← Rod Squad: The Urology Podcast for Students
Rod Squad: The Urology Podcast for Students
Ep. 48 Testes Cancer Initial Treatment and Staging
00:28:20
In this episode, I quickly overview the high points of testes cancer, the intitial steps to take,...
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- [00:02]
A
Hello and welcome to Rod Squad, the urology podcast for students. I'm Parker Adams and I want to do urology. Welcome to episode 48. This is going to be on testis cancer, the initial treatment of it, as well as how to stage it. I got my information mostly from the AUA core curriculum, but I also supplemented that with Smith and Tanago's general urology as well as Weider's pocket guide to urology. So to jump right in. So testis cancer is the most common tumor in young men from the age of about 20 to 40 years old. It's most common in Hispanic or non Hispanic whites, and it's least common in African Americans. 95% of these tumors are going to be germ cell tumors. The other 5% are considered like sex cord or stromal tumors. These include things like your Leydig cell or your Sertoli cell tumors, but 95% of them are going to be germ cell. This is further broken up into seminomas and non seminomas. Seminomas are fairly self explanatory, but non seminomas contain a multitude of different cancers. And this includes embryonal carcinomas, yolk sac tumors, choriocarcinomas, teratomas, or even a mixed germ cell tumor that contains a multitude of these.
- [01:29]
The most common presentation of a testis cancer is a localized seminoma. And this accounts for about 50% of cases. And it's important to note here that 2.5% of these patients that are presenting with a unilateral testis cancer, two and a half percent of those patients are gonna end up with a cancer in the other testicle. The median age for this presentation of this other cancer is at six years. So even though two and a half percent might not have that cancer at that time of diagnosis, in five or 10 years, maybe they might have a cancer in their other testicle.
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The risk factors of of testis cancer. So there's three big ones I want to talk about. So the first one is cryptorchidism and has a relative risk of about four to six. But if you do orchidopexy prior to puberty, it drops it down to about 2 or 3 relative risk for cryptorchidism. The next risk factor for testis cancer is intratubular germ cell neoplasia, kind of a precursor to cancer, and then family. The third risk factor is family or personal history of testicular cancer.
- [02:53]
Okay, so the presentation and evaluation of these patients. So classically a testicular cancer will present as a painless testicular mass. But it's important to know that not all testis cancer is necessarily limited to the testicle and causing this painless mass. It might have spread, so it might have gone around your body. It might have gone to somewhere in your abdomen. It could go up to those supraclavicular nodes that are so unique.
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In cancer. I know, like, gastric cancer can make that node as well. It can cause lung symptoms, so it can cause shortness of breath or hemoptysis from going to your lungs. So it can present differently, like an abdominal mass, different masses, like supraclavicular mass or shortness of breath or hemoptysis. And then so that's kind of how it presents. What's the first thing that you guys do for this? So the first thing you do is get a scrotal ultrasound. It's the initial study of choice, and it's pretty good. It measures anything that's greater than 2 to 3 millimeters as far as the size of the mass is concerned. And just to break it up a little bit, if it's heterogeneous, then it signifies like a non seminoma, whereas if it's homogeneous, it would signify more of a seminoma. Okay. And the way I remember this is, like, hetero means like, different, and non seminomas have, like, multiple, like, different types of cancers in it, whereas homo means, like, all the same. So seminomas is like, just the seminoma, you know, so it's. It's not contained to this multitude of different cancers, and then there's no role. So the AUA made sure to note that there's no role for ct, mri, or other advanced imaging at.
