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From the “guardian of the genome” P53 gene to breakthrough therapies targeting cancer cells, this episode explores science, resilience, and hope. Plus, a powerful personal journey from diagnosis to advocacy with The Brain Tumour Charity.
Listen now and discover why understanding the brain could unlock life-saving treatments.
CONOR: Welcome to Discovery Matters everyone. I'm Conor McKechnie.
DODI: And I'm Dodi Axelson. Today's episode is gonna be a heavy duty one. We're gonna take you inside the world of brain tumor research and well, besides just being heavy, it's also fascinating because there's mystery, there's complexity, and some incredible and inspiring people working tirelessly behind the scenes.
CONOR: We'll be hearing from a researcher whose story is one of curiosity, passion, and frankly scientific serendipity that we're so familiar with coming all along the way.
VERONICA: We talk about cancer as one disease, but it's really hundreds of diseases that have been compiled into the same term. The brain is a very complex organ and up to this point, we're still discovering new cell types in the brain and their functions through state-of-the-art technology.
DODI: Plus, we'll explore work on the legendary guardian of the genome, the P53 gene, which could help unlock new treatments. And we'll hear why compounds targeting proteins might hold the key to killing cancer cells without harming the healthy ones.
CONOR: And because research never happens in a vacuum, we will also hear a powerful personal story from someone we know and love who is living with an inoperable brain tumor and hear about the support that she has received from organizations like the Brain Tumour Charity in the UK.
SOPHIE: Only by understanding what's happening, can we develop solutions and medicines and ways to help people live with or even cure brain tumors.
DODI: That is what matters on today's episode of Discovery Matters.
THEME TUNE
VERONICA: So my name is Veronica Rendo. I'm a group leader working with Brain Tumor Research here at The Rudbeck lab.
DODI: Originally Veronica, comes from South America.
CONOR: How did Veronica end up working with Brain Tumor Research in Uppsala in Sweden of all places.
DODI: Well, I did ask her if she came to Sweden for the sunshine and the cheap beer.
CONOR: That's definitely not the reason.
DODI: Not the reason at all. But she arrived in Sweden much in the same way I did many, many moons ago.
VERONICA: I'm more originally from Venezuela. And then came to Sweden as an exchange student and then one year became many years.
CONOR: Okay. An exchange student. I'm not sure if our audience knows that about your past, your exchange student past.
DODI: Nor do they really need to.
CONOR: Okay. So shall we skip the anecdote about how you washed up on the shores of Sweden?
DODI: We'll do that.
CONOR: So now we know what brought you both to Sweden specifically, but what exactly brought Veronica into the field of brain tumors?
DODI: She started off studying biology.
VERONICA: Always genuinely interested in how cells coordinate themselves to exert multiple functions in our body and how those processes are affected with disease. I remember taking a course from a very talented teacher I had in Venezuela about cancer genetics, and I just became fascinated by how all these processes and cells become altered and how these cancer cells always find a way to evolve in a timeline of months or years as compared to millions of years, right? Like we get to know from like Darwin and so on, and they become resistant to treatment and they like escape all the therapeutic approaches that that have been tried so far. So I think that really stuck to me as a biologist.
CONOR: You can hear the passion in her voice for this, can't you?
DODI: Mm-hmm.
CONOR: It sounds almost as if she has some kind of intellectual admiration for cancer cells because of their resilience, and I found that in many researchers, actually.
DODI: Yes, I very own Daria Donati.
CONOR: Exactly.
DODI: She just loves the way they are determined to live.
CONOR: Mm-hmm.
DODI: And there is admiration.
CONOR: Yeah.
VERONICA: Don't get me wrong, it's a incredibly devastating disease, and we're all either affected by it or have a loved one affected by it. I think the current statistics is like one in two will get diagnosed with some cancer around their lifetime, but from a biological perspectives, like getting understanding of those processes and integrating different disciplines to then see how we can hit them hard to disrupt them and be able to cure the disease has been really a research interest of mine for many years.
DODI: You know, for all her passion and interest in the field. Brain cancer research specifically was just not her original field.
VERONICA: Yes, I did my PhD working with colorectal cancer, which is one of the most common types of cancer that is diagnosed in adults worldwide, and I was really looking at this disease from a genetic perspective, so I was trying to understand what are the genetic alterations that happen in colorectal cancer cells as they progress and become aggressive and what makes them different from normal cells in the colon, in this case, but in the rest of the body, and how we could exploit that knowledge for therapeutic purposes.
