Don’t Give Up on Testicular Cancer

Genetics and Testicular Cancer – Insights from a Public Health Researcher - Episode #26

July 30, 2021 The Max Mallory Foundation - Joyce Lofstrom host Season 1 Episode 26
Don’t Give Up on Testicular Cancer
Genetics and Testicular Cancer – Insights from a Public Health Researcher - Episode #26
Show Notes Transcript

Geneticist and cancer epidemiologist Charleen Adams, Ph.D., shares her insights on the genetics of testicular cancer and cancer, in general. She began her career as a chaplain in Manhattan, NY, a position that led her to study disease prevention through genetics. She is now a bioinformatics Postdoctoral Research Fellow in the Lemos Lab at the Harvard School of Public Health.  Listen to Charleen on Don't Give Up on Testicular Cancer, a podcast from the Max Mallory Foundation.

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Genetics and Testicular Cancer Insights from a Public Health Researcher – with Charleen Adams, seasons 1, episode 26

 

Welcome to Don't Give Up on Testicular Cancer, where cancer survivors, caregivers, and others touched by cancer share their stories. The Max Mallory Foundation presents this podcast in honor and memory of Max Mallory, who died at age 22 from testicular cancer. I'm your host, Joyce Lofstrom, a young adult and adult cancer survivor, and Max's mom.

 

JOYCE: Hi, this is Joyce, and with me today for our podcast is Charleen Adams. And Charleen is a geneticist and a cancer epidemiologist. She earned a PhD in genetics from the University of Washington and an MPH in genetic epidemiology from Johns Hopkins University. She studied the incidence of familial testicular germ cell tumors as a cancer research training fellow at the National Cancer Institute and is currently a bioinformatics postdoctoral research fellow in the Lemos Lab at the Harvard School of Public Health. She is focused on cancer predisposition and aging. So Charleen, thank you so much for joining me today and sharing your wonderful background with us on cancer research.
 
 

CHARLEEN: Thank you. Thank you, Joyce. It's an honor to be here. I was moved by your son Max's story.

 

JOYCE: Thank you so much. That's how we got started with the podcast, and how I found you, because I know you've done some research into testicular cancer. But before we get to that, I know you have lots to talk about. And we'll start with one of your early positions as a hospital chaplain and how that really influenced what you do now. Can you share that story with us?

 

CHARLEEN: Yeah, absolutely. So when I was in my early 20s, I had just finished a graduate degree in linguistics and was wanting to help people. Didn't really have all of the words for what that was, but now I know it was something, what we call it a humanistic instinct, and I followed it all the way to divinity school. And in divinity school, I was trained as a chaplain and worked at Columbia Presbyterian Hospital in Manhattan. And so what I did there was walk around to different patient rooms and floors. I had a cardiac intensive care unit, a pediatric neonatal unit, really, and a cancer wing.

 

And so normally what I would do is just make rounds and check in on whoever was there, but often I would be paged to show up when there was an emergency. It could have been because a baby just died, or somebody came in from a car accident or something. And so the nurses wanted me to be there for the families. And it was a moving and highly emotional job. The hardest part about it was feeling so powerless over everything. I mean, the very nature of it was that people didn't want to be there. And there was a lot of confusion, anger, fear, and not just from the patients and the families and the hospital staff, but then I would also feel those emotions, being part of all of it.

 

And so that was a lot of what the job was, was dealing with all of the unknowns and the inability to intervene in something that was out of everybody's control, even though the doctors and the nurses were doing everything that they could. And so that experience of feeling so helpless and out of control led to some deep soul-searching, as we could say, on my part, where I wanted to be, I wanted to have the job, I wanted to be the chaplain, if you will, that prevented people from being in the hospital, not the person who was there once people were in the hospital. But yeah, what was that? And at 22 years old, I didn't know what that was.

 

JOYCE: Right. I don't think any of us would. So, I know you've told me that this this job influenced how you studied or led the rest of your life. So how did that happen as a chaplain?