- [04:56]
A testis mass presentation. And then that's half of it. So half of it is to get this ultrasound. The other half is to get tumor markers. And you need to get these prior to orchiectomy. And that makes complete sense, right? You want to measure these tumor markers when they're elevated so that when you do an intervention, like, do an orchiectomy, you can measure them after that intervention to see if it's worked. So you measure them high, you take out the cancer. You see if they drop to normal. And if they don't, then that would signify that there might be something else in that person's body or some other tumor that you didn't take out, like a metastasis or something that's still causing those tumor markers to be elevated. So there's three big tumor markers to remember with testis Cancer. And there's other ones, too. Smith and Tanagos talks about a couple briefly, but apparently they're not used commonly as far as prognostic evaluation goes and working these patients up. But there's three. One, there's three that are very important. So they're afp, beta, hcg, and ldh. And for each of these, I'm going to tell you the half life. And this is important because the half life will tell you how long you need to wait after you do an orchiectomy on this patient to reliably check if their levels should be below normal. Right. So you can calculate, okay, if the half life is a day, then I can wait, you know, a week or whatever it is, and just keep dividing it in half and half and half. And see, based on their values prior to orchiectomy, when you would expect those values to be in normal range. And then you can check the values on that date and you can see are they in the normal range or are they not? And if afp, for example, has a half life of five to seven days, so every five to seven days, it should be cut in half. And if you do it and you're like, man, every like 10 days, it's getting cut in half and it's really not dropping as quickly as I thought or. Or as much as I thought, then that would raise a flag and be like, huh, maybe there's something that is still producing afp. So AFP is the first one I'm going to talk about again. Half life, five to seven days. It's commonly elevated in yolk sac tumors and embryonal carcinomas. This is not all inclusive. There's other ones as well, but these are the common ones. And then what's interesting to me is you can have false positives. So when. What else do we measure AFP in? Hepatocellular carcinoma. Right. So if this guy has liver cancer, then their AFP could be falsely elevated. It can also be elevated with, like, other types of cancers, like lung, biliary system cancers, pancreatic cancer, stomach cancer. So there's really a smattering of different cancers or diseases that can falsely elevate your afp. So just keep that in mind. And because of this, because it's not specific and there's multiple things that can elevate it, the AUA really recommends we don't treat testis cancer based solely on an AFP level that's less than 20. So you really want to see, not want to see, but you really should see that AFP above 20 before you start making management decisions in regards to testis cancer based off that value. So next one I'm going to talk about is beta HCG. So this half life is 24 to 36 hours. So it's a lot shorter than AFP. And it's positive in like 20 to 60% of non seminomas and it's positive in 15% of seminomas. And the big. What's the big non seminoma that elevates beta hcg. So it's the choriocarcinoma that elevates it just a ton. I think, like Smith and Tanego's mentioned, that 100% of choriocarcinomas elevate beta HCG, and that's because they make like the syncytchotrophoblasts or whatever that form this beta hcg. I think it's just important to remember that even though that's the one that's classically associated with beta HCG, there's other tumors. Like 15% of seminomas can raise this marker as well. So it's not specific necessarily to just choriocarcinoma. Embryonal carcinoma can also cause this to be elevated. And then similarly to afp, there's other things in your body that can make beta hcg. So it can be observed in liver, biliary, pancreas, stomach, all the things that we talked about with afp, it can be seen in those types of diseases and whatnot. So just keep in mind that these tumor markers, although helpful, can be elevated in other situations. And the weird one here is that if they smoke a ton of pot, if they smoke a bunch of marijuana, it can elevate their beta hcg. Just a little fun fact for you to know. And then LDH is the last one that I want to talk about. And this one's interesting because it doesn't really narrow down the type of tumor that it is. It only narrows it down to the point of germ cell tumor, and it's not specific past that. So it really narrows it down. Well, we're not in that 5%, you know, we're in the 95% of germ cell tumors for testis cancer. Whoop de doo. Why do we get this level if it's just going to tell us something that we basically already know? And it's interesting because apparently it can help us guide and learn more about the amount of burden that this patient has. So it's not really used as a identifier as far as what type of tumor it is, it's more used of how much of that tumor, of whatever it is, do they have in their body? And it can be used as it can go into prognostic calculations and stuff like that.
- [11:02]
Ooh, I should mention that the LDH half life is 24 hours.
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Okay.
