In Episode 2 of In Plain English, presenter Gloria Marino and guests Teodora Stoica and Jacob Walker discuss the paper “Tumor Microenvironment Components: Allies of Cancer Progression” by Pablo Igor Ribeiro Franco et. al. They discuss the ways in which cancer cells can modify their environment to grow, multiply, and spread; the importance of individualized medicine for cancer treatment, and why equitable access to healthcare may be our best tool in the fight against cancer.
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Episode Transcript
[Intro music]
Jamie Moffa: Welcome to In Plain English, a podcast where we discuss scientific research in terms that are accessible to everyone, not just the experts. I’m your host, Jamie Moffa. Before we get started with today’s episode, a few reminders. You can download the paper for each episode at inplainenglishpod.org by clicking on the episodes link in the main menu. You can also listen to previous episodes there. We believe in open access science for all, so the papers we choose will always be free for you to download. If you have a question or comment about a previous article, you can submit it under the Continue the Conversation tab. In future episodes, we will begin by reading and responding to some of the questions and comments that you send in. If you are interested in being a guest or presenter for a future episode, you can click on the Become a Guest tab on the website. You can also reach out to us on Facebook or Twitter @plainenglishsi, that’s P-L-A-I-N-E-N-G-L-I-S-H-S-C-I. To listen to this podcast, you can find us on Google Podcasts, Spotify, SoundCloud, or wherever you listen to podcasts. With that out of the way, on to today’s paper.
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JM: On today’s episode, we will be talking about cancer, specifically all of the stuff that surrounds cancer cells and helps them to grow, survive, and spread. Our expert presenting today’s paper is Gloria Marino. Gloria, would you like to introduce yourself?
Gloria Marino: Sure. Thanks for having me, Jamie. I’m super excited. So my name is Gloria. I am starting my fifth year of my PhD program. I’m in the Biochemistry and Molecular Biology program at Johns Hopkins University. I study cancer, as is probably obvious. Specifically, I study melanoma, which is the type of skin cancer, and how the environment around melanoma, our skin, changes as we get older. And then how those changes as we get older contribute to differences in how old versus young people survive and adapt to having melanoma.
JM: Great. Thanks, Gloria. And joining Gloria for this discussion are our two guests for this episode, Teodora Stoica and Jacob Walker. Teodora, Jacob, would you each like to briefly introduce yourselves?
Teodora Stoica: So my name’s Teodora. I’m a postdoc researcher at University of Arizona, and I’m looking at how brain networks change as we age.
Jacob Walker: And my name is Jacob Walker. I am a political activist, organizer, and I have started a nonprofit, among many other things. And right now I’m studying for the law school, and I’m here on the podcast to be the person that doesn’t know a lot about the subject. So I’m excited to learn from people that are here. I’m really excited to be here. Thanks for having me, Jamie.
JM: Yeah. Thanks, everyone, for being on this second ever episode. And without further ado, Gloria, would you like to take it away with an introduction of the paper we’re going to be talking about?
GM: Sure. So today we are doing a literature review as our paper. So a literature review is a little bit different than a traditional scientific paper, in that normally a scientific paper is very data focused. So lots of graphs, lots of charts and pictures. Whereas a literature review is kind of what it sounds like. So it’s much more where somebody takes a topic, a scientific topic, and they will summarize sort of what we know about this topic. And in a literature review, they will cite many, many, many different data papers to just kind of give us an idea of a whole particular field, or something even very, very specific. So in this case, we are talking about a paper that’s near and dear to my heart. It is called “Tumor Microenvironment Components, Allies of Cancer Progression.” So we’re really talking about the tumor microenvironment today, which is a really cool and important topic that doesn’t get a lot of love in the cancer field, but really should and is sort of changing how we treat cancer. The tumor microenvironment is kind of a good name because it’s really sort of what it sounds like. It is the small environment that surrounds whatever a tumor is in our body. So as I sort of mentioned, I study melanoma. And the microenvironment of melanoma, since it’s skin cancer, is the skin. And then kind of similarly for lung cancer, we think about the environment being the lung and everything that’s around it. And what’s important is that these environments contribute to how cancer grows. I like to say that tumors don’t exist in a vacuum, tumors exist kind of in mesh. They exist in 3D. They exist in a specific place, in a physical place. And that place has a lot of different components and a lot of different things that kind of cause cancer to change, spread, adapt, all these different things.
And so just kind of like as a brief story time of kind of the history of how we got here: kind of back, you know, way back when we think about how we study cancer, a lot of it is just based on the tumor itself, right? What does the tumor look like? What are the cancer cells doing? And how do we stop it? And that is all very important. But if we kind of start to think about, you know, we’ll say the mid-1800s, 1858, to be exact, this very, very smart man named Rudolph Virchow started noticing that cancer would often pop up in places that had chronic inflammation. And chronic inflammation basically means anywhere where immune cells are a lot. So when we think of inflammation, we think of when we get like a cut, and it gets all kind of red and inflamed. That’s what we’re talking about. They can be anywhere in your body. So he noticed, he’s like, “hmm, it seems like cancer pops up a lot here. Maybe, you know, where cancer pops up, or maybe when the environment is inflamed, it might cause cancer.” This was in the 1850s, so he didn’t really know. But he kind of, you know, planted the seeds.
Then in 1889, my good friend, Stephen Paget, he invented or kind of coined what is sort of become the tumor microenvironment field. So he coined what he called the seed and soil hypothesis. So seed and soil is interesting. What he basically did is, I think he was an MD, and if he wasn’t, he got a lot of cadavers somehow. So he basically noticed that women who had breast cancer, like very, very, very frequently, upon their death, he saw that upon autopsy that these women had cancer in their ovaries. And he was like, this is very weird, because if we’re thinking about tumors as just cancer cells, and cancer cells can move and spread basically indiscriminately, you would think that among these hundreds of women, we would see kind of a random pattern of where this cancer winds up, all these metastases. But no, like many of them, the majority of them, were in the ovaries. So that’s when he started thinking like, maybe the cancer seeds only grow in a specific soil and a specific tissue. So there is something sort of inherent about the tissue and inherent about the cancer cells that have to work together to grow.
And now today, we really kind of think of the tumor microenvironment as a really critical part of cancer. The last kind of historical thing I want to tell you is we’re going to fast forward to 2011. So 2011, Hardy Weinberg and Hanahan, they published this landmark paper, it’s got like a bazillion citations, one of the biggest in the field, and it was called the hallmarks of cancer. And they basically outlined all the things that have to happen in order for a cancer cell to be a cancer cell. And one of them is that it has to have these very specific and unorganized and detrimental interactions with this environment.
TS: Thanks, Gloria. I was wondering if you can talk about this really fun term that I highlighted in my reading of “replicative immortality?”