 

CHARLEEN: Indeed. So part of this was that, it was the patients that I had when I look back at this. I had the newborns, and I had the cancer patients. And so my first job after leaving divinity school was helping babies. I ended up working the time [without] having any training in genetics, but I knew what to say to them. So this is a program where every baby born in the U.S. in a hospital is screened for a bunch of genetic disorders. I'm not talking about things like Down syndrome or things that people might think about during pregnancy. These are disorders that are very, very rare and that most people wouldn't even [know], but we have an ability to test for them. So these are conditions that are usually what people would think of as sudden infant death, where the baby looks totally fine. Everybody thinks the baby is fine. And then all of a sudden, they're dead. And this happens because the baby has a genetic mutation. It is a mutation. But the conditions that get screened for in newborn screening are ones that, if you identify that the baby has this in time, there's a treatment. So that's the idea, identifying who has these conditions and then getting them on treatment. And that prevents them from either dying or having, in many cases, some pretty serious disability.

 

So I ended up working, doing exactly what I'd had that impulse to do as a chaplain,  figuring out how to find the invisible thing that is making people sick, and coming in and intervening before the sickness even happens. And so that was my entry into genetics and public health. So on the job, I learned Mendelian genetics and also the sciences of public health, which are epidemiology, the study of diseases and their prevention in populations, and biostatistics, which is the statistics that you apply to biology. I was using all of those in what we call an applied position. I wasn't acting as a researcher. I was using the science similar to how doctors use science to make treatment decisions. We were treating the population, really. But in doing that, I found that I wanted to do more and to understand even more. And what that meant is that I wanted to be a researcher.

 

And so I'm getting even closer to that goal of being able to help far in advance that I had the instinct for as a chaplain. I went from the newborn screening job into a master's program at Johns Hopkins, a master's in public health and genetic epidemiology. And what that is, is you're looking at genetics of the population. So it's different than figuring out what a particular person's genetics are. It's using knowledge of genetics. You have like a whole pool of people. And then as most people who are in research end up doing, I went and had a fellowship somewhere, which just means you get more training by people who are already doing what you're interested in. I did that at the National Cancer Institute in their clinical genetics branch. And they were studying testicular cancer and they were studying ribosomopathies and telomere biology disorders and neurofibromatosis and other diseases that run in families. And so it was similar to newborn screening in that they were looking at these rare mutations that happen, but in families and you can track a disease in families. And so I learned about testicular cancer there. My first paper was on that. Then I went to the University of Washington for my PhD. So now I'm a postdoc, what we call postdoctoral, which means that I've got my PhD and now I'm working as a scientist in a lab in the Lemos lab. That's sort of how that came together.

 

JOYCE: Wow, that's very impressive. And I think, too, as I listen to you, [it] tells me how closely intertwined all of our biology, genetics, everything really comes together. And you need an understanding, I think, of a lot of it or all of it to really, I guess, research.

 

CHARLEEN: Oh, absolutely. And I think that's such an important insight. In fact, this came up just yesterday in my lab, in the Lemos lab, where we were talking about what it is that we do, and even what identity we have as scientists. And my boss, the investigator I work for, said, well, you know, when people ask him what he does, he says,  it depends on who's asking, because sometimes you will say, well, I'm a geneticist, or sometimes you'll say, you know, I'm an epidemiologist, but really, you throw everything you have at trying to understand disease. So if you need to be an epidemiologist, you learn epidemiology to answer the questions, or you learn genetics to answer the questions. You just have to keep learning. So that's exactly right. There is a real blend of the different sciences to answer these questions.

 

JOYCE: With that in mind, I think it's a good segue then to your specific area of research because I know you are working in public health. You also are working in cancer research, which in my mind are pretty broad terms. Can you narrow it down and just give us a look at what you're studying in cancer research?

