TED2005
Eva Vertes: Meet the future of cancer research
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Eva Vertes -- only 19 when she gave this talk -- discusses her journey toward studying medicine and her drive to understand the roots of cancer and Alzheimer’s.
Eva Vertes - Neuroscience and cancer researcher
Eva Vertes is a microbiology prodigy. Her discovery, at age 17, of a compound that stops fruit-fly brain cells from dying was regarded as a step toward curing Alzheimer's. Now she aims to find better ways to treat -- and avoid -- cancer. Full bio
Eva Vertes is a microbiology prodigy. Her discovery, at age 17, of a compound that stops fruit-fly brain cells from dying was regarded as a step toward curing Alzheimer's. Now she aims to find better ways to treat -- and avoid -- cancer. Full bio
Double-click the English transcript below to play the video.
00:26
Thank you. It's really an honor and a privilege to be here
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spending my last day as a teenager.
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Today I want to talk to you about the future, but
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first I'm going to tell you a bit about the past.
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My story starts way before I was born.
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My grandmother was on a train to Auschwitz, the death camp.
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And she was going along the tracks, and the tracks split.
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And somehow -- we don't really know exactly the whole story -- but
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the train took the wrong track and went to a work camp rather than the death camp.
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My grandmother survived and married my grandfather.
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They were living in Hungary, and my mother was born.
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And when my mother was two years old,
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the Hungarian revolution was raging, and they decided to escape Hungary.
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They got on a boat, and yet another divergence --
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the boat was either going to Canada or to Australia.
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They got on and didn't know where they were going, and ended up in Canada.
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So, to make a long story short, they came to Canada.
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My grandmother was a chemist. She worked at the Banting Institute in Toronto,
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and at 44 she died of stomach cancer. I never met my grandmother,
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but I carry on her name -- her exact name, Eva Vertes --
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and I like to think I carry on her scientific passion, too.
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I found this passion not far from here, actually, when I was nine years old.
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My family was on a road trip and we were in the Grand Canyon.
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And I had never been a reader when I was young --
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my dad had tried me with the Hardy Boys; I tried Nancy Drew;
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I tried all that -- and I just didn't like reading books.
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And my mother bought this book when we were at the Grand Canyon
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called "The Hot Zone." It was all about the outbreak of the Ebola virus.
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And something about it just kind of drew me towards it.
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There was this big sort of bumpy-looking virus on the cover,
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and I just wanted to read it. I picked up that book,
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and as we drove from the edge of the Grand Canyon
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to Big Sur, and to, actually, here where we are today, in Monterey,
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I read that book, and from when I was reading that book,
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I knew that I wanted to have a life in medicine.
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I wanted to be like the explorers I'd read about in the book,
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who went into the jungles of Africa,
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went into the research labs and just tried to figure out
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what this deadly virus was. So from that moment on, I read every medical book
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I could get my hands on, and I just loved it so much.
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I was a passive observer of the medical world.
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It wasn't until I entered high school that I thought,
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"Maybe now, you know -- being a big high school kid --
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I can maybe become an active part of this big medical world."
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I was 14, and I emailed professors at the local university
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to see if maybe I could go work in their lab. And hardly anyone responded.
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But I mean, why would they respond to a 14-year-old, anyway?
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And I got to go talk to one professor, Dr. Jacobs,
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who accepted me into the lab.
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At that time, I was really interested in neuroscience
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and wanted to do a research project in neurology --
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specifically looking at the effects of heavy metals on the developing nervous system.
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So I started that, and worked in his lab for a year,
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and found the results that I guess you'd expect to find
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when you feed fruit flies heavy metals -- that it really, really impaired the nervous system.
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The spinal cord had breaks. The neurons were crossing in every which way.
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And from then I wanted to look not at impairment, but at prevention of impairment.
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So that's what led me to Alzheimer's. I started reading about Alzheimer's
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and tried to familiarize myself with the research,
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and at the same time when I was in the --
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I was reading in the medical library one day, and I read this article
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about something called "purine derivatives."