GM: So replicative immortality is this very, very sci-fi and scary thing about cancer cells is that our cells, our normal human cells that are not cancerous, they can only divide a certain number of times. And that number is relatively low, you know, somewhere between 40 and 70. But it’s pretty tightly regulated. And cell growth, if you kind of think about it, it doesn’t happen that much in our bodies. The only time cells really need to grow is if you get a cut or something and you kind of need to fill in that empty space or if you need to sort of make a bunch of immune cells if you’re sick. But other than that, our cells are just kind of at stasis and they sort of grow whenever they need to fill in. So because of that, we have this super strict limit on ourselves. The cancer cells bypass that and override it. So basically what they do is they just keep dividing and dividing and dividing forever. They are immortal cells. They never stop dividing.
TS: So why can’t we take this concept and live forever then?
GM: This is a great question, Theodora. Many before you have thought of this, but you’re right. No, you bring up a great point. Like if our cells are capable of dividing forever, why don’t we just do that then, right? The problem is, is that the reason that our cells don’t divide forever normally is because when our cells divide when they copy the DNA, there are errors. And the ends of your DNA don’t get copied all the way every time. It’s not very much, but there’s kind of like a slight mismatch where it doesn’t quite make it to the end. So you can imagine if you’re not replicating your entire genome every time and it starts getting shorter and shorter and shorter and shorter, it can start to get really bad really quickly. So our cells, luckily, have a fail-safe mechanism in place and they have these things called telomeres and they’re basically like taps kind of on the ends of our DNA and they’re just nonsense. Like it’s just a bunch of, you know, genomic bases. They don’t mean anything. They’re never transcribed, never used. And so we have these caps.
TS: Junk. They’re junk.
GM: Yes, we have taps of junk, but it’s good because that way every single time when the cell divides and gets shorter and shorter, we’re just losing junk and not anything important. So our cells know to stop dividing when we’re getting close to the end of the junk cap, basically. This is important because any time the cell starts to divide more than that, we are going to start to have problems very quickly. We’re going to start having a bunch of different gene mutations. We’re going to start losing gene function. And that is what happens in cancer cells. Cancer cells get mutated. They start losing, as they keep growing, they’re losing all these crazy gene functions and then they’re up-regulating stuff to kind of make up for it. So if we try and make ourselves live forever, we will just give ourselves cancer.
TS: I’m really bummed, Gloria. That’s all I got to tell you.
GM: I know.
JW: So as cool as replicative immortality is, or sounds, maybe not the best thing to have in you.
GM: If you have cells in you that are replicating forever, you have cancer. There is no cell in your body that if it is dividing uncontrolled is healthy.
JW: Generally a negative thing if that happens.
GM: Generally bad.
JW: Perfect. Okay.
GM: So we kind of think of cancer really as more of a disease classification as opposed to a specific thing. And so really cancer, quote unquote, the disease describes a disease where you have cells that are dividing out of control. And then that can be breast cancer. You have breast cancer. You have breast cells that are dividing. You have, you know, melanoma cells, you have liver cells, like the type of cell, but like the disease overarching describes the phenomenon of having cells inside you that won’t stop growing.
TS: On that line of thinking, you mentioned the soil hypothesis. So how come each particular way that cancer grows in particular parts of the body is different?
GM: That’s a great question. It’s a combination of things. So you’re starting with cells that are growing out of control, but they’re not growing out of control the same way question mark as other people. So let’s say person A and person B, they both come into the clinic, they both have brain cancer. That means that they both have a disease where some cell in their brain is dividing out of control. We have many different types of cells. So any one of those types of cells or cells from that you know, lineage could be the ones that are growing out of control. So that alone makes a difference. Let’s say that person A and person B, it’s the same cell type that’s growing out of control. There are a lot of different ways that a cell can lose its regulation in growing. And we usually like in the field, a common like, way to talk about it is sort of the gas and break. So you basically have genes that when they are on, they actually gas. So genes get turned on and they start the growth process. And then you also breaks. So you have genes get that gets turned on that stop growth. So you kind of have the start and stop genes. So you can get cancer one of two ways: you can either get a mutation in a gas gene where it’s always on, the foot is on the gas all the time, so no matter how much you try and hit the breaks, you are always going to be growing. Alternatively, you could also have a mutation in a gene that’s the break, and then the breaks don’t work anymore. So even though you’re only putting your foot on the gas, you know, as much as you normally would without breaks, you’re still growing. And there are multiple different genes that are gas and break, and you could have a mutation in any of those. And so, the odds of person A and person B having the same mutation in the same gene: very low. And then you want to add to that, you know, the specific microenvironment of their brain, you know, the—any sort of specific immune cells they have, you know, it’s very, very, very, very different. So that’s kind of why these things tend to manifest dramatically differently within people, even with the same quote unquote type of cancer.
JW: As I was reading this, I mean, I’m coming from a very different background from Teodora or Gloria or Jamie. So like, you know, I’m kind of like zooming out a little bit and understanding a decent amount of what’s in here. But also kind of like looking at what does this mean in like the larger context, and one of the things that jumps out to me really clearly is just the way we talk about cancer, especially in like the nonprofit space which I have worked in organizations that have worked along like organizations like the American Cancer Society. And it’s been in like healthcare advocacy capacities and stuff like that to like expand access to healthcare. And what is really interesting to me is: I think there’s a huge disconnect after talking to you, Gloria, and hearing like the initial start of this, and reading this article about how people think about cancer and what the reality actually is, because I think that there are a lot of people out there that are waiting for A Cure to Cancer, all capital letters. So I think that that’s kind of an interesting thing that jumped out to me. So I’m wondering like just what your take is on that because you have to see the fundraising that goes on with the American Cancer Society. And you have to see like, you have to notice even with talking to patients, the disconnect between like, what the science is showing: these micro environments are so important and that they’re very different, the different cancers are very, very different, versus what people’s like—the popular understanding of cancer. I’m just wondering what you think about that.
GM: No, it’s a great point and you’re totally right. I mean, I think sort of going back to the initial war on cancer, you know, mid-century, sort of the idea of that initial funding for “The War on Cancer” was that we’re going to find the magic bullet that is going to cure all cancer. No matter where it is, no matter who you are, all cancer. And sort of as you guys have seen, even just reading this article or talking about it, right, like, even the same type of cancer can be dramatically different between people, right? So I—the Cure for cancer with the capital C doesn’t exist because there just isn’t a one size fits all approach to this.
JW: I really think people would be so surprised to hear that. I mean, I think that that is very shocking.
TS: Yeah.