DODI: Veronica discovered an enzyme that is present in colorectal cancer cells but absent in normal cells, and that meant they could develop compounds that specifically target the cancer cells and make them toxic to only those cells.
VERONICA: The normal cells in the body could detoxify, but they could, colon cancer cells could not, and then they would die.
DODI: After this, Veronica went to a conference in the US to present her research, and there she met other groups that had been thinking about similar approaches to hers, but in different cancer types.
VERONICA: And among one of these cancer types was brain tumors. So I met with these groups and then later I had the incredibly welcome pleasure to join one of these teams in Boston and continue my journey there in the context of brain tumors. And I encounter here biology that is related to a gene called p53, which is now a big focus of my research.
CONOR: Aha, the famous p53 gene, I know about this one. It's essentially the built in cell police. It stops damaged cells from becoming cancerous. Is that right?
DODI: That's right. And Veronica told me that it has been termed the guardian of the genome.
CONOR: I feel a Marvel movie coming on here, don't you?
DODI: I do too.
CONOR: Mm-hmm.
VERONICA: So when you have a cellular stress that can either come from inside the cell. Or externally, for example, DNA damage that is caused from radiation. When we treat our body, this gene is able to tell the cell, okay, we have DNA damage that we need to repair. Can we do this? Yes. Okay. Cells should stop growing. Can we not repair this? Okay, the cells should die. Under different mechanisms, and the one that we start is called apoptosis. So it's really a key regulator of what happens, what's the fate of a cell when we have this kind of stress. And of course you can imagine that a protein that has such a key function wants to be hijacked by cancer cells because cancer cells want to keep growing and dividing no matter what.
DODI: Veronica said that as you look at many cancer types, take for example, ovarian cancer, then you can see that in 95% of the tumors there is always a genetic mutation inactivating p53.
CONOR: Essentially defunding the police.
DODI: That's right.
CONOR: And shutting down its functions.
DODI: That's exactly right. But in the context of brain tumors, actually half of them retained the p53 police function.
VERONICA: And we thought this would represent a unique opportunity to then make use of compounds that enhance the effect of this protein that remains functional and active in the body so that we can really go and kill cancer cells.
CONOR: She's sending in the backup.
DODI: Yes.
VERONICA: And the way that backup looks is you have p53, but then there are other proteins. One of them is called, for example, MDM2, which suppress p53 function. And the way they do that is by physically binding to the protein, so it's not able to exert it's roll in the cell. So there are compounds now that disrupt the protein-protein interaction between p53 and these negative regulators, in this case, MDM2, so that then MDM2 keeps bound to this drug It can no longer suppress p53. While p53 is then liberated and it can exert its function in the cell.
DODI: As interesting as all of this is, I think sometimes when we talk about genes, protein interactions and cells and things like this, we often lose sight or forget that there are people behind this, all real patients, those who are affected by the very tumor that Veronica is working so hard to research. And so let's leave Veronica for a moment with her eye to a microscope studying a p53 gene and head to London to hear from a colleague of ours, Conor.
CONOR: Yes, let's do that. Let's check in with our own communications teammate. Sophie White.
DODI: As you and I know, but the listener won’t, a few years back, Sophie started noticing that something was off with her body.
SOPHIE: I thought what I initially had was a gym injury, which I then didn't go away and didn't get better. And I was feeling really tired, thought that was to do with work. Eventually ended up speaking to a doctor on the phone. When she heard my voice, she said that I needed to go to A&E, which I was quite shocked about.
DODI: And this is just, this is really hard to listen back to.
CONOR: Mm-hmm. I can imagine.
DODI: For the whole team, of course for Sophie, but also for the whole communications team, this became just an unforgettable trauma, but there's victory at the end and it's a glorious story. So let's, let's get on with Sophie's story. So, once at the accident, an emergency ward of her local hospital, the doctors performed a CT scan of her brain and they could see a mass near her brainstem. And let's just let Sophie tell the rest here.
