutamide, then Lupron, wait for their Abbey script to come in and then switch them from the biclutamide to like, what are you actually doing with the biclutamide?
And are you actually impacting their survival in any way by giving them the two or four weeks of biclutamide? So I think, you know, not to say that there's been a movement away, but I think we are seeing less utilization of the first generation antiandrogens in the clinic because of the fact that we have these next generation agents and many individuals are getting such agents.
I don't feel so strongly that somebody must absolutely get biclutamide to suppress the T-flare. I think in the localized context, where I'm not using an ARSI, then I will absolutely do that.
But when I am using an ARSI, I think it just gets very complicated for the patients to also have to worry about getting their first generation antiandrogen while we're getting their Abby on board or Enza on board. You know, we may just tell them to start their Abby or Enza first and then come in later for the injection. So at the end of the day, do I think that that impacts overall survival? No.
Yeah, I mean, I would tend to agree. And I think in those contexts, those kind of extreme contexts, cord compression, saddle paresthesias and so forth, it's pretty easy to use a GNRH antagonist and just kind of be done with it and get castrate, you know, in the order of hours. You know, I think that's also a context where bilateral orchiectomy still, you know, remains in the toolkit.
All right, so side effects. You know, my usual, and it's always a little bit tricky, especially when you're talking to people with a new diagnosis of prostate cancer and they're a candidate for surgery or radiation and you're talking about hormones. I almost feel a little bit bad because when you run through the litany of stuff, it sounds so awful that...
you know, people are just like, there's no way I'm going to do that. You know, there's going to be loss of muscle mass, increase in fat mass, or maybe some cognitive impact, some cardiovascular risk, osteoporosis, weight gain, loss of libido, erectile dysfunction, fatigue. I mean, do you like run through this?
I do. You know, I've actually, I do run through the side effects because I think at the end of the day, patients want to know, And I hate it when somebody comes back in the clinic and they're like, nobody ever told me this was going to happen. So I really want patients to be informed about the side effects that they may experience and the different things that may happen.
And we certainly can't go through every little possible thing that could certainly happen. But I think it's key to go through the key ones that you're worried about when starting ADT. And I think it's important because then you can help with prevention. So that's going to be key. So I think the first thing is kind of going through the fatigue side effects.
Many patients want to know, am I going to be able to continue working? Am I going to be able to continue exercising? And so kind of level setting is important around there. The vasomotor symptoms, I think, are really important to describe.
You know, the other thing that I think is really important is the sexual side effects and not just with regards to libido, but the body dysmorphism that can happen from going on ADT. I think patients want to know that. And not be like, what is happening to me?
Like the testicular atrophy that could potentially happen, you know, hair loss, you know, changes in even smell, you know, the different kinds of things that can happen when patients are on treatment. I think it's important to go through that. You know, the other thing is the bone health.
Some patients might need a baseline DEXA scan if they're certainly if they're going to be on treatment for a prolonged period of time.
and optimization around bone health, muscular loss, mood, you know, irritable mood, sleep, metabolic changes is critically important, you know, and some and actually even thinking about doing a cardiovascular risk assessment or make sure somebody is doing that, whether it be their internist, cardiologist or you yourself as their oncologic care provider. is important.
So I think kind of, I think it's key to go through that. I think this is also an opportunity where our nursing team can be leveraged, our APP team can be leveraged. You know, they're really fantastic and kind of going through the detailed summaries of the different things that patients may experience.
Yeah, I think that's clutch. And, you know, the body dysmorphism, I don't know if I mentioned, but the gynecomastia that can be very troublesome to patients. And, you know, of course I do too. And I don't know necessarily why, but I feel like there's still this like surgery, radiation kind of situation. And I always feel like a little bit bad, like bad mouthing the other option. Yeah.
You know me well enough that it's like, you should just understand all your options very, very well and then pick the one that suits you better. So maybe I subconsciously downplay some of the adverse effects that I don't want it to come across as biased, which is silly. You know, I think it's an...