GM: You’re totally right, Jacob. Like, I think that if the magic bullet existed, we probably would have found it by now, especially with, you know, I think that people also get disappointed because they watch all this funding go into cancer research year after year after year, right? But I think really where we’re going or where the future is, which we’re sort of starting to see the beginnings of now, is personalized medicine for cancer. And I think a lot of different fields are sort of thinking about personalized medicine. But with cancer, specifically, because as we discussed, it’s just so different depending on who the person is, you really have to treat it person by person. And we’re trying to see the beginnings of that because tumor sequencing is happening now right like, you know, we’ve heard of triple negative breast cancer right? That triple negative basically refers to what receptors or what things are sticking off of cancer cells that we could possibly target. And the way that we figure that out is we basically take the tumor, we crush up a biopsy of it, and then we sequence the cells, and we figure out what the mutations are. And this is the case for a lot of different cancers because some cancers have common mutations. So, not all cancers but for example, in melanoma, there is a gene called b-Raf, and it’s a growth gene. And something like 60 to 70% of people who have melanoma have a mutation in this particular gene. So, we’ve been able to find a specific drug that targets that gene and basically put the break back on. And that has helped numerous people, right, but not everyone. Like you need to know if you have that mutation in order to see if this medicine is going to work for you.
We’re kind of I think I see us sort of at the very beginning, sort of like the infant part of personalized medicine with things like that. But I think going forward, once we get more sophisticated with the amount of drugs that we have and the amount of sequencing we’re able to do, I think you’ll probably be able to get like, this is your tumor person A, these are all your mutations, and we’re going to target this and this. And then if and when we see it recur, we’re going to re-sequence it and then we’re going to target, boom, boom, we’re going to target the new mutation.
TS: So, back, back to my original question, if you do all of that, can you live forever?
GM: You would probably live a lot longer, but I think that’s something else we’ll get you like—
TS: No I’m genuinely interested in the science, but I’ve heard so much about how, for example, CRISPR can, and you can talk about more about what that is, Gloria, but I’m sure that has to do with an advent of personalized medicine in cancer treatment. But at the same time, if you take all of what CRISPR can do, all right, so we’re going to edit our own genome, we can at least get rid of—not get rid of, but I guess make sure that cancer isn’t one of the things that makes us die.
GM: As far as CRISPR, CRISPR is a really interesting technology. So for, you know, any listeners and or—so Jacob, what do you know about CRISPR, not to put you on the spot, but just to get a pulse on this?
JW: I know of it as the thing that you put your vegetables into in the refrigerator and forget about them, or they freeze. So then, you know, related to health, because they make you not eat vegetables, I think, so I think it’s a net negative for me in my life, CRISPRs have been a net negative.
GM: Okay, so CRISPR, it’s a super interesting tech, but essentially, it is a way of doing precision gene editing. So you can basically like put this system, if you will, into the cell, and then you can essentially like almost like laser target it to a specific gene, and you can cut that gene out of the DNA. Or they’re kind of working on, you know, changing, you know, even just a single base pair, so you could change—like I like the idea that I think Theodore is getting at is that if you have a mutation, it is usually in one base of a gene, right, that’s causing it to become a new gene or causing it to be weird. And you could go in with CRISPR, woop, cut that, replace it with the right thing and fix the mutation.
So the problem is that CRISPR works really well if you’re doing cells in a dish, they can basically just like put a whole bunch of these, you know, CRISPR systems in and they’ll go into all the cells and it’s kind of a closed system. And, you know, and then kind of once CRISPR is done, you can then like sort the cells based on who was successfully CRISPRed and who wasn’t. But you like, can’t do that in a person right like that system doesn’t work. CRISPR would really only work if we’re talking about a single cell, so we could probably do it as just a sperm and egg that had initially—
JW: So if you—so basically, that was going to be my question because it sounds like if you CRISPR one cell, and then—or one person—but then you couldn’t just like, put it back in their body because then they would just have one CRISPR cell and—one cell that had been CRISPRed—and then a bunch of other ones that haven’t?
GM: Right, exactly. Like that would do nothing.
JW: Because you’d have to change each one individually, which I imagine would take some time.
GM: And how would you even do it, right? How would you make sure that you were, if we knew how to get all the cancer cells, we wouldn’t need to CRISPR them, because we could just pluck them all out, right? Like, that won’t work.
Circling back though to sort of like, I think that you guys are on the right track with like, can we take your cells and reprogram them and then put them back at you, right? That is sort of like what you guys are getting at. But kind of the closest thing that we have a) to truly personalized medicine and b) to a cancer cure is CAR-T cells. Have you guys heard of these or know what they are? No. Okay.
It’s literally CAR dash T. And basically, so T cells, they’re a type of immune cell in your body. And basically their function is that they kill cells that are infected with virus. So, you know, kind of like now, if we were to get COVID—
JW: Oh, because that’s when they measure people with HIV, that’s like one of the, like, isn’t that one of the diagnostics that they do to determine something about—
GM: You’re right. So like in HIV, the virus attacks your white blood cells, and T cells and B cells are two subtypes of those so-called white blood cells. So yeah, if you have low T cells, it basically means, hey, the virus attacking your T cells, your HIV is progressing.
Anyway, your T cells, your B cells are the ones that make antibodies. Your T cells are kind of the search and kill machines. So like, essentially, when a cell, a healthy cell in your body is sick, is infected with virus, it will basically throw up a flag that’s like, help me. An antibody recognizes that and binds to the cell. That antibody is basically like a big giant X on the cell that’s like, kill me, like kill this cell, this is disgusting, get this out of here. And so T cells are the ones that do that.
So, given that sort of setup, you can imagine that T cells would be very, very, very helpful in cancer. If we could just get a T cell to recognize a cancer cell, we could make the T cells in your own body kill the cancer cells. Turns out they were able to do that. So, CAR-T cells—
TS: Great!
GM: I know, it’s actually very happy.
So CAR-T cells, they take—the downside is that this only seems to work in liquid tumors, so blood tumors, like lymphoma, leukemia, lipoma, all those different kinds. But they take your T cells out, and they reprogram them so that they recognize the cancer cells in your blood. And then the T cells, when they put them back in, the T cells will seek and destroy all those cancer cells. And it is remarkably successful. There’s like, one of the best, like, examples that they always use, there was a 10-year-old girl, unfortunately blood cancers, like, are predominantly found in children, especially leukemia. It’s a very, like—
TS: That’s sad.
GM: It is. It’s like, it is mostly a pediatric cancer. It’s very rare for adults to get it. So the 10-year-old girl, she had leukemia, was, like, on death’s door. CAR-T cells are an experimental treatment that she qualifies. They do it. That was 10 years ago. She is, like, right as rain, like, hasn’t had, like, has been in remission for 10 years, all of her scans come back to me every single time.
TS: So since those cells are still in her body, then does that mean that if she were to perhaps have another occurrence of cancer, would that be, would the T cells just be like, no, not today?