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And they seemed to have cell growth-promoting properties.
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And being naive about the whole field, I kind of thought,
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"Oh, you have cell death in Alzheimer's
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which is causing the memory deficit, and then you have this compound --
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purine derivatives -- that are promoting cell growth."
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And so I thought, "Maybe if it can promote cell growth,
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it can inhibit cell death, too."
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And so that's the project that I pursued for that year,
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and it's continuing now as well,
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and found that a specific purine derivative called "guanidine"
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had inhibited the cell growth by approximately 60 percent.
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So I presented those results at the International Science Fair,
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which was just one of the most amazing experiences of my life.
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And there I was awarded "Best in the World in Medicine,"
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which allowed me to get in, or at least get a foot in the door of the big medical world.
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And from then on, since I was now in this huge exciting world,
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I wanted to explore it all. I wanted it all at once, but knew I couldn't really get that.
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And I stumbled across something called "cancer stem cells."
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And this is really what I want to talk to you about today -- about cancer.
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At first when I heard of cancer stem cells,
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I didn't really know how to put the two together. I'd heard of stem cells,
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and I'd heard of them as the panacea of the future --
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the therapy of many diseases to come in the future, perhaps.
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But I'd heard of cancer as the most feared disease of our time,
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so how did the good and bad go together?
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Last summer I worked at Stanford University, doing some research on cancer stem cells.
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And while I was doing this, I was reading the cancer literature,
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trying to -- again -- familiarize myself with this new medical field.
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And it seemed that tumors actually begin from a stem cell.
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This fascinated me. The more I read, the more I looked at cancer differently
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and almost became less fearful of it.
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It seems that cancer is a direct result to injury.
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If you smoke, you damage your lung tissue, and then lung cancer arises.
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If you drink, you damage your liver, and then liver cancer occurs.
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And it was really interesting -- there were articles correlating
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if you have a bone fracture, and then bone cancer arises.
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Because what stem cells are -- they're these
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phenomenal cells that really have the ability to differentiate
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into any type of tissue.
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So, if the body is sensing that you have damage to an organ
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and then it's initiating cancer, it's almost as if this is a repair response.
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And the cancer, the body is saying the lung tissue is damaged,
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we need to repair the lung. And cancer is originating in the lung
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trying to repair -- because you have this excessive proliferation
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of these remarkable cells that really have the potential to become lung tissue.
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But it's almost as if the body has originated this ingenious response,
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but can't quite control it.
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It hasn't yet become fine-tuned enough to finish what has been initiated.
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So this really, really fascinated me.
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And I really think that we can't think about cancer --
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let alone any disease -- in such black-and-white terms.
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If we eliminate cancer the way we're trying to do now, with chemotherapy and radiation,
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we're bombarding the body or the cancer with toxins, or with radiation, trying to kill it.
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It's almost as if we're getting back to this starting point.
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We're removing the cancer cells, but we're revealing the previous damage
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that the body has tried to fix.
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Shouldn't we think about manipulation, rather than elimination?
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If somehow we can cause these cells to differentiate --
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to become bone tissue, lung tissue, liver tissue,
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whatever that cancer has been put there to do --
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it would be a repair process. We'd end up better than we were before cancer.
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So, this really changed my view of looking at cancer.
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And while I was reading all these articles about cancer,
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it seemed that the articles -- a lot of them -- focused on, you know,
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the genetics of breast cancer, and the genesis
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and the progression of breast cancer --
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tracking the cancer through the body, tracing where it is, where it goes.
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But it struck me that I'd never heard of cancer of the heart,
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or cancer of any skeletal muscle for that matter.
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And skeletal muscle constitutes 50 percent of our body,
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or over 50 percent of our body. And so at first I kind of thought,
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"Well, maybe there's some obvious explanation
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why skeletal muscle doesn't get cancer -- at least not that I know of."
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So, I looked further into it, found as many articles as I could,
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and it was amazing -- because it turned out that it was very rare.