SOPHIE: So at that point they tell you that you've got a tumor, but they don't know what type it is. Then everything moved quite quickly from there. I had surgery to have a biopsy to determine what brain tumor type it was. I also had procedure to drain some of the fluids that had built up near the tumor. I had to wait for weeks for the results of that biopsy, and really the waiting is one of the worst parts of the experience. And then I found out that it's high grade and it's inoperable. So we need to act very quickly to minimize the effects it might have on me. I go on to have radiotherapy directed at the point of the tumor and chemotherapy to attack it in a different way. My symptoms then start to get worse again. I'm struggling with walking now. And my speech is even worse. The doctors, they order a second surgery this time to put a shunt into my brain, so that means they can drain fluid and continue to drain it if it builds up again. They're not doing anything with the brain tumor because it's inoperable. It's too dangerous where it is, but I wake up from that second operation and I just feel dramatically better. So my speech is as it is now completely clear, I'd have an hour-long conversation with a friend over the phone, which I just wasn't able to do before. So it was like a miracle of going back to pre any symptoms coming on. That was amazing, and almost back to normal walking again, but knowing that the tumor is still there and that it's incurable obviously leaves then an emotional challenge to overcome, to live alongside the uncertainty that these kind of conditions can bring. And I'm fortunate in that since then my tumor has remained stable and I've been able to get back to normal life, enjoying my hobbies, but having to still live alongside the uncertainty that it might come back and it might progress.
CONOR: When you hear personal stories like Sophie's, it is very hard to imagine how you would act yourself in the same situation, and you find this difficult relationship with the story being, could I, would I? But you only have one choice, which is to be brave and move forward. I don't know how well or otherwise people feel about being told that their stories are inspirational, but you can only hope that you could act the same way.
SOPHIE: I don't see it as a strength or being brave or any of those things. I just think that people acting in different ways when they get presented with a health challenge and no way is right or wrong. So my way of coping with it is to be open about it.
DODI: Part of Sophie's openness included starting a social media account online. This was a huge step for Sophie, who is an introvert, right?
CONOR: Indeed.
DODI: I mean, she does not call attention to her, to herself, but she opened this social media account called The Brain Babe, please do follow the Brain Babe, on social media, and she was filming herself and she's been sharing her treatment and sharing her story, and sharing her fundraising efforts.
SOPHIE: So before when I set up an account to share my story was the idea of sharing what I wanted to share with the people who cared about me. Share those updates, but I didn't realize that actually a lot of people in my, my loose ties in my outer network would actually care as well. So I was really surprised to see a bit of a following build and people engaging with what I posted. And then that really led on to me thinking what to do with this. And so I set a lofty goal of raising 10,000 pounds for the Brain Tumour Charity.
DODI: The Brain Tumour Charity is a UK based organization. It funds research, spreads awareness works to speed up diagnoses, and offers support and information to people like Sophie who are affected by brain tumors. And they also support the loved ones of the patients.
SOPHIE: I wasn't aware of the Brain Tumour Charity before I got diagnosed. These organizations are often sought out when people need them, so getting closer to the charity. Since I was diagnosed, I realized they're the largest funder of research into brain tumors globally.
DODI: So there was Sophie taking power of her diagnosis and sharing her story online in regular social media posts as she went in and out of hospital, getting more and more and involved with the Brain Tumour Charity, which often included public events.
SOPHIE: I went to an event where I met researchers that were working on brain tumors, and the one that I was paired with was Veronica.
DODI: That Veronica. And now we're coming full circle. We heard from Veronica Rendo earlier on in this episode. Let's bring her back.
VERONICA: So. My first contact with the Brain Tumour Charity in the UK came ironically through my postdoctoral training in the US because I received funding to pursue my work there. And my research project at the time was to evaluate the use of MDM2 inhibitors in a phase one clinical trial in adults diagnosed with glioblastoma. So we essentially were tasked to understand, does this m inhibitor cross the blood-brain barrier, which is a natural mechanism that we all have evolved to protect our brains from virus and bacterial infection. So we wanted to know if this compound could cross that sort of filter that protects our brain and exert a function on the brain tumor cells.
DODI: Veronica says that she and her team got really encouraging results, which they then shared with the scientific community and platforms like the Brain Tumour Charity, which has been so important to our Sophie.