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So the initial treatment. So the initial treatment for these guys is radical orchiectomy. And there's certain situations where you can consider a partial orchiectomy. And these are usually when the tumor is super tiny, so you could just snip it off. The tumor is bilateral. So the way I've envisioned this at least is that, like, oh, man, you have this guy, he only has two testicles. So if he has a tumor on both testicles, then you want to at least consider just cutting out the tumor so he at least has, like, a half of two testicles left, which, like, kind of is one testicle. You know, that's the way at least I think of it in my head. So you consider it in bilateral tumors, and then you also do it when you have increased suspicion for a benign tumor. And I have a hard time wrapping my head around this because I thought you considered all testes. Testes tumors to be. To be malignant until proven otherwise. So I don't really know what would heighten your suspicion. Is it, like, negative? Like, is it negative serum markers? Is it, like the homogenicity on ultrasound? Or like, what. What is it that raises your suspicion enough to say, yeah, we don't need to cut this out. We can sit on it? And then the other thing to consider at this time before you do orchiectomy is sperm banking. So there's a couple people that sperm banking is especially important for, and that's when they don't have a normal testicle on the other side. So maybe they had torsion when they were 11, and now they're 30 and they have a mass on their other testicle. So that's someone you want to consider sperm banking. And then the other one is someone that's, like, seen you for 10 years because they never could have kids, and you did a whole fertility workup, and they're like, sub. They have, like, sub fertility, and it's really hard for them to have kids. Then that would be someone that you also want to consider sperm banking for. So you take out this testicle, you do a radical inguinal orchiectomy, you send it off to pathology, and then once the. You get the pathology back, now's the time to complete your staging. So this is when you do your CT scan. You do a CT scan of the chest, abdomen, pelvis, with oral and IV contrast. And there's this, like, weird thing about you could get a chest X ray instead of a chest CT if they have negative post orchiectomy tumor markers as well as no abdominal metastases. But I don't really get that because it just doesn't make any sense to me because it's like you're already ordering a chest, abdomen, and pelvis, so you'd be taking off one of the three. You're still getting the two other CTs. And then you have to wait almost like a month after their orchiectomy to see potentially, potentially depending on how high their levels are, to see whether they actually have negative post orchiectomy tumor markers. So I just don't really get if that's like, worth. Like, is. Is it, I don't know, is that beneficial to wait that much time? And you're already getting this other. These other CTs. Like, is it really worth it to get an X ray instead of the ct? And if the X ray, like, showed anything, my guess is that you'd probably end up getting the CT anyways. So it just doesn't make a ton of sense to me. But I'll chat it over with my resident tomorrow and see what he thinks. And then in addition to ct, you can consider brain imaging. This is really dependent on, like, your clinical eval. So if they have, like, significant altered mental status or something that would raise your suspicion that there's possibly a metastasis to the brain, then you'd want to get some imaging. And then the AUA notes that there's no PET scan imaging in the initial staging of testis cancer. Okay, so I've talked a little bit about staging. I'm going to go over it. It's kind of brutal, but I wanted to at least get down to the podcast. And I'll do my best to make it mildly interesting and try to bring out the highlights of how the staging works so you guys don't go completely crazy. But I would recommend that you guys go into the AUA curriculum. Go into Smith and Tango's. They have a nice table and look at these different things so you can kind of see the nuances of it, because what I'm going to be telling you brushes over some of those nuances that I want you guys to read about. So the staging of testicular cancer, so it's broken up into four different categories. The pathological tumor so PT or T, the pathological N or node, so TN and then metastases, so M and then serum markers, so S. So they actually add, instead of the normal, like T, N and M, they add the S at the end of it as well. And it's taken into consideration when you're staging these patients. So I'm going to start with tumor T. So, and I'll do a broad overview first. So if there's an X after any of these, it means that it couldn't be evaluated. If there's a zero, that means it's not present. That's common amongst basically all staging. So now I'm going to get into like the ones, twos and threes and whatnot. So the first one is PTIs, and that's actually a germ cell neoplasia that's in situ. And I just envision, like in situ cancer, just filling up the epithelium and not breaking the basement membrane of whatever part of the body that you're in. So it's like filling it up, but it really hasn't breached that membrane to actually be called, like, invasive cancer, you know. So that's like. The first one is just in situ germ cell neoplasia. And this is where it gets interesting. The T1, T2, T3, T4. And how this works is that for each level, there's a structure that wasn't involved and now is involved, and it bumps you up to that level. And that's how I want you to think about it. So T1. The only structure that's involved is the testes. It's limited to the testes. And if that's the case, you're T1. And that means that you have no lymphovascular invasion. That means that you haven't involved your epididymis, your spermatic cord, your scrotum, your hilum of your testicle. None of that stuff has been involved. You're just limited to the testicle.