 

CHARLEEN: Yes, that's right. And that's also a good question because there are people who will use maybe an animal model or cells to study mechanisms of cancer. What I'm looking at are what we call exposures or risks. Yeah, exposures are risk factors for cancer, but in the population. So I'm not going to be able to say to any given person, look, I think you have this risk. But what we can say is, I'm looking at something that a lot of people in the population are exposed to. And so we get an understanding of what is going on in the population. Again, I keep using the word population because that's what it is. It's population science.

 

JOYCE: So it's the group of people that make up a population, right? That's a good reference to when I think about cancer in general, but let's just start with testicular cancer and that whole possibility of a genetic predisposition. Is that true? Is there a genetic predisposition to testicular cancer?

 

CHARLEEN: Yes, there is. Testicular cancer is what we say highly heritable, meaning that it runs in families and we know this. What makes it especially challenging is that it's not like breast cancer where we have certain genes that we know if you have a mutation in them, like in the BRCA1 and 2 genes, that genetic counselors might say to you, oh, you have this mutation in this gene, then we need to [look at that.] We're not screening the population for particular mutations in genes for testicular cancer, even though there is that genetic component.

 

But the other thing I would want to say about genetics goes, it's going to shift from testicular cancer to just cancer broadly. And that's that cancer is fundamentally a genetic disease caused by mutations. But the mutations aren't always the ones that we inherit. We get mutations all the time. after birth, or even in the womb, we can get them. Most of these get healed, like our body has these mechanisms for healing mutations. But every so often, our mechanism for healing, called DNA damage and repair, every now and then that machinery just messes up, and a cell will divide, and it'll still contain an error. If it's the right type of error, then a cancer might develop. And so this explains some of the weirdness. You know, we all know about smoking and lung cancer. But we also all know somebody who's 105, who smokes three packs a day, and they are fine, and they like go running and everything. So weird, right? But that doesn't mean that smoking isn't causing mutations that cause cancer. It means that that person hasn't had the bad luck of a mutation occurring in just the right spot and then it not being repaired or something like that. So it's like cancer is stars lining up in a constellation of really bad luck.

 

JOYCE: See, that's interesting, Charleen. I'll just talk a few minutes, because I always wondered--I mean, I've had thyroid cancer and breast cancer, and the thyroid cancer was caused by exposure to radiation in my teens for acne. And it was what they called light treatments, but it was radiation. And so that's, I think the doctors told me it's pretty much cause and effect. But I wonder then about--we can get into the environmental side of it too--exposure to things in the environment. There are so many components. How do researchers or scientists feel about the whole angle? It's like I have glaucoma, not glaucoma, but cataracts. And it's just your luck that, you know, who knows why you get those, but some people have [them] and some people don't. And does that make sense? Like the luck factor, I'll call it. I just, man, I don't like it.

 

CHARLEEN: I don't either. So when we study carcinogens, those things that cause mutations, they have some key characteristics. And so if we know about these, then we can try to reduce our exposure to these. And that's the good news about cancer is if you know what the carcinogen is, you can try to avoid it. That's one of the reasons why we say don't smoke. We can't always figure out where that mutation is going to happen from the smoking. That's part of the bad luck. And the other bad luck is sometimes the machinery that tries to repair it just gets a quirk and it doesn't work. So what we do is  like in a 12-step program: you're doing what you have control over. And what we do have control over, if we know what these exposures are, what these risk factors are, then we can avoid them. But it's a challenge to figure out what the risk factors are. And we know going back to testicular cancer, what some of them are.

 

JOYCE: Well, Max was born with one testicle. And we knew that when he had surgery [to find the other testicle] when he was like 12 months old, 18 months, and they said, oh, there never was another testicle. Don't worry about it, which I now know was not accurate. But that's a risk factor for what I've read about testicular cancer is born with one testicle, you really need to pay attention to your health long term. So that's just a statement, I guess, of being aware of the ones we can identify, the risk factors.