VERONICA: And from a scientific perspective, I think this results really motivated us to see. Whether there were other brain tumor types beyond glioblastoma that not only affect adults, but also young adolescents and children where we could apply this treatment with MDM2 inhibitors, and by interacting with the Brain Tumour Charity, you really get an aha moment in the sense of weight. This is just not devising, coming up with a drug that kills cells for killing cells, but at the end of the day, this is gonna be used to treat a person, so we need to define biomarkers, right? Which alteration needs to be present in a patient at the time of diagnosis that will allow the clinician to make an informed decision whether you will benefit or not from enrolling in a clinical trial where we test a treatment of interest. Toxicity, it's also something that perhaps not everyone in the lab bench thinks about because when you're doing your experiments, you kill cells, and that's it.
CONOR: Okay, but how does this actually affect the brain? Is Veronica also killing normal cells in the brain at the same time as she's killing cancer cells?
VERONICA: So I think these kind of interactions have really allowed us to think about these components already at early stages of devising treatment combinations and approaches that synergize with standard of care with radiation chemotherapy, to really put not only the best treatment suggestions forward, but also the ones that are safest and have the less toxicity.
CONOR: It must be really difficult and risky trying to work out which genes to amplify or send backup for and which ones to turn off and inhibit and not allow. So, how does Veronica manage, like what we know is real complexity, it's called off-target effects when she's arranging for a clinical trial or in her research?
VERONICA: From the research side, really what we try to do is we try to evaluate, in this case, the effects of treatment in a panel of as many models as we can. For example, we have patient derived cell lines that once upon a time came from a patient's biopsy that then were cultured in the lab and we try to test our combinations and profile sensitivity of as many cells as possible. So for example, for MDM2 inhibitors, we have really looked at over 50 cell line models that are derived from patients both with adult and pediatric disease. Then when it comes to trying to understand the toxicity and the treatments, and if these things like translate into models of larger biological complexity. We're doing work in a model that really excites me, which is called assembloids, where you can essentially take cancer cells and put them in contact with brain organoids.
CONOR: Basically mini brains grown in the lab.
DODI: Organoids.
CONOR: It's another favorite topic. We can, of course, go into how this is the origin of the name of Cytiva, but we won’t. Let's stick with Veronica.
VERONICA: And this is a model that allows you to study not only how the cancer cells invade the normal brain, but also assess what are defects of a treatment of interest, not only in the cancer cells, but also in the normal brain compartment. And this allows to understand, okay, do we have what we call a therapeutic window? Are we killing cancer cells more than we're killing the normal cells? So in terms of knowing which genetic alterations we can turn on and off, I think this is a very important step, and then we still use a lot of animal modeling where we can go and inject these cancer cells in the brain of a mouse, for example, and then see what the effects of the treatment are in terms of tumor growth and survival.
CONOR: Am I right in thinking we're still a way from actually unleashing these experiments for humans? Is that right?
VERONICA: Yes, and there's an incredibly heterogeneity that we see in patients like not only like you can zoom in into the same brain tumor of one patient, and you'll see that there are coexisting cells with different molecular alterations. So of course that means one treatment will not kill all of those cancer cells that are so different. But then also when you compare patients diagnosed with the same brain tumor across each other, they can also look very different. And then we also have to bring in the component that this is a rare disease compared to other cancer types. To your initial point, you really have to join forces to have enough models and enough understanding of the disease to make sure that you can come up with treatments that are relevant.
CONOR: Can we get back to organoids though? You know how much I love them, these tiny little, little organs in a dish. They're just so incredible. And I'm wondering why would we still need animal experiments? What are the pros and cons of organoids as being the only path? Why do they just form part of the path?
DODI: Yeah, Veronica and I spent some good time talking about that, beause I wondered the same thing, Conor. She said there are different models that can be used to answer biological questions and there are just advantages and disadvantages either way.
VERONICA: Something very exciting with the organoids is that of course you can have in the lab are representation of an organ. In this case the brain, and you can start modeling how tumor cells invade, they become aggressive, how they do this, what are like the molecular processes behind that. You can assess treatment effects as I was exemplifying with these MDM2 inhibitors. But we're still at a point where we're a bit limited in terms of which cell types and interactions we can study. So for example, traditional brain organoids are lacking vasculature. They're lacking components of the immune system that maybe if you would go and study these in an immunocompetent mouse, you would get a much better answer. At the same time, organs are expensive to generate, but you get results quicker. So I think at the end of the day, it really depends on which biological question you wanna answer. But so far, I think it's really an integration of the models that gives you true power to understand how your treatment is working.