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Now, there is a little stipulation here. So it breaks it into T1A and T1B. The nice thing about it is that it's broken down just by size. So if it's less than 3 cm, it's T1a. If it's greater than 3 cm, it's T 1b. But both of those are just limited to the testicle. So what structure involvement bumps you up to a T2. So there's three different ones. And this is where it gets kind of brutal. T2 is the hardest. So the first one is Lymphovascular invasion. So if you have lymphovascular invasion, you're a T2. Okay. Or you could have hilar soft tissue involvement or epididymitis involvement. Okay? And this is where it gets interesting. So everything after this, so including hilar soft tissue or epididymitis, and everything after this, I talk about when it involves this structure that could be involved, whether it's with or without lymphovascular involvement, and it'll bump you to that level. Okay? So if you have hilar involvement, you're a T2, and it doesn't matter whether you have lymphovascular involvement or not. And it makes it complicated because lymphovascular involvement is also something that bumps you up to T2. But that gets more important when you're in T3 and T4 and involving those more severe structures. Because if you're involving that, you don't necessarily need to have your T2 lymphovascular involvement to be able to jump up to a T4 if you have scrotal involvement. Okay, so it's just a little bit of a nuance that they mention here. So T1, and I keep reviewing this because you guys are listening, and it's hard to get this in your head. So T1, limited to testicle, broken down by size. Less than 3 cm is A. Greater than 3 cm is T1B, T2. A few things bump you into T2 lymphovascular involvement, hilar soft tissue involvement, or epididymitis involvement. You can have any three of those, and you don't need the other two to be able to bump you up to T2. All right, T3. So what's the next structure? Past the hilum, past the epididymitis or. Sorry, past the epididymis, past the lymphovascular invasion. What's the next structure that we need to involve to bump this up to a T3? And that's the spermatic cord. So spermatic cord involvement brings you up to a T3. And again, you don't need lymphovascular invasion with spermatic cord involvement for it to be a T3. You can have spermatic cord involvement without lymphovascular involvement, and you're still a T3. I know I'm, like, hitting that hard, but I think it's important to know because they mention it in literally every step of the staging table. And then what's the structure that bumps you up into a T4. And I mentioned it just a minute ago, it's the scrotal involvement. So if you involve the scrotum, you're up to a T4. And the same nuance with lymphovascular invasion. Okay, so nodes. There's a bunch of mumbo jumbo in here about nodes. It's really broken down by size. So an N1 is nodes that are less than 2 centimeters. Okay? If you breach 2 centimeters in size, then you're.