An opportunity to empower the patients that while these things are being done to them, you can get vitamin D and calcium for bone health, get the DEXA scan, weight-bearing exercises, heart-healthy diet, sleep hygiene, supplements, maybe even potentially that you don't have to be like a passive victim in this, that there are things that you can do, plugging me in with sexual health counseling, a men's health team.
So, I mean, maybe for me in the events that I still do, vitamin D, calcium, baseline DEXA, run through it. And by all means, if they've got cardiovascular risk factors, that's where I'm going to probably engage a team. And you kind of mentioned there's some controversy around it. What do you think? You know, GnHRH antagonists, do they have some cardio protection? Do they not? Hard to say.
Yeah, you know, I think the big take home message is that, you know, you can't just like put somebody on their ADT and check out because what we saw from the PRONOUNCE study, which was actually designed to look at cardiovascular risk in people that were getting an agonist versus an antagonist. And in the context of the trial, they had very robust upfront cardiovascular risk assessment.
Patients on both arms were getting seen by cardiology or, you know, kind of getting ongoing kind of cardio prevention. And at the end of the day, the study had to close down because that rate was so low and in both arms and wasn't any different in either arm. So I think the key take home is Like prevention is key and staying on top of it is key.
Now, I think, you know, certainly if I have somebody before me who's got an extensive cardiac history and they really need to be on ADT, they've got high risk disease and you're treating them with a curative intent and they need to start treatment. Like, yeah, in that context, I'm going to go ahead and prescribe medication.
an antagonist, you know, every day over an agonist just to do everything that I possibly can to mitigate their cardiovascular risk, like whether it be a thrombotic event or arrhythmia or something. So, you know, I think at the end of the day, I think there's probably a little bit more hype than true data. And I think the data that is out there has some flaws in it.
But I think that, you know, it doesn't necessarily put the person in any worse off situation from an efficacy standpoint or side effects standpoint, and may potentially mitigate some CV tax.
Yeah, that's essentially my understanding. And I guess if there was going to be a difference that seems a little bit more real, if you will, it would be the testosterone recovery when you're on a, you know, non quote unquote lifelong plan, six months, you know, 12, 18 months of a GnRH antagonist versus let's say, you know, six monthly luprons.
Do you feel like they're similar in terms of testosterone recovery or different?
You know, I do think the antagonists are associated with more rapid time to T recovery. And, you know, I think the other thing that we don't necessarily know is how that potentially plays into their long-term outcomes. You know what I mean?
I don't think there'll ever be a study that'll look at this, but when people, most of the older studies looked at the role with agonists and therapy was that much longer with an agonist as you waited for their T to recover. So does the fact that the T recovers faster, is that gonna impact long-term outcomes? I don't think we really know, but I think it's very much,
You kind of want to give patients the duration of the treatment that you want to give them and stop as opposed to having this protracted time that you don't know when they're going to recover. And, you know, so I think it's it's nice to use the antagonist when the course of therapy is finite and you want their T to recover.
Makes sense. So is there any kind of meaningfully different counseling when it's favorable versus high risk? Let's just not, we would start with the ADT element, not necessarily the ASRIs and second generation and, you know, potentially triplets. You know, is your counseling for somebody who's basically intermediate risk or high risk, similar, comparable, different?
you know, I think it's slightly different because of the fact that they're going to be on therapy that much longer. You know, I think it's the, you know, muscular loss, the bone loss, metabolic changes can be way more pronounced.
You know, you have patients, they come into clinic, they're on 24 months of ADT and first visit, they're up two pounds, up two pounds, up two pounds in a year, they've gained 10 pounds and now they've got some, you know, pre-diabetes. And so, you know, The propensity for that to happen with somebody just being on therapy for six months is not as high as, you know, two years of therapy.