GM: That is a great question. I actually don’t know if we know the answer to that, because in your immune system, basically your body will create, you know, antibodies and upregulate T cells and kind of get the whole immune system going when you’re sick or when you have cancer or whatever. And then it dies down. And that’s important, right? Like, we don’t want to have our immune system on high alert all the time. It doesn’t really work like that. It’s supposed to be kind of like crank it up, put it back down.
So as far as the CAR-T cells, what you really need in order for them to continue to be effective for years and years and years, is you need what they call memory T cells. So they’re sort of like, once your body is sort of like, okay, the danger is past, you’re no longer sick with the flu, we can kind of die down again. It’ll mostly just kind of let all these like T cells die off, like we don’t really need them. But it’ll keep like a very, very, very small few, kind of like in reserve. And so those we call the memory T cells, so they could if need, they’re kind of like our like reserve forces. So they could if need be spring back up. So we don’t actually, I’m not sure if we know whether CAR-T cells are able to make memory T cells.
The other thing that makes it complicated is if the cancer were to quote unquote come back, would it be exactly the same?
TS: Okay, I have a quick question. A very, very selfish personal question. I live in Arizona. There’s lots of sun. The sun is out, like, I want to say 24 hours a day because it seems like that. What is the number SPF, what’s the magic number that I should be wearing at all times on all parts of my body.
GM: This is an excellent question. I’m a huge sunscreen advocate, a common thing that people think is that you can get a base tan and then you’re fine, or if you are a person who is very rich in melanin that you are fine. But the truth is, everybody needs to wear sunscreen. I think people kind of think that SPF is like a linear scale like 50 gives you like 20 times—20 more protection than 30 or whatever, and that’s hardly the case. So you really need SPF 30 at a minimum. Anything beyond like 50, you’re not getting like that much more coverage.
TS: Wait, what’s wrong with a tan?
GM: Oh, well, like, now, don’t all right, don’t tell my PI this, but I also love to be tan. I love to go to the beach. I always wear sunscreen, but I will still usually get tan if I wear sunscreen. And the truth is, is that there’s really no such thing as a safe tan, because if you are tanning—When we get tan, we get darker because there’s more melanin in our skin. So melanin is what produces our skin pigment. The only people who don’t have any melanin are people who have albinism, who are albino. Everybody else has some level of melanin, and that kind of depends on what your relative skin tone is. So melanin is produced by cells in your skin called melanocytes, so they produce melanin, and it is actually fascinating. So these, these melanocytes in response to UV radiation specifically, in response to the sun, the melanocytes will start to produce melanin. And basically melanin look under the microscope like these black masses, just like totally black. And you can see that the melanin will start to sort of cover your healthy cells, kind of like an umbrella.
TS: That’s fascinating.
GM: Yes, like the melanocytes like bloom almost, and it’s like these big black shades that are trying to shade your cells so that we aren’t getting as much radiation. When you are tan, your body is like, holy crap, I need to protect myself. I need to put up these, you know, safety umbrellas. Once you’ve gotten to that point, there’s already some kind of sufficient damage. Obviously, if you are wearing sunscreen, it is better than nothing, but avoiding the sun is best way you can avoid that.
TS: So melanoma is when you have, so the melanocytes have cancer, or which part of you have cancer, the melanocytes?
GM: Yes, the melanocytes are the like cell of origin. So the melanocytes start to divide uncontrollably.
TS: So we don’t have any more umbrellas.
GM: Or you have like too many umbrellas that aren’t really doing their job. Another like common critique of sunscreen is that you aren’t going to get enough vitamin D, because when you are exposed to sun, you make vitamin D. But like, if you could eat like one vegetable a week, you’ve probably got enough vitamin D.
JM: Can we talk about the actual tumor microenvironment? So what are the components? If you have like a melanoma in your skin, what is all the stuff around it? And how is that affecting how the cancer is growing and spreading?
GM: Okay, this is a great question. So I really like studying melanoma for the tumor microenvironment because the skin is a really, really great subject to study. So sort of what I study and what I very, very biasfully think is like the most one of the most important parts of the microenvironment is actually something called the extracellular matrix. So, or the ECM. So the extracellular matrix is again very aptly named. It’s basically a whole bunch of different proteins that makes like the mesh that everything in your body fits in. So basically anything that isn’t an organ or like a blood vessel is extracellular matrix. It’s kind of like all the filler. So, ECM, it has a lot of like important functions, including sort of retaining water and kind of allowing for structure. And so the water retention part is really important because as we get older and we get wrinkles, what’s basically happening is your ECM is starting to break down. And it’s not like through any really fault of your own, but like, it just happens over time.
But if we circle back to cancer and why the ECM matters in it, sort of what we see is that over the course of the natural aging process, we start to see this breakdown in the structure of the extracellular matrix. Interestingly, you see a very, very similar kind of breakdown in cancer. So when a tumor like forms, one of the first thing it’s going to start doing, it’s going to start breaking down ECM around it, and it does that for a lot of reasons. One, your ECM is like protective and providing structure and your tumor doesn’t like that it doesn’t want that it wants to be free. But also, your tumor wants to grow and it wants to move. So cancer cells want to move that want to get out of the primary tumor and kind of travel throughout your body. If they try and go through the ECM, it’s going to be really difficult because it’s just like, mushy, messy, you know, it’s really kind of hard to get through and designed that way. So what cancer will start to do is it will start to send out a whole bunch of little proteins and a whole bunch of little, you know, things into the ECM that will break down the structure and will make it stiffer. So when ECM stiffens, the cancer cells can start to use it more like a road. So rather than it like—cancer cells kind of walking in this like squishy swamp, it gets really stiff and then they’re easily, easily able to kind of crawl along your ECM and move.
TS: You know what, Gloria? Cancer—
JW: It’s horrific.
TS: Yeah, it’s horrific. I think the name of this podcast should be cancer is a bitch.
GM: You are right. The like cruel irony of cancer right is that it’s your own cells, like it’s not like it’s an alien thing like, it’s your own cells and all they’re trying to do is survive. One of the things that they need to do in order to survive is they need to start changing their environment to help them. So changing the ECM: huge, huge step. And actually, some specific cancers, I think like some of the most common examples are breath and liver, they can actually when they do initial biopsy, sometimes they will look at how stiff your ECM is when they do the biopsy, because that is a huge prognostic marker. Meaning like if they take the biopsy and they see that you have a really stiff ECM, they can kind of start to adjust your treatment they, can kind of start to adjust maybe even your survival timeline. Because they know stiff ECM means this cancer can spread a lot faster it’s a lot more aggressive, you know, all of these things.
TS: What are stages?