 

CHARLEEN: That's right. And younger age with testicular cancer is a risk factor. Younger men are more likely to get this, [also] being white, being European ancestry. We don't know why, but that's a risk factor. And of course, that's not one we can do anything about, except for, but you know, just generally know [about a] family history or a personal history of testicular cancer. Carcinoma in situ, that’s essentially the possible transformation into it being malignant, but we call it a risk factor because not everybody who has carcinoma in situ goes on to have the malignant version, having the undescended testicle. So those are what we consider more or less established risk factors. These are things that maybe a physician would be thinking about, like if you told them there was testicular cancer in the family, they might ask questions about these things. But what I'm doing is looking for the unestablished risk factors, the things that we don't have general agreement on yet, but there's some signal that there might be a reason to think that this is something we might be able to do something about.

 

JOYCE: So does that relate to what you're doing research-wise on DNA and ribosomes? Is that something you want to share with us, too, [in your] work with cancer?

 

CHARLEEN: Right. Well, that's similar, but a different pathway that we think of. So it's a different set of risk factors. With the ribosomes, so ribosomes are machines. I mean, that's the metaphor for them. So we have our DNA, and the DNA contains information. Well, we have to get that information made into proteins. And the ribosomes take the message and turn the message into a protein. So it's fundamental. If there's even a minor error in that machine or process, then you can end up predisposed to all sorts of problems. That's why I'm interested at this point in looking at that molecular mechanism that takes us a bit away from testicular cancer, but it's, who knows? I don't think that there's a relationship at this point between ribosomes and testicular cancer. But the idea of looking for molecular mechanisms is similar. And maybe we can talk if there's time about some of the molecular parts. But I think I have some general thoughts about the biology of testicular cancer.

 

JOYCE: Go ahead.

 

CHARLTEEN: Okay. So I think that'll help us get into some of the hypotheses for risk factors that are specific for testicular cancer. So before doing that, this is what I know of testicular cancer. Most testicular cancers that impact young men are what we call testicular germ cell tumors. And these arise from something we just mentioned, testicular carcinoma in situ. What this is, are cells that haven't but could migrate outside of the walls of the seminiferous tubules. So testicular carcinoma in situ is believed to arise from arrested gonocytes, ones that fail to differentiate. So gonocytes then are the precursors to sperm cells. So what we're talking about here is what's going wrong in the most common types of testicular cancer--some are these particular cells, the cells that become the sperm. So gonocytes, these cells that become the sperm, they differentiate even from something else that is more broad, and that's the primordial germ cells. And they do this early in the fetal development, around week seven in the fetus. So this means that if something stunts them--so when we say it stunts them, it means that it's going to stop them from developing in the way that they should. So if something stunts them at that phase, this happens early on in life, which is why we were saying that testicular cancer, most men who get it, get it early on between, you know, 15 to 45 in that range. And this means that the transformation happens very early on in life. So when stunted, the gonocytes, they can't go on. And so what we think happens is they stay stunted until puberty, and then transform into this carcinoma in situ. And yeah, and so that's the most common types of testicular cancer come from carcinoma in situ. And these are our seminomas and the non-seminomas. And Max had a non-seminoma, right?

 

JOYCE: Yeah, he had cryocarcinoma, so it was non-seminoma.

 

CHARLEEN: Yeah, and non-seminomas tend to present earlier than the seminomas, and so that kind of--it explains why, because how old was Max when he was diagnosed?

 

JOYCE: He was 22.

 

CHARLEEN: So that's consistent with the non-seminomas. People who have the seminomas, they can be diagnosed 10 years later or so, you know, that speaks also to the possibility of it--you know, of this, whatever's happening is going on pretty early.