And so I do think that the counseling is important, especially for people that are doing longer course treatment.
And how are you following these patients in terms of, you know, labs, obviously, testosterone and PSAs, anything kind of beyond that?
I mean, like I said, DEXA scan for select individuals, depending on duration of therapy, making sure they're up to date with their lipid panel, making sure they've had a hemoglobin A1C, if you've looked at their fasting glucose, and somebody is tracking that, you know, some patients may warrant, you know, being on a statin or being on an aspirin if they're high risk when they go on ADT.
And so I think making sure that that's evaluated. You know, some of these therapies can cause high blood pressure, so monitoring against that. But I think with regards to testing, for me, it's basically a hemoglobin A1c, glucose level, you know, lipid panel. You know, there's been some recent enthusiasm around coronary calcium scores with regards to CV risk.
I don't know that that's been consistently implemented across oncologic practices, but I think the education is really key.
And where do you like to see their testosterone levels kind of level out?
On treatment?
Yeah.
Undetectable. You know, hope to get it down low. And then, you know, patients always ask me this question. Well, what about if we get it down to a certain level and whatever? And I'm like, everything that we do is to drive the levels even lower. And what we measure in the blood is like not even what is measured in the tumor.
And studies have actually demonstrated that the interprostatic and intratumoral androgen levels are even higher than what they are in circulation. And even when the levels are undetectable in circulation, you can still detect potent androgens within the tumor. So that's just my rationale to like continue to drive the T levels as low as you can get them. When you're on therapy, you're on.
When you're off therapy, you're off. But
doing this halfway thing is not really you know constructive yeah i mean it used to be like less than 50 then less than 20 then it's basically undetectable and i think you kind of hit the nail on the head and you know there's been just a explosion of medications really trying to eradicate any testosterone from any source you know beyond just the hypothalamic pituitary testis access
And it kind of segues into, so, you know, maybe for finite favorable risk, of course, there's a counseling and it's kind of like, I just got to get through this and you'll be fine. For the higher risk, it's a longer duration. Maybe some of the metabolic elements become a little bit more front and center. And then there's kind of you're in the long haul and, you know, whether that's going to be.
intermittent or continuous as very person-specific, disease state-specific, whether they're sensitive or resistant. But just talk a little bit about maybe how you think about continuous versus intermittent ADT when appropriate.
Yeah, very good question. So I think certainly in the biochemical recurrence setting, that's where I'm thinking of more intermittent ADT. And there's really no data to suggest that continuous ADT is associated with better outcomes, probably increases the risk of toxicity. And so giving them opportunities where they can have, patients can have, you know, T recovery is critically key.
I think in the metastatic setting, I think in general continuous, but, you know, there are caveats to that. And I think a lot of the caveats stem from what PSMA PET imaging has done in the field, what Saber has done in the field with regards to localized treatment for metastatic disease, particularly in individuals with oligometastatic disease.
So I think we've really challenged the paradigm a little bit in the metastatic setting for those patients that have low volume oligometastatic disease, actually giving more finite treatment and actually thinking about introducing a holiday if the primary has been treated, the metastatic foci have been treated, and they've received intensified therapy.
I think that's sort of how I like to think about the continuous versus intermittent strategy.
And intermittent, so you've got them on your ADT du jour, their cast rate, their PSA is undetectable, and then you decide to give them a little bit of a holiday. Can you talk a little bit about the triggers to get them back on treatment? Are they PSAs? Are they doubling time? Are they patient anxieties or provider anxiety? What does that kind of look like?
You know, it's all the above and everybody's different. And what I will say is you're never going to find in a textbook a number for which, yeah, when you hit that number, go ahead and resume because everybody's different. So I think it depends on what's their risk, their PSA kinetics, what's their rate of rise. What's their rate of rise in the context of what their testosterone is doing?