GM: Stages of cancer. Great question. So generally speaking, if we’re thinking about what we call solid tumors, so any tumor that’s not in the blood, it basically refers to how quote unquote deep the tumor is, if that makes sense. So if you have a melanoma tumor, it usually starts as a weird looking mole, and it’s just kind of on the surface of your skin. That’s usually stage zero or stage one, however you want to think about it, and eventually your skin cancer instead of sort of growing out on your skin to be larger, it’ll start growing into your skin, it’ll start growing vertically. So once it starts growing in, then we start to hit all the stuff in the microenvironment that we don’t want it to be near. And then that’s when we start to get into the ECM, you know, we kind of reach that skin layers, if you will. The level of reach determines the staging. So usually, once it’s kind of breached the skin, and it’s deep, then it’s a stage two. Stage three is usually what they’ll do is if they think that you have aggressive melanoma or they think it’s stage two or higher, they’ll do a biopsy of your lymph node, whatever the closest one is. And so, if they see cancer cells in your lymph node, then you get stage three, because that means that they’ve already traveled, right? Stage four is usually reserved for anything that is metastatic. So metastatic means that you have a secondary tumor somewhere else in your body, anywhere else. So that is sort of the level of staging.
So obviously, catching cancer really early is what is really critical to treatment right now. So if you can catch it at stage zero one, even two, before it’s really started to travel, that’s usually when surgery is really effective, you know, because you can cut it out. And you know that things haven’t moved that much. Once we start getting into stage three and stage four, when things are really moving, you know, we’re talking about trying to track cancer cells through your body, and we’re just not there yet medically, right?
JW: So something that I thought was pretty interesting when reading the article also with the, talking about the micro environments, like where a tumor happens to be, if it happens to be near a bony place in your body, or near kind of a fatty place in your body, or wherever it may be, is kind of like, I kind of thought about the local like new stations that are always like, oh, red wine is like good for like not getting cancer. And then like a couple of weeks later, they’d be like, oh, it’s like, red wine is really bad, it can give you cancer, or it can be bad for you, you know, they have these like constantly conflicting things. But then reading this and then hearing about how different all the different cancers are, I’m like, well, obviously, like, you know, for one type or one part of your body, like something could be good and contain something that’s good. And then for another part of your body, if something else or a different type of cancer happened, like, it could be really bad, you know, or like, oh, this is something people complain about all the time, like you can’t really get good health advice and the local news just throws it on there with no context. And then it’s like, well, no wonder, because everyone is mistaken about cancer, like the very base fact about cancer.
GM: You’re exactly right. And it kind of ties into like what Teodora was talking about earlier, too, is that like, that’s sort of the reason we don’t have this magic bullet, right, like, every organ, you know, if we even think of cancer as like, organ specific, right, every organ needs different things, right, so it’s not like you can treat lung cancer the same as we treat brain cancer, the same as we treat like a sarcoma that comes from the muscle or like a heart or like all of these things are so dramatically different, that exactly like when you start talking about anti-cancer, again, it’s like, what cancer are you talking about?
TS: I will also say, Jacob, that whenever they say that red wine is bad, I immediately turn everything off. I’m like, no, you will not tell me red wine is bad you will not tell me that like—
GM: Well, what’s interesting, kind of thinking about like, sort of cancer prevention or whatever, it is untrue that eating blueberries is going to like prevent you from getting cancer right? Like what is interesting is that I don’t think, I don’t think last year because obviously COVID really messed with everything, but I think in 2019, it was one of the first years that we actually had a decline in global cancer rate. It wasn’t much it was like somewhere between one or 2%, but it was still a decline and like, especially like if you’re looking across the globe it was a pretty big deal. Interestingly, like it wasn’t necessarily because we have some new great cutting edge, you know, treatment. It was really that global smoking rates are the lowest they have been in a very long time. And so lung cancer, like, far and away is like killing people at a massive rate globally, and it’s mostly due to the fact that so many people around the world smoke. And so, you know, there are so many cancers that you really can’t prevent like, you know, these cancers that just arise from random mutations with this bad luck, like there’s no amount of blueberries or kombucha or green tea that can prevent that. But there are cancers that are definitely preventable or at the very least, like, you can massively reduce your risk of getting it. And lung cancer, liver cancer and melanoma are these big three. And lung cancer is obviously, you know, not smoking; melanoma is avoiding the sun, wearing fps, and then liver cancer is not being an alcoholic essentially, not like over consuming alcohol. Unfortunately, the things that we know work, like not smoking and not handing don’t really want to stop doing, so.
Let me talk a little bit about sort of the role of blood vessels, kind of when we think about this tumor microenvironment, because this is another really sort of important part, both blood vessels and lymphatic vessels. So your blood vessels and your lymphatic vessels: blood obviously carries blood; lymphatic is essentially carrying all of your immune cells, and also cell waste. Both of these vessels are kind of all permeated throughout your body, and they basically kind of weave through the extracellular matrix as well. So again, if we’re kind of going back to skin, if we’re thinking about the surface area that we can all see that isn’t very deep, where stage one cancer might occur, and we start thinking about stage two, that would be if it goes down into the extracellular matrix where all these vessels are kind of living. And so again, we’re thinking about cancer and cancer is our own cells, our cells need nutrients and oxygen to survive. What cancer tumors and cells will start doing is they will start sending out signals that are like, “Hey, I need more nutrients, I need more oxygen, I need to like be fed,” essentially. And your body will start to create more blood vessels that will go and feed the tumor. That’s sort of another thing that when physicians or whatever look at the tumor, they will look at its quote unquote vascularization: how many vessels are in it right. Because again, if it’s a lot of blood vessels connected to it, it is aggressive, it is going to get big and—
TS: Hungry tumor.
GM: It’s very hungry. And that’s the thing is it kind of starts to like siphon—you know what I mean, like your blood, like your body is making blood for everybody and then your tumor is just like siphoning it for itself, basically.
JW: So, I mean, I so if you have a like, say you have a melanoma that has advanced and it’s like on your arm and it’s gone down and it’s like gone to a different place. Like, what makes cancer actually fatal? Is that when a cancer cell lands in a place you really don’t want it to land that’s like vital for body, like vital for the continuation of life and then it grows there to the point that it disrupts?
GM: That is essentially what will eventually kill you is that like—
JW: Okay, so it goes back to the microenvironment also then of like the next place that it lands too, even at like the end stage of the whole thing?
GM: Yeah, because basically, like, you know, you could die from a primary tumor if it’s in a really really bad spot right, but like, really what kills you is that, and this kind of goes back to what we talked about the blood vessels, is that the main way that cancer cells start to move is they enter your bloodstream because your bloodstream goes everywhere, it’s a superhighway. So, if your cancer cells can enter, zip into your bloodstream, they can go anywhere and they can just leave at any point. So, the more blood vessels that a tumor has going to it, right, it’s got like all of these highway entrances right there, so the odds that at least one cell is going to make it in is really high.