SOPHIE: There's over 120 different types of brain tumor and there vary in terms of grades from grade one up until grade four.
DODI: That's our Sophie again. Today, she lives with an inoperable brain tumor and, you know her, Conor, she's really amazing. She's working full-time again and just doing excellent work as she always has.
CONOR: She just cracks on.
DODI: Yeah.
CONOR: Absolutely.
DODI: The fact remains, however, that the brain and brain tumors are still surrounded in such mystery. And for Sophie, the only way she sees this mystery being solved is through research, research and more research.
SOPHIE: I would hope that firstly, the researchers who choose to go into studying brain tumors stay in that field. We know that it's underfunded compared to other disease areas. I hope that they discover how brain tumors work how they, how they progress. Because only by understanding what's happening can we develop solutions and medicines and ways to help people live with or even cure brain tumors.
DODI: And Veronica Rendo, whom Sophie met at a Brain Tumour Charity event, is one of the researchers working tirelessly to solve this mystery.
VERONICA: So the brain is a very complex organ, and up to this point, we're still discovering new cell types in the brain and their functions through state-of-the-art technology, such as imaging, through high resolution microscopes and so on. I think that in terms of cancer, we've done a pretty good job of understanding what causes different brain tumors. We also know that brain tumors can grow in different ways and some grow what we call diffusely. So imagine like a spider web. So it's really hard. To go into an organ where every little bit matters for coordinating essential functions in life and trying to resect that mass. It's not possible sometimes. So this means that in contrast to other cancer types, where we have seen tremendous advances in precision medicine, in immunotherapy, in viral gene therapies, here we’re mostly limited to radiation and chemotherapy to try to kill those cells. But of course these approaches are not selective to cancer cells, so then you end up with tremendous side effects and toxicity also affecting the healthy body.
CONOR: Veronica is talking here about a kind of cancer that is both very complex and very high risk.
DODI: The riskiest of the risky.
CONOR: Not even that, it's also rare, the rarest of the rare and the most expensive to treat. What keeps us going and not giving up?
VERONICA: I think for me, the opportunity to have been in close contact with brain tumor survival and advocates and understand what this means for themselves, their families moving on with their lives, has really given me inspiration to try to make a difference in a population of patients that are in desperate need for better treatment options. So I think that's what keeps us going, and then, from a scientific perspective, I have to say that because as you mentioned, this is a rare tumor type, you really need an international community of preclinical and clinical researchers joining forces so that we can really integrate our scientific outputs, device, ways to generate more models and rejoin forces to test our treatments in a safe way. So I think that has been as a researcher at an early stage of my career, very inspiring to see really how you need to come together to enable each step of the way.
DODI: This hard work is starting to pay off.
VERONICA: So I was incredibly lucky to participate in a phase one clinical trial where we studied the effect of these MDM2 inhibitors in patients with glioblastoma, so in adults. And the goal of this study was to understand if this inhibitor had blood-brain barrier penetrance, it could cross permit into the brain and exert effect, and we were able to demonstrate that it has the potency and capacity to do, even though it cannot do its job alone. It's not sufficient as a single agent to fully kill the tumor cells. So we know that we need to combine it with something else, and that's what we're trying to figure out in the lab. And that's something else is very dependent on which brain tumor type we're studying. So now we have really exciting projects where we have looked at brain tumors that occur in children that can also benefit from this approach. And we have generated data in the last two years that suggests what we can combine this inhibitor. And luckily we have compounds that are clinically relevant that we know can cross the blood brain barrier and can be studied. So now we're doing all the work in the models I describe in the patient derived cell lines, in the assembloids, in mouse models to try to validate that these combinations can actually kill the brain tumor cells. So I'm very hopeful for the five years to come.
CONOR: That is an extraordinary journey. Today, we've learned so much starting with how Veronica's early fascination with biology and cancer genetics eventually led her into the world of brain tumor research.
DODI: We heard how cancer cells can hijack key systems like p53, the body's own cellular police force, and how scientists like Veronica try to send in backup using new compounds that help p53 fight back against tumor growth.
CONOR: And we also explored the sheer complexity that researchers face from working with patient derived cells and organoids essential pieces of the puzzle in understanding how treatments might work safely in the future in the human brain.