 

JOYCE: Okay, that's interesting to me just to think about that. That's probably what happened with him because the undescended testicle was there and it just didn't come down and we didn't find it or know about it, I guess. As you just described, it became malignant or cancerous. I think that's good information though for our listeners just to understand that in terms of checking. There's a lot of promotion out there for testicular cancer awareness saying that men ‘check your balls’ or pay attention. But there's other kinds of cancer like what Max had that didn't show up in his testicles. It was in his abdomen. Anyway, I appreciate you going into that and explaining it because I think that's something I didn't really understand and it's helpful to know that.

 

CHARLEEN: I think that brings us to some of the hypotheses that are specific for testicular cancer. Part of these come from these two questions that are out there for testicular cancer, and they're related to critical periods. So what's happening early on in life that's stunting these pre-sperm cells and making them go dormant? So this is all invisible to us. We don't know what's happening. I mean, most of us don't know that this might be happening. So something [is] happening early on. And then also what happens at puberty, that for some reason, these cells go from being dormant to the carcinoma in situ that possibly could become testicular cancer?

 

So there we have it. Something might be happening early on that might, because it's early on--that implies heritable genetics. So that's one thing, but also the things that can possibly influence the development in the womb. And then we have something that might be happening during puberty. that might increase risk. And so I'll start with the latter. I'll start by talking about something that might happen during puberty or later. So interestingly, marijuana has been on the rise at the same time that cases of testicular cancer have increased. And so marijuana is not considered to be an established risk factor, but there's a hypothesis that it might increase risk for it by impacting the endocrine or the reproductive systems. There are edibles and there are, you know, and just smoking it. So we would think that maybe the edibles would be more involved in the endocrine bits. But if you're smoking marijuana, then you would be exposed to some of the potential carcinogens that are just from smoke as well. So it's difficult to figure out exactly what aspect of marijuana might be doing what.

 

But in 2009, there was a study done in Seattle at the Fred Hutchinson Cancer Research Center, which incidentally, is where I did my dissertation for my PhD. And they found that there was an increased risk for testicular cancer among current marijuana smokers compared to healthy controls, and that this was primarily an increased risk for non-seminomas.

 

JOYCE: Really? Okay.

 

CHARLEEN: Yes, non-seminomas. And they also saw that those who started smoking marijuana at a younger age and were using more of it were also at a greater increased risk. So that's highly suggestive data--but it's one study.

 

JOYCE: Right. And that's important to emphasize too, I think.

 

CHARLEEN: Right. So they're picking up on a potential signal. So since then, other people have looked into this in various ways. There have been what we call meta-analyses. And this is where several studies are combined together and people kind of look at the evidence across them. They looked for patterns in the published literature and in some of these meta-analyses that have been done. And they concluded that the signal between marijuana and non-seminomas seems credible. So that's another piece of evidence. It's still not definitive. But it's saying that when you look at not just one study, but several studies, the signal still is there. And they said that the strength of the evidence is weak. What this really means is that it looks like there might be something there.

 

And there are some unanswered questions. Maybe it has to do with you whether the route, what we call the route of exposure, was this due to, as I said a minute ago, the smoking and what's happening with some of the chemicals in the smoke versus the cannabinoids--which might be more relevant for your reproductive system? It's an important question that we don't have an answer to yet with suggestive evidence. So if it were me and I were a man and there was a family history of testicular cancer, I would probably avoid marijuana. But again, that's just being cautious and there's not enough evidence out there. So that's kind of the unsatisfying thing about a lot of the hypotheses, is that exactly what they are: they're hypotheses.

 

 

JOYCE: The other thing I think, when I listen to this too, is it takes me back to the luck factor. I would agree with you, if I were a young man and knew this and had a family history, I would try to avoid marijuana too. I think it's like so many things out there that it really comes back to trying to be as healthy as you can be and avoid, I guess, what's the right term? I was going to say known risk factors, but like alcohol, drinking alcohol. There are many studies out there that talk about cut it out completely, have one drink. I think that's the challenge of being human, perhaps, is we all have to decide how much of a risk will we take? And I think it's very easy to fall into the, oh, it won't happen to me attitude. You don't know. I think that's life. But you bring up another good point for people to know about and just think about: what do you want to do if you have that risk factor in your family for testicular cancer?