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Some articles even went as far as to say that skeletal muscle tissue
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is resistant to cancer, and furthermore, not only to cancer,
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but of metastases going to skeletal muscle.
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And what metastases are is when the tumor --
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when a piece -- breaks off and travels through the blood stream
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and goes to a different organ. That's what a metastasis is.
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It's the part of cancer that is the most dangerous.
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If cancer was localized, we could likely remove it,
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or somehow -- you know, it's contained. It's very contained.
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But once it starts moving throughout the body, that's when it becomes deadly.
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So the fact that not only did cancer not seem to originate in skeletal muscles,
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but cancer didn't seem to go to skeletal muscle --
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there seemed to be something here.
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So these articles were saying, you know, "Skeletal --
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metastasis to skeletal muscle -- is very rare."
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But it was left at that. No one seemed to be asking why.
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So I decided to ask why. At first -- the first thing I did
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was I emailed some professors who
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specialized in skeletal muscle physiology, and pretty much said,
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"Hey, it seems like cancer doesn't really go to skeletal muscle.
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Is there a reason for this?" And a lot of the replies I got were that
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muscle is terminally differentiated tissue.
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Meaning that you have muscle cells, but they're not dividing,
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so it doesn't seem like a good target for cancer to hijack.
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But then again, this fact that the metastases
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didn't go to skeletal muscle made that seem unlikely.
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And furthermore, that nervous tissue -- brain -- gets cancer,
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and brain cells are also terminally differentiated.
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So I decided to ask why. And here's some of, I guess, my hypotheses
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that I'll be starting to investigate this May at the Sylvester Cancer Institute in Miami.
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And I guess I'll keep investigating until I get the answers.
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But I know that in science, once you get the answers,
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inevitably you're going to have more questions.
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So I guess you could say that I'll probably be doing this for the rest of my life.
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Some of my hypotheses are that
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when you first think about skeletal muscle,
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there's a lot of blood vessels going to skeletal muscle.
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And the first thing that makes me think is that
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blood vessels are like highways for the tumor cells.
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Tumor cells can travel through the blood vessels.
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And you think, the more highways there are in a tissue,
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the more likely it is to get cancer or to get metastases.
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So first of all I thought, you know, "Wouldn't it be favorable
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to cancer getting to skeletal muscle?" And as well,
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cancer tumors require a process called angiogenesis,
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which is really, the tumor recruits the blood vessels to itself
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to supply itself with nutrients so it can grow.
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Without angiogenesis, the tumor remains the size of a pinpoint and it's not harmful.
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So angiogenesis is really a central process to the pathogenesis of cancer.
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And one article that really stood out to me
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when I was just reading about this, trying to figure out why cancer doesn't go to skeletal
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muscle, was that it had reported 16 percent of micro-metastases
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to skeletal muscle upon autopsy.
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16 percent! Meaning that there were these pinpoint tumors in skeletal muscle,
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but only .16 percent of actual metastases --
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suggesting that maybe skeletal muscle is able to control the angiogenesis,
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is able to control the tumors recruiting these blood vessels.
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We use skeletal muscles so much. It's the one portion of our body --
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our heart's always beating. We're always moving our muscles.
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Is it possible that muscle somehow intuitively knows
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that it needs this blood supply? It needs to be constantly contracting,
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so therefore it's almost selfish. It's grabbing its blood vessels for itself.
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Therefore, when a tumor comes into skeletal muscle tissue,
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it can't get a blood supply, and can't grow.
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So this suggests that maybe if there is an anti-angiogenic factor
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in skeletal muscle -- or perhaps even more,
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an angiogenic routing factor, so it can actually direct where the blood vessels grow --
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this could be a potential future therapy for cancer.
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And another thing that's really interesting is that
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there's this whole -- the way tumors move throughout the body,
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it's a very complex system -- and there's something called the chemokine network.
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And chemokines are essentially chemical attractants,
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and they're the stop and go signals for cancer.
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So a tumor expresses chemokine receptors,
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and another organ -- a distant organ somewhere in the body --
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will have the corresponding chemokines,
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and the tumor will see these chemokines and migrate towards it.