DODI: And Sophie's story reminded us why all this research matters. Behind every gene, every protein, every experiment, there are real people, real lives, and real families navigating the uncertainty of a brain tumor diagnosis.
CONOR: And Sophie's openness, her positivity and determination from sharing her journey online. Follow the Brain Babe to raise money for the Brain Tumour Charity. Just show what a powerful patient voice can do to help drive change and drive research.
DODI: And hearing how Veronica's work is already moving into clinical trials gives us real hope the next five years hold exciting possibilities. Smarter drug combinations, more precise treatments, maybe even breakthroughs for children and adults with rare and aggressive brain tumors.
CONOR: That's what I take away from today. Curiosity sparks research.
DODI: Yep.
CONOR: Research drives progress.
DODI: Yep.
CONOR: And progress gives patients a fighting chance.
DODI: Oh yeah.
CONOR: And now it's time for every day as a school day. You know how you have a dog.
DODI: Oh my God. I'm doing doing a dog story too. Alright, what's your dog story?
CONOR: Mmine is not quite a dog story, but we both have dogs.
DODI: Yes.
CONOR: And we all...
DODI: And we love them more than any other creature on the planet.
CONOR: It's ridiculous.
DODI: Yeah.
CONOR: Well, what's super interesting is how dogs and wolves don't look the same. And this idea that dogs have evolved to look and be perceived by their humans –
DODI: Yeah.
CONOR: – is not just something that's happened in dogs.
DODI: Accidentally. This is my story too. We learned the same thing. I love this.
CONOR: Is it the raccoon story?
DODI: Let's do it. No, no. It's not. Okay. All right. You go.
CONOR: Oh my goodness.
DODI: Keep going.
CONOR: So, raccoons appear to be showing early signs of domestication. City dwelling raccoons are evolving shorter snouts, something that happens to dogs or happened to dogs and other domesticated animals, and their cheeky little masks and their little childlike hands.
DODI: Wow.
CONOR: They are becoming more human-y friendly type, looky likey. There's gotta be a scientific word for that, but there's a study that shows that there is a case for the domestication process. Not being initiated by humans, but by actually the raccoons capturing humans themselves and evolving slowly to become more habituated to human environments and looking more like animals that are domesticated.
DODI: And that short snout that's key because supposedly humans find that cuter.
CONOR: It's cuter.
DODI: Yeah.
CONOR: And it drives what's called a selection pressure.
DODI: Oh god.
CONOR: And that selection pressure is super intense. So proto dogs, pre-dog dogs that would've been wolves, may have dug through human trash heaps exactly the same as raccoons do and over time, the individual animals that had a reduced fight or flight response would feed more successfully around humans, and they would pass that non-reactive behavior onto their offspring. And that drives tameness and that appears to be happening in raccoons.
DODI: My goodness. Okay, well my dog story is from nature.com. It's also about the shape of skulls, and this was 11,000 years ago. Humans were already shaping the future of dogs, so researchers studied over 600 skulls and genomes from dogs up to 10,000 years old. Some really ancient skulls there, finding that dog-like skulls appeared around the end of the Ice Age. So size and shape. Diversity exploded soon after the Ice Age, meaning early humans were not just taming wolves, they were selectively breeding and trading dogs across regions. To hunt, guard and be their best pals.
CONOR: So effectively teaching old dogs new tricks.
DODI: Exactly.
CONOR: I couldn't resist. Sorry.
DODI: Exactly. Oh, I love that we both had dog stories this week.
CONOR: I miss my dog when I'm traveling. Oh. I mean, I miss my family too, but you know, there is a special welcome home when you get jumped on by your dog.
DODI: So Peter Barker on this, on this trip? Lars made pizza, and we left the pizza on the table and Peter helped himself to pizza. And I think he was mad because he saw my suitcase out.
CONOR: So he ate your pizza?
DODI: He ate the pizza.
CONOR: There you go.
DODI: Terrible, Peter Barker.
CONOR: My name is Conor McKechnie. If you'd like to get in touch with us, write to Discovery.matters@cytiva.com. Our producer, mixer, and very patient sound magician is Tom Henley.
DODI: I am Dodi Axelson. Please do give us a rating on Spotify or wherever you choose to listen to this podcast from. Thank you so much for listening to Discovery Matters brought to you by Cytiva.