 

CHARLEEN: Yes, that's right. In this case, it would be kind of an informed guess to say, we don't know if it would make a carcinoma in situ that might be there transforming. We don't know. So then to switch on from something that is a little bit more satisfying.  You mentioned radiation. And so I wanted to bring up, there's been a longstanding question in cancer research about what we call transgenerational radiation exposure. And what this means is a question of whether if you have been exposed to radiation and you're not yet pregnant, or if your partner-to-be has been exposed to radiation. Is that exposure having some impact on your body in a way that it would make the mark of that inheritable? So could your future children inherit the radiation exposure, the mutations that possibly come with that? The question is, if a person has been exposed to radiation, will their future children have an increased risk of cancer?

 

There's been a recent paper that I thought I could share because it has an interesting answer to this question. This is a bit of background on this. It's a statement that you know, is kind of funny to say out loud, but most nearly all of our DNA that we are born with comes from our parents. But the funny part about that statement is saying ‘nearly  all’ because you can think, well, how in the world can I have some DNA that I didn't get from my parents?

 

JOYCE: That's right.

 

CHARLEEN: So that's what I wanted to explain right here. I say nearly all, because we can have some random mutations in our DNA that we didn't inherit from either the mom or dad. And these mutations are what we call de novo, which just means new. They're new. And these are known. We know that they happen. they're an important source of evolution. Some of these might make us more resilient. Some of these might cause disease. Depending on the luck of the draw, we think that some of these de novo mutations can increase risk for autism, for example. So these sorts of mutations are what were being looked at in this paper. Scientists wondered, speaking of radiation, whether the children that were born from the Chernobyl nuclear power plant accident, whether the Chernobyl survivors, the children of the Chernobyl survivors, had extra de novo mutations. If the children had more of these mutations than the rest of us, that might predispose them to cancer because you would think--the idea is that the radiation from the Chernobyl meltdown causes mutations in the parents, gametes, so in their eggs or the sperm cells. That's why we can say that they're new mutations because in the parents' bodies, they don't have them, but if the radiation caused them that's why it's called new. So mutations in the DNA of the eggs or the sperm are, if it's in the sperm, this is going to be relevant for testicular cancer, possibly. But fortunately, and this is why I say it's somewhat satisfying, is, the results of the study revealed that the children of the Chernobyl survivors did not have more of these new mutations than the rest of us. And this is one study, but it's hopeful. When we think about all of the terrible things that are out there, there's at least some evidence that this reduces the concern for this particular exposure.

 

JOYCE: And you know, I think what it also says is how certain things affect DNA or mutations and other factors in the environment don't. And that's why we need people like you who can study it and just help us understand if those things are going to affect us, like radiation exposure or anything that gets there. It could be other things in the environment. I think it's fascinating [remembering] watching that Chernobyl program that was on one of the [streaming] platforms. I mean, it was a horrific, horrific incident. And what happened there in that town, still abandoned, but the kids were okay. I mean, that's fascinating. I can see why you must enjoy what you do, because there are so many stories. Not stories, but just evidence and things that you uncover when you are looking at genetics and the things that you do.

 

CHARLEEN: Well, speaking of genetics again, I have a few more thoughts going on.

 

JOYCE: Oh, yeah. Go ahead.

 

CHARLEEN: The familial end. One of the established risk factors is the family history of testicular cancer, but there's some research that is suggesting that it might not be only a family history of testicular cancer, but a family history of other cancers too. And so this comes from some work that's been done in Norway. They observed increased risks for testicular cancer in families that may have underlying cancer predisposition. And so that's something. Again, it's one paper, but it's saying that maybe there's a broader predisposition to cancer. And that suggests that there might be a mechanism. I don't think it's the ribosomes, but something that is kind of global like that, that might be able to affect multiple organs. Because if you have, in a family, an aunt and a brother and a great-grandma who all have these different types of cancer. And you see that that is associated with testicular cancer. That suggests that there's something that is a general mechanism. That's another avenue of research is determining whether the cancer predisposition for testicular cancer is broader than what happens in testis.