And so really what tends to happen is, like you said, you know, let’s say you have melanoma one of the places that tend to metastasize to the lungs. So, you know, you’re battling this melanoma sort of growing in your skin, and then it gets to your lungs. Okay, well now you have this thing growing in your lung and like, can you like get enough oxygen. Okay, even if we were to like get rid of one of your lungs. Oh, shocker, like it’s moved to your other lung, you know what I mean or like cancer also tends to—or melanoma at least—it also tends to metastasize to the brain. I mean, maybe we can remove from your brain but then it might get into your spinal column, you know, it’s just like, it eventually just gets that you’re chasing the thing around the body and it’s going to eventually get somewhere where it is just incompatible with life basically.
TS: I’ve never seen anyone in person personally die of cancer like in front of me but on the media I see that they died in pain. Why is there pain?
GM: So, often there is pain, because like, you have something growing that is pressing into other like organs and pressing into space, you know what I mean so it’s pressing on nerves that are sort of all around it where things shouldn’t be. It’s like, yeah, like imagine the pain, it is like alien or like a parasite like imagine the pain of something growing like in the center of your arm and growing right? Like—
TS: I see.
GM: —pushing. Yeah, so that is like, usually where the pain comes from. If you wanna get really dark, the most like intense pain I hear for cancer is bone cancer, and I think it’s because it’s like so deep in there and it’s like it is always going to push on things.
TS: Right. Because there are some cancers that you don’t know that you have. So you’re not in pain, you don’t even know.
GM: Right, so one of the like, um, biggest perpetrators of that is pancreatic cancer, like, of all the cancer types, since 1990, your prognosis for every single cancer type has improved, some more significantly than others but all are better, except for pancreatic cancer. We have made no progress on that tumor in forever like, since whatever the dawn of time. And a lot of the reason is because your pancreas is this like, smallish organ, it’s kind of tucked up in there so it’s not like it would, you know, some people will see cancer pop up like, you know, if they have something up with their lungs or if they have something up their bowel, like sometimes it’ll just pop up like they find it by accident. Like, your pancreas is not really part of like a normal screen. And it’s so sort of hidden that by the time you start to experience pain, the size of the amount of that tumor has to have grown is huge. And usually when a tumor is very big, some cells of it have already moved, have already gone off. So the problem is, is not necessarily that we don’t know how to treat pancreatic cancer, the problem is, is that we can’t detect it early enough. So most people who get it, they’re usually in stage like three or four already. And then by that point, you’re already at the, “oh crap, we have to chase this around the body” stage. That’s why your prognosis is so bad. Not because that cancer is necessarily like intrinsically better or worse than another one, but it’s just our ability to detect it is so bad.
JW: I feel like cancer is like real estate, almost, like it, like it’s all about the location.
GM: And it’s a lot of, like, luck or bad luck, like it’s, it’s so random. I mean, really, because like, they kind of call it like the two-hit hypothesis of cancer, which is sort of like how cancer starts. Our body has a lot of failsafes built in, right, you have lots of pairs of gas and breaks, we have lots of things that can compensate for each other should something go wrong, you know, we have a lot of failsafes built in. So basically what they think happens is one of the failsafe that your body is built in is that you have two copies of every gene, right, one from mom and one from dad. The idea is that if one of those gene copies were to become nonfunctional for any reason, no worries, because you’ve got a whole second copy backed up. So you could just stop transcribing the crap one and you know, we’ll just go with the other one. So the two hit hypothesis is basically that lightning strikes twice, and you get two random mutations in the same gene. So you get boom they knock out one copy of your gene, boom it knocks out the other. Now you have a non-functional gene. And so kind of like, stemming from that is BRCA mutation is a very like, famous mutation in a specific gene called BRCA that makes women more susceptible to getting breast cancer. So if breath cancer runs in the family women will often get screened for mutation. And you have—oh it’s something crazy like you have like a 40% higher chance of getting breast cancer than the average, some like crazy metrics like that.
And the reason is, is that if you have a mutation in this gene called BRCA, that means that one of your copies is already faulty. That means that you’re starting with only one functional copy.
JW: So it’s the one hit hypothesis.
GM: And then it becomes the one hit hypothesis, exactly, right? So like then the odds are not in your favor because like something happens, you’re screwed, right? So that’s kind of where it comes from, and it just so happens that that gene is involved in DNA repair. So it fixes mutations. So if you have a nonfunctional gene that is supposed to fix gene mutations, it’s bad news bears, right?
JW: Interesting, yeah, interesting. And then I think when we’re talking you said that, like, just the process of aging just provides more opportunities for that firing to not be good.
GM: Pretty much. I mean, essentially, you know, kind of how we talked about like with, you know, telomeres are like big junk caps on our DNA, DNA transcription is 99.999 or whatever percent accurate. But it is still 0.001% inaccurate. Again, we have all these failsafes in place. We have DNA repair mechanisms where, you know, we kind of do like when cells are dividing, we do a quick check. So these proteins will go along the DNA and they’ll make sure yes, yes, yes, yes, everything’s good. They see something that’s wrong. They’ll fix it. With those in place, right 99.999, which is really, really good. But there’s always a chance that something goes wrong. And, you know, if that goes wrong in, again, one copy of a gene and one cell, no big deal. Two copies, and that cell starts to go haywire, then it’s trouble, right.
The last bit of this paper that I wanted to talk about, talk with you guys, is the immune system and immune cells as members of the tumor microenvironment. And we kind of talked about this when we talked about CAR-T cells and stuff, because your immune system is built to get rid of the threats in your body, whether that be viruses or parasites or bacteria or even cancer cells. And there’s actually a lot of evidence to show that throughout your entire life, your immune system is very good at getting rid of potential cancer cells, like early in your life. Like, there is evidence to show that like, we have a cancer cell or two or what—something that could become cancer floating around that our immune system is just taking care of.
So it is actually very, very effective. But the problem is, is that once you get a cancer that really, really, really gets going, it kind of overwhelms your immune system, and you start to get this thing where—they call it like immune—immune exhaustion or even T cell exhaustion, where your immune system, like we talked about, we want to turn on and we want to turn it off. Once your immune system is on and it’s trying to get this tumor for, you know, we’ll say days and months, it just doesn’t, it just loses its effectiveness, like the cells get tired like they just don’t work as well. And then that kind of translates to sort of the rest of your body, because your whole immune system is just not as functional as it should be because it’s just been on, on, on, on all the time. And so it really just kind of makes you a little bit more susceptible to other things. So we kind of go back to thinking about like diet, for example, something that, I can’t remember who actually pointed this phrase, but they basically called cancer is the wound that doesn’t heal. You have these cells that are growing, trying to fill in a missing gap and you have your immune system that’s often active, trying to fix it like trying to fix it, but then it just never heals. So you just are in this like chronic state of like, we need to fix this, we have something wrong, we have something wrong. So if you have a very poor diet, or if you are very overweight, your immune system is already kind of high. You just have kind of a lot of toxic things coming through your body that your immune system has to deal with.