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Is it possible that skeletal muscle doesn't express this type of molecules?
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And the other really interesting thing is that
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when skeletal muscle -- there's been several reports that when skeletal
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muscle is injured, that's what correlates with metastases going to skeletal muscle.
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And, furthermore, when skeletal muscle is injured,
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that's what causes chemokines -- these signals saying,
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"Cancer, you can come to me," the "go signs" for the tumors --
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it causes them to highly express these chemokines.
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So, there's so much interplay here.
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I mean, there are so many possibilities
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for why tumors don't go to skeletal muscle.
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But it seems like by investigating, by attacking cancer,
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by searching where cancer is not, there has got to be something --
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there's got to be something -- that's making this tissue resistant to tumors.
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And can we utilize -- can we take this property,
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this compound, this receptor, whatever it is that's controlling these
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anti-tumor properties and apply it to cancer therapy in general?
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Now, one thing that kind of ties the resistance of skeletal muscle to cancer --
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to the cancer as a repair response gone out of control in the body --
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is that skeletal muscle has a factor in it called "MyoD."
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And what MyoD essentially does is, it causes cells to differentiate
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into muscle cells. So this compound, MyoD,
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has been tested on a lot of different cell types and been shown to
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actually convert this variety of cell types into skeletal muscle cells.
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So, is it possible that the tumor cells are going to the skeletal muscle tissue,
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but once in contact inside the skeletal muscle tissue,
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MyoD acts upon these tumor cells and causes them
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to become skeletal muscle cells?
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Maybe tumor cells are being disguised as skeletal muscle cells,
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and this is why it seems as if it is so rare.
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It's not harmful; it has just repaired the muscle.
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Muscle is constantly being used -- constantly being damaged.
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If every time we tore a muscle
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or every time we stretched a muscle or moved in a wrong way,
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cancer occurred -- I mean, everybody would have cancer almost.
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And I hate to say that. But it seems as though muscle cell,
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possibly because of all its use, has adapted
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faster than other body tissues to respond to injury,
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to fine-tune this repair response and actually be able to finish the process
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which the body wants to finish. I really believe that the human body is very,
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very smart, and we can't counteract something the body is saying to do.
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It's different when a bacteria comes into the body --
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that's a foreign object -- we want that out.
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But when the body is actually initiating a process
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and we're calling it a disease, it doesn't seem as though elimination is
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the right solution. So even to go from there, it's possible, although far-fetched,
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that in the future we could almost think of cancer being used as a therapy.
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If those diseases where tissues are deteriorating --
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for example Alzheimer's, where the brain, the brain cells, die
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and we need to restore new brain cells, new functional brain cells --
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what if we could, in the future, use cancer? A tumor --
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put it in the brain and cause it to differentiate into brain cells?
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That's a very far-fetched idea, but I really believe that it may be possible.
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These cells are so versatile, these cancer cells are so versatile --
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we just have to manipulate them in the right way.
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And again, some of these may be far-fetched, but
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I figured if there's anywhere to present far-fetched ideas, it's here at TED, so
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thank you very much.
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(Applause)
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ABOUT THE SPEAKER
Eva Vertes - Neuroscience and cancer researcherEva Vertes is a microbiology prodigy. Her discovery, at age 17, of a compound that stops fruit-fly brain cells from dying was regarded as a step toward curing Alzheimer's. Now she aims to find better ways to treat -- and avoid -- cancer.
Why you should listen
Eva Vertes may not yet have the answers she needs to cure cancer, but she's asking some important -- and radical questions: If smoking can cause lung cancer, and drinking can cause liver cancer, is it possible that cancer is a direct result of injury? If so, could cancer be caused by the body's own repair system going awry?
She asks this and other breathtaking questions in her conference-closing 2005 talk. Her approach marks an important shift in scientific thinking, looking in brand-new places for cancer's cause -- and its cure. Her ultimate goal, which even she calls far-fetched, is to fight cancer with cancer.
Eva Vertes | Speaker | TED.com