 

JOYCE: Interesting, because I have that kind of family background. All of my aunts and my birth mother all had some kind of cancer. Boy, another thing to just think about and maybe learn more, just in terms of my own background. Anything else on your studies or hypotheses that we should know?

 

CHARLEEN: Well, the only thing else that's really coming to mind for me right now is it gets more molecular. But one thing I mentioned with marijuana is that it's possibly an endocrine disruptor. And so when we think about something that's going to mess with your endocrine system, how could that possibly do that? So we have what we call molecular mechanisms or something that may be the way in which an exposure has an endocrine-disrupting effect that might be through these molecular mechanisms.

 

JOYCE: In our previous conversations, you've brought up something that is a potential endocrine disruptor. And so I don't know. These are those, I hesitate to try to say this, but I'm going to try. So these per- and polyfluoroalkyl substances.

 

CHARLEEN: The PFAs, yes. Yes, the PFAs. So these are ubiquitous synthetic chemicals that have been around since the 1940s. They're used in industrial manufacturing and in household products. And when we say ubiquitous, this is because a lot of our products have them. Most people, if they're tested in the US, will have some of these in their bodies. We know that diet, water, household products, food packaging, all of these are potential sources of these chemicals. And there's a group of people that over in France called the International Agency for Research on Cancer. And what they do is set the kind of global standards for what is considered to be a carcinogen. So they classify different exposures into whether we think they are or aren't a carcinogen. And they classify these PFAS as being possibly carcinogens, which means that there's some evidence that they may be, but we don't, again, they don't have definitive evidence. What we've seen is that they're possibly endocrine disruptors that increase the risk for disorders in males that start early in life, including undescended testes.

 

JOYCE: Wow. Yeah, and I read several articles about it. It's one of those chemicals. I mean, it's out there and it's something we weren't aware of. And to our discussion about the different research papers that are out there, hopefully there'll be some more study into this and its relationship, if there is one, to testicular cancer. But I think one of the articles I read and I mentioned to you was a young man in Ohio who had testicular cancer twice, I think, and they thought [it was] related to this. Also, there's been another area of Ohio that they're studying for this appearance of this chemical or this compound, I think in the water.

 

CHARLEEN: People are aware of it, that’s right. I had read the study that was done in the mid-Ohio Valley near a chemical plant where drinking water was contaminated with this. And so the authors in this case were interested in cancers generally, but they had an a priori hypothesis that they would see a particular increased risk for testicular cancer. And this comes from some animal studies where they'd seen that some of these chemicals can impair testosterone production.

 

JOYCE: Oh wow, okay.

 

CHARLEEN: Yes, and induce some Leydig cell tumors in rats. And they had this knowledge from what they'd seen in animals. So when they were wanting to know whether the people who lived near this chemical plant, if there was an increased risk in cancer for them, they were particularly interested in whether they would see more testicular cancer. And in fact, they did. So that's pretty suggestive evidence. This is currently being studied at the National Cancer Institute. They're looking at this, a big study, in relation to contaminated water with PFAS. In particular, it appears that the firefighting foams are emitters of some of these that then gets into water. So what they're looking at are military sites that, and I'm not sure why military sites in particular, but it may be that maybe, maybe military sites are more, I don't know, maybe they use more of these products as possible. They've got a Department of Defense study, where they're looking at whether military personnel are exposed to PFAS through water. And they've got a case control study on this that's underway. So I think there's going to be some interesting results that come out from that. But I don't know if they're still at the quantifying stage or if they're still collecting data. So I don't know how long that'll be. But it's hopeful that they'll have It'll be informative.