JW: Is that coming from the food or from the impacts of being overweight, or both?
GM: Both. So, if you kind of—there, there’s some evidence to show that like, you know, if you’re eating super, super processed food, it causes kind of inflammation or some immune cells coming in to like the gut to kind of calm everything down. And when you’re overweight, also often your heart has to work harder, which does kind of impact, like, how your like, aorta works and that can become inflamed, as well as your joints, they tend to have a little bit more stress on them so they can become inflamed. So you kind of have like all of your body, your body’s trying to kind of put out fires, a lot with your immune system. So the reason that these things kind of sort of preclude you to cancer is you can imagine if our immune system is sort of like, picking off these cancer cells periodically because it’s like, working properly. If your immune system is already like doing 800 billion other things, like a cancer cell might slip through the crack. So that’s sort of where the connection is. So it’s not necessarily like that you’re eating this one particular thing or that you are not doing this one particular thing. It’s that like, you are creating this environment, your body, where your immune system is like hyperactive all the time. And then, like, ironically, the hyperactivity leads to less effective immune system.
TS: So if you don’t get sick often, and you have a really good immune system, then does that mean that so that—so the healthier you are in general, like if you don’t get colds and, you know, does that mean that that also lowers your risk of cancer?
GM: Yes. Like, the thing about cancer, right, is that it’s random. So you could have something in your DNA, you know, that is just kind of a ticking time bomb. But it’s one of those things where it’s like, your eating habits, your exercise habits, will not contribute to increasing your odds of getting cancer, if that makes sense. So it’s more like, it’s less of like, oh, you’re less likely to get cancer than somebody else, which is probably true. But like, just because it’s so random, like, you know, it’s hard to say for sure. But you are doing much more to decrease your chance of getting cancer.
JM: It’s more like a harm reduction then.
GM: Yeah, because cancer is random, right, there’s like not very much control, but like what you can control, like, of the things you can control, we know that being overall healthier, making sure your immune system is sort of like, able to function correctly and then turn on and then turn off. All of these things kind of help you just be like, give yourself the best chance, basically, right, like, I mean, I think like the good thing about like, if we want to sort of end on a higher note or at least like what is what is exciting. I think personalized medicine is going to be the way of the future and I’m excited about it because I think that cancer is really kind of leading the way for personalized medicine with a lot of other diseases. You know, I think that, for example, like neurodegenerative diseases, you wanna talk about the brain and how complicated that is? You know, there are so many different things where I think that the medical field has really tried to simplify it, where I think that a lot of people could really benefit from personalized medicine in so many different facets of care. So I think that kind of as cancer care becomes more personalized, my hope is that that will really extend to a lot of other things that so that maybe one day like you know, way, way in the future, it’s like, okay, we have like the Jacob like health plan like we you know, sequence your tumor, we know that you have like a nonfunctional copy of this gene that you know me make you more likely to have heart disease, so we’re going to make sure that we were like screening for that, you know. Like that I think is like my prime skydream of health care.
The other thing I’m excited about is actually the FDA approval of mRNA vaccines for coronavirus is a huge win for the cancer field, because mRNA vaccines, as you guys might know, have been sort of in the works for the last 20 years. We really just needed apparently a global pandemic to really light a fire under the FDA’s butt to get them going. Being able to just use a short mRNA sequence to program, like essentially your immune system, it’s kind of like CAR-T cells but in a shot. Because like essentially what you’re doing is you’re priming your immune system to recognize a certain threat and make antibodies against something. And because it’s like a short mRNA sequence that they put in the vaccine, you can easily switch it up and it’s very cheap like you just change, you know, the sequence and then you just put it back in.
So for cancer patients, that’s huge, right, like, rather than having to like, take the T cells out and change them in a dish, and put them back in you, and you know, wait to do all this, like, you could just get somebody a vaccine to make your immune system recognize your cancer cells. And then they’ll wipe them out and then if they pop up again, you can just give them a new vaccine. So that is like super exciting, and again it kind of ties into like personalized medicine. But I think those two things at least of what we see now, I think will really kind of radicalize cancer care in a really good way.
JW: That is hopeful, I think, and also hopeful that maybe we can get ahead of some of the variants of COVID as well.
GM: Yeah, exactly. I mean, I think the other thing too about us making progress with cancer is a lot of the progress that we’ve made has been because we have lowered the ages of screening for a lot of cancers, we started screening earlier, and we have a lot more advanced technology for imaging, right, we have like MRI machines, we have CT scans, we have all these different things, rather than just, you know, like X-ray or whatever. So I think as well as our technology gets better and better and better, we can increase our resolution of imaging. And I, you know, because it’s a technology thing and it’s just like exponential, I mean, I have no reason to believe that we couldn’t one day achieve single cell or maybe multi cell resolution and imaging. That could be like really important, like that could really radicalize, you know, how early we’re able to detect things.
TS: But I wonder if there’s like a proxy that we could get to that we don’t have to put people in an imaging scanner, but I don’t know, like have a really consistent way of saying, okay, we’re going to take this piece of your blood and then figure out where your cancer is. I don’t know, I just feel like there’s so much testing and testing costs money and people don’t have money to pay for the testing and testing money time, etc. It just elongates this process of actually getting the frickin treatment. So if there would be like an easy way to detect it, that would be even better.
GM: Yeah, I think a lot of, again, Teodora, she’s on it with what people have thought of. So like, what you’re describing is what we call biomarkers in the field, but basically like, similarly, you know, can we take a sample of blood and figure out what type of cancer you have. Sometimes, yes, but if you have cancer, like, if you have cancer cells in your blood, it is very, very, very bad news, right. So it’s not incredibly helpful. Yet. But hopefully, we can get there. They’re kind of starting to look to see if they can find tumor DNA in the bloodstream which doesn’t like—the good thing about when cancer cells get in your blood is your blood and going at a very, very fast rate. So it’s kind of, rather, maybe not so with them getting onto a highway, but more like them going to like rapids. So a lot of times they don’t survive in your bloodstream and they’ll like blow apart. But there are traces of DNA that are left behind if the cancer cells are blown apart, right. So that is something that they tried to look at, but I agree that would be obviously the best because you just do a little finger prick.
TS: Yeah.
GM: But, conversely—
TS: Oh, come on, Gloria.