Are they just rapidly rising because their testosterone is recovering and that's what's driving their doubling time? Or are they... Do they have a stable testosterone and they're rising? What's the absolute number of the PSA? How do they do with hormone therapy before? Do they want to go back on hormone therapy? What does their PSMA PET scan shows when their PSA gets up to a certain level?
So I think it's all of these factors. that will weigh in when is the right time. And, you know, the right time is what's right for the patient, quite honestly. So there's no, you know, in the BCR setting, not to say you're treating a number, but you kind of are. There's no clinical symptoms. They don't have metastases.
You're trying to ward off the development of metastases and improve their longevity. But Whether you start at three months or at six months or wait a little bit longer, there's no data to say that doing something one way versus another way improves outcomes.
Yeah, I couldn't agree more. I mean, there's people that really get taken for a ride with ADT. There's people that it's not so noticed. There's people that really are upset with PSA levels at various thresholds, and there's people that are not. So I agree, it's individualized.
And like you said, you know, earlier PSMA PET scanning has kind of flipped everything on its head when it comes to detecting METs. Well, you know, I think this is a topic that can be reviewed enough.
I mean, I certainly learn plenty every time and, you know, not to, I absolutely think that a lot of people, you know, med-oncs, radoncs, urologists can safely and effectively prescribe ADT, but it behooves us to kind of stay up with it, make sure patients are well-informed and, you know, do everything we can at our end as well as the patient and to help mitigate side effects.
So maybe as we're kind of wrapping up here, Raina, any kind of parting thoughts for the audience on how you approach ADT or things you're excited about in the future?
Yeah, no, very good. I mean, I think the way to approach it is to be systematic about it. and provide education. I think, you know, actually in communicating with patients about their different experiences in when they started ADT, I think one of the biggest take homes was like, everybody does it different. Every doc doesn't different. There isn't sort of like a system.
So I think like kind of being a little bit more systematic about, you know, these are the options that you have and these are the side effects and just, you know, You know, at our institution, you know, Aditya kind of we piloted together kind of like an ADT order set, you know, like when you're going to start ADT, these are the things to think of. These are the labs to think of.
This is the imaging. Here's the teaching. And I think that that really kind of takes out a lot of bias from the process. So I think standardization is important and also kind of seeing what the goals are for the patient and aligning with them is really key. I think what's really cool that's coming down the pike is, you know, we continue to bat away at the androgen receptor in prostate cancer.
And I think the next generation of hormonal agents, we've got CYP11 inhibitors that now not, you know, the abiraterone is a CYP17 inhibitor, blocks a little bit lower down in the adrenal hormonal axis. You know, MK5684 is a CYP11 inhibitor that blocks even higher up. preventing cholesterol from entering into the hormone production pathway.
And it can be associated with adrenal insufficiency type symptoms. So mineralocorticoid deficiency in addition to glucocorticoid deficiency. And so that is coming down the pike. We've seen some pretty promising data. There's also AR degraders, AR protags. There are different kinds of ways to further kind of block the androgen access.
So I think there's a lot of cool stuff coming down the pike that hopefully will enhance patients' survival and not be associated with too much toxicity.
That sounds perfect, Raina. Well, thank you, as always, for your keen insights. Always a pleasure. And best of luck with the ASCO elections. Again, Raina is on the nominating committee. She's amazing. Vote for her. All right, Raina. Thank you so much.
Thank you, Aditya.
Thank you so much for listening. If you haven't already, make sure to follow, rate the podcast five stars, and share with a friend.
If you have any questions or comments, you can direct message us at underscore Backtable Euro on Instagram, X, or LinkedIn.
Backtable is hosted by Aditya Bagrodia and Jose Silva. Our audio team is led by Kieran Gannon, with support from Aaron Bowles, Josh McWhirter, and Josh Spencer. Design and digital marketing led by Brian Schmitz.
Social media and PR by Chi Ding. Administrative support provided by Judy De La Cruz.
Thanks again for listening and see you next week.