 

 

[marker]

 

JOYCE: Right. It sounds like it, because that's a lot of different people. I mean, populations of people in the military and firefighters and young men. So I mean, it'll be something worth watching.

 

So as we talk about [these] things, going back to testicular cancer, just from your perspective as a researcher in this area, do you have any thoughts on what people should be aware of around tests? I mean, general thoughts. You know, a young man with testicular cancer, family, caregivers, any thoughts about things to think about or be aware of?

 

CHARLEEN: You know, I think that's an important question. As I was preparing for this podcast, this is about a month ago, maybe a month and a half ago, I put a question out there to the Twitterverse, to people on Twitter to see a poll, just to see if anybody knew what the risk factors were for testicular cancer, or if people even knew that it impacted younger men. What I got back from that is, first of all, most people know nothing about it.

 

JOYCE: I think that's interesting, and I agree with you based on the people I've talked to. They don't know anything about it.

 

CHARLEEN: They don't know anything about it. Whereas, in contrast, if you ask people about prostate cancer, you know, people will generally have more to say about that. So, people don't know that this is something that happens to young men. Generally, people don't know, and they don't know about the undescended testis. That it seems so obvious maybe to you and I, you know, but for people that have no reason to be thinking about it--aren't thinking about it, I think that just continuing to have some public education, that this is something that happens to young men.

 

JOYCE: Yeah, I think so too. I know some of the survivors I've talked to were like, oh, we knew nothing about this when I found a lump on my testicle or whatever. I guess I want to say maybe that's true for all of us, but with different kinds of cancer. But yes, public education is very much needed. I would agree. So my last question, Charleen, is really about what's next for you and your research or just anything you're doing that you'd like to share with us.

 

CHARLEEN: Yeah, so I'm interested in cancer predisposition. And so, as we had said at one point earlier in the talk, this is throwing whatever at it that I have to throw at it. So right now I'm looking at ribosomes, but there's something called epigenetics that is one of those molecular mechanisms that I'm currently looking at. I'm going to continue to look at both the heritable genetic components, but then how that interacts with the environmentals. And those environmentals being, you know—with some of them, trying to figure out how much evidence there is, like with marijuana for testicular cancer. That seems such a broad answer to the question, but I'm at this point where my general goal is to continue with the molecular mechanisms.

 

Speaking of luck, there's some part of being a scientist where you end up going with the flow of things. Right now, I'm looking at the ribosomes and aging. How that morphs into the future is hard to say, because it depends on, will we get a grant in this? So your research ends up as, you follow the trail of grants. It's a combination of those sorts of things. I can say that talking to you has reinvigorated my interest in exposures that happen early on in life.

 

JOYCE: Okay, well, we'll have you back to talk about that. I think it's so interesting. I think your perspective helped me a lot to understand some of the dynamics of cancer, and I think for some of our listeners too, because we talk a lot about survivorship or with survivors, but I think getting down into why it's there is really important to know as well. So I thank you for taking the time to do this with me.

 

CHARLEEN: Thank you so much, and I think that your podcast is very important for the world and education and getting knowledge out there. And for survivors, but also for researchers, because the more that we interact with families, the more that it becomes real and gives us to think more about the mechanisms. Because it's very much like being a chaplain where you face the situation: where there's this unknown, and how to fix it. I admire what you're doing. Well, thank you.

 

JOYCE: I really appreciate those kind words, Charleen. And I think it's a good way to end our program. And I did mean it. I would love to have you come back sometime down the road with some more insights for us. So thank you.

 

CHARLEEN: Great. I would be happy to. Thank you, too.

 

JOYCE: Thank you for joining me today on Don't Give Up on Testicular Cancer from the Max Mallory Foundation. Go to maxmalloryfoundation.com to learn more about testicular cancer, to donate, and send your suggestions for guests on the podcast. And join me next time for Don't Give Up on Testicular Cancer.




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