GM: It’s—no, but like a good thing. Like if we’re talking about imaging and sort of technology, technology necessarily gets better and it gets cheaper. That’s just like how it goes, right. I mean, obviously the most high tech, you know, is going to be the most expensive. But like, as we increase our resolution, our technology, what was considered state of the art is going to become less state of the art, but cheaper, you know what I mean. So like, once we’re getting into like these insane imaging, all of a sudden, maybe everyone doing an annual MRI isn’t going to be that expensive. So, you know, it’s kind of one of those things that I think that that could really work in people’s favor where, you know, even if it’s not the best, best, best resolution, it’s way better than what we have now and it’s cheap and relatively easy.
JW: And I think, I think what’s been interesting about this entire discussion is just how you really, if you like scratch the surface at all it seems like on cancer research and, you know, the search for cure or whatever you wanted to call it, or you know, whole ecosystem around solving this problem which is really a lot of different problems that are kind of tangentially related to each other. I think what’s interesting to me is like the way you have to change your expectations and I think like, it’s interesting Gloria to hear from you and hear how excited you are about technology and about earlier screening and stuff like that because I think we all do just instinctively, you know, the dream of like healthcare for a lot of people is to take a pill and be cured of like everything that could be wrong with you, and I think that that’s the expectation for a lot of people and I think that, you know, there have been miracles like that with antibiotics and stuff like that. But with something that originates in your own body, I think it makes it harder. And I–what’s interesting, you know, as someone who has worked in a field of trying to expand access to healthcare to more people, like talking about earlier screening and like stuff becoming more accessible is really the fight to cure cancer. Like that is really like someone having a primary care doctor and not having to worry about whether they can make it to a primary care doctor or not, is the cure for cancer. I mean, maybe it’s a little bit of hyperbole, but I’m going to go with it. You know, we kind of have the cure for a lot of these cancers, especially like a melanoma the cure is finding it early and like having surgery or doing whatever needs to be done to get rid of it and like that is the cure. And so it’s in some ways you can say that there’s, you know, this is a really sad conversation. But in other ways you can say it’s actually really hopeful because it’s not really, you know, technology or know how or expertise that’s preventing us from curing most cancers, it’s people not finding it soon enough.
GM: You are 100% correct. Like if I think the field was being honest with itself, most of the reason that we have made significant improvements in cancer treatment is because we have much, much, much better screening and much better education. You know, people kind of know, hey, if you have a suspicious mole, maybe you should get a check. And it seems like second nature but that’s not by accident. That’s by a very, very, like, specific and strong public health campaign, right, or like, I should wear sunscreen, like public health campaign, you know what I mean, all these things like educating people about what to be wary of what to look for and, you know, having people have access to a provider that could potentially give them a yes/no. And these are all things that and like, you know, of course, like people delay treatment because they can’t afford it or because they have, you know, lack of access and like, when you’re talking about cancer, delaying treatment by even a matter of weeks or months, I mean that can make or break sort of your survival.
The other thing that we talk about a lot with cancer field is the disparity among different ethnicities and survival rates, and I’m sure you can all guess who has the lowest survival in the United States right of course people of color. And it’s for a lot of different reasons, but most of the data shows that really due to lack of access and people’s inability to afford care. So, and, and also, not to get on my soapbox here but especially in melanoma, melanoma presents quite differently on people who have darker complexions because melanoma is a very dark tumor it looks, it looks black like on skin. But that color contrast is not as pronounced as somebody who is more darkly complected. So, oftentimes dermatologists don’t really know how to diagnose it, or they don’t recognize it because it’s not in textbooks, not taught. Right? You kind of have this like whole systemic problem that permeates into, you know, all these inequalities. So I agree, I mean I think that health care equity, if we could kind of get even closer to health care equity would be massive decline in cancer, or I guess, increases in survival, decline in late-stage cancer diagnosis.
JM: Alright, and on that note, we are going to wrap up. Thank you, all of you for joining us for this excellent discussion, and before we go, I’d like to give each of you the opportunity to promote any projects that you all have in the works, social media etc. So Gloria what do you have to promote?
GM: Sure. Also, thank you again Jamie and also Jacob and Teodora, this is great. Um, so I actually write a blog, it’s called Bare Bones Biology. It’s barebonesbio.wordpress.com. I basically write about a topic in biology, kind of in the, in the spirit of this podcast where it’s accessible to any listener anybody at any level. So if you want to go ahead and check that out if you’re interested, and also follow, it’s @_barebonesbio on Twitter. I also write periodically for Massive Science. I actually wrote about sort of inequality in the dermatology field recently, so you can check out my profile on Massive Science as well to read more of my work.
JM: Thanks! How about you, Teodora?
TS: So I write on my blog curiouscortex.com. I write about neuroscience topics that just interest me and apparently other people. So you can find some of my writing there, and that has kind of got picked up by other people like Scientific American. And so, if there’s anything, if there’s anything on Scientific American, I’ll let you guys know and it’ll be linked there on curiouscortex.com. And then, in the process of putting together a, I think it’s going to be a nonprofit right now. We don’t know what it is as of yet, but we, a team that I met at ComSciCon, we are putting together a mental health, Google like platform, where people can just put in their questions and we as the researchers go behind the scenes and get the answers in a very scientifically minded way. And mental health is very, very sort of—people that have mental health issues they don’t want to talk to anybody about it, so we thought this would be a great way to get that going. It’s going to be called mentallyminded.com. We don’t have a website yet, but it’s coming. So, that’s exciting.
JM: Great. I can’t wait to check that out. And Jake?
JW: Yeah, so I am—I mean, I’ve been working on a few things but one of the things that comes to mind is the organization Jamie and I founded with some other friends with St. Louis Quarantine Support, where we were delivering food to people who were having to quarantine at the onset of the pandemic, and it kind of morphed into just kind of a hunger alleviation organization and a mutual aid organization. So my Twitter handle is @BankonJake, and if you’re interested in how an organization like that would like get going or something like that, feel free to reach out and I can give you some pointers on how you can set up a similar mutual aid organization in your community. It’s been really enriching experience, I think I can speak for myself and Jamie for doing that. So that’s about it, I mean and on Twitter if you want to see me in my natural habitat fighting with people about politics like you can find me @BankonJake.
JM: Great. Well thank you all once again for joining us on our second ever episode of in plain English. We have been talking about the paper called “Tumor microenvironments, allies of cancer progression.” You can find that free to download on inplainenglishpod.org. And once again, you can follow us on Twitter @plainenglishsci, that’s p-l-a-i-n-e-n-g-l-i-s-h-s-c-i, or find us on Facebook at facebook.com/plainenglishsci. And you can find our podcasts on Google Podcasts, Spotify, SoundCloud, or wherever you listen to your podcasts. We’ll see you next time for another paper presented In Plain English.
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In Plain English Podcast 