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Sorry. If you're greater than 2 centimeters in size, then you've earned yourself an N2. And if you're greater than 5 centimeters in size, then you're in N3. So it's less than 2 is N1, 2 to 5 is N2, and greater than 5 is N3. Okay? And then the metastases, the way that they wrote this down in Smith and Tanago's is breaking it up between M1A and M1B. And the lungs are a common place of metastasis for testis cancer. So M1A is non retroperitoneal nodal. So if it was retroperitoneal nodal, that would go into your nodal category, not your metastasis category. So non retroperitoneal nodal or pulmonary metastases. So this is kind of what you're expecting when you have progression of disease, right? You're going to go to nodes outside of your retroperitoneum. You might end up leaking into your lungs because that's a common place for it to go. That's kind of the next step in progression. So it would make sense that that's M1A. Now to go to M1B, you have to get even further in that progression. So you need to have non pulmonary visceral metastases to be M1B. And that makes sense, right? They're first going to go to your lungs, A great harvest place for metastases of a ton of different cancers. So they're first gonna pop over there, you know, grow a little bit, get stronger, get stronger. And then they're gonna go to your visceral organs. And that would classify you as an M1B. And then I know this is brutal, but the serum markers is the last category of your staging, and the it is broken down kind of by value. And they look at LDH, HCG, and AFP, okay? And they do LDH by a certain multiplier of normal, and it's S1, S2 and S3. Okay. And for each value, they have it broken down into each one. I suggest you guys look at this yourself. I'll read it off to you just because I want to be complete, but I know it's probably going to go in one ear and out the other. So I'm going to start with LDH. S1 is an LDH of less than one and a half times normal value. Okay. S2 is an LDH 1.5 to 10 times of normal and an S3 is an LDH of greater than 10 times normal. Alright, HCG. Think of fives for HCG. So an S1 for HCG is less than 5,000, an S2 for HCG is 5,000 to 50,000 and an S3 for HCG is greater than 50,000. And for AFP and S1, think of like the ones for AFP. I know that's a terrible memory hook, but for AFP, for S1 you're less than a thousand, for AFP, for S2 you are 1,000 to 10,000. And for S3, you are greater than 10,000.
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So I know that was kind of brutal. And then you use all of the things that you do from that chart. You kind of put it together and it puts you in a certain stage of this cancer and you use that for your management strategies. And there's some complexities to this as well. They have a great chart in the AUA curriculum. I suggest you go look at it to paint in huge brushstrokes for you guys, it's broken up into stage one, two and three. And then it's kind of escalating as you go up those stages. Which makes complete sense, right? So in stage one, your N0, your M0, and you're basically S0 except for one exception. Okay. You are T positive, though. You're anywhere from T1 to T2 to T3 to T4, and you work your way up to any PT, okay? Any type of tumor level.
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So epididymil, epididymis involvement, scrotal involvement, you work your way up to that through stage one, but everything else is absent. Okay. And then starting in stage two, then you jump over to your nodes. But in stage two, your metastases are still negative. Okay. But in all of stage two, you're at. It doesn't matter what your tumor stage is, it's just focused really on the nodes. So it's nodes one through three, nodes two notes three. And that's compared to your, your S's as well. They start to come into, come into play in stage two. But it's important you guys, to remember that Metastasis in stage two is still M0. Okay? And then in stage three, again, you're still at any tumor stage, right? Could be confined to the testicle. Could be. Or not confined to the testicle, but it could be like, what do they say? Limited to testes. Or it could have epididymal involvement or scrotal involvement. Doesn't matter. But this starts to take into consideration metastasis. So if you have distant nodes that are positive or visceral or lung involvement or something like that, that would start to come into play and put you into stage three. Whereas the nodes become less important. They start to say, any nodes is just will suffice for stage three. And really the deciding factor of where in stage three you are lies on the amount of metastasis that you have. And then throughout all of this, stage two and stage three, especially, the S comes into play. So very complex. I guarantee that you guys probably don't need to memorize this, but I think it's just good to have in the back of your head that's like these different stages, these things are negative or they start to matter a little bit more as you progress through. So I wouldn't worry too much about that. But I think it's interesting to look at at the very least. So I hope this episode was helpful. I know it was getting kind of brutal near the end going over all those details, but you can listen to this multiple times. If you have any questions, please reach out to me. Or if you have any suggestions, please reach out. You can email me@rodsquadpodmail.com you can go to my website@rodsquadpod.com or you could even out to me on Twitter, Oddsquad, Pod. And then other than that, I hope you guys are doing well. I hope you guys are staying safe and take care.