Thank you. It's really an honor and a privilege to be here spending my last day as a teenager. Today I want to talk to you about the future, but first I'm going to tell you a bit about the past. My story starts way before I was born. My grandmother was on a train to Auschwitz, the death camp. And she was going along the tracks, and the tracks split. And somehow -- we don't really know exactly the whole story -- but the train took the wrong track and went to a work camp rather than the death camp. My grandmother survived and married my grandfather. They were living in Hungary, and my mother was born. And when my mother was two years old, the Hungarian revolution was raging, and they decided to escape Hungary. They got on a boat, and yet another divergence -- the boat was either going to Canada or to Australia. They got on and didn't know where they were going, and ended up in Canada. So, to make a long story short, they came to Canada. My grandmother was a chemist. She worked at the Banting Institute in Toronto, and at 44 she died of stomach cancer. I never met my grandmother, but I carry on her name -- her exact name, Eva Vertes -- and I like to think I carry on her scientific passion, too.
謝謝你們!真的很榮幸能在這裡 渡過我身為青少年的最後一天。 今天我想與你們談論未來, 但是我要先跟你們分享一點我的過去。 我的故事遠在我還未出生前就開始了。 我祖母曾身處在前往奥斯威辛死亡集中營的火車上, 她乘坐的火車沿著軌道前進,來到分岔處。 不知何故,我們並不知道整個事件的來龍去脈, 但結果是,那列火車沿著錯誤的鐵道抵達某勞動營,而非死亡營。 祖母活了下來並與祖父結了婚。 他們那時住在匈牙利,在此時期我媽媽出生了。 當我媽兩歲大時, 匈牙利發生了革命,於是他們決定逃離匈牙利。 他們搭上了一艘船,又是一個命運的分岔點, 那艘船的目的地可能是加拿大或是澳洲, 他們雖上了船卻不知將前往何方,最後抵達了加拿大。 所以,長話短說,他們來到了加拿大。 祖母是化學家,任職於多倫多的班廷研究所, 她在 44 歲時死於胃癌。我從來沒見過我祖母, 但我繼承了她的名字,她的全名 - Eva Vertes 而且我認為我也繼承了她對科學的熱誠。
I found this passion not far from here, actually, when I was nine years old. My family was on a road trip and we were in the Grand Canyon. And I had never been a reader when I was young -- my dad had tried me with the Hardy Boys; I tried Nancy Drew; I tried all that -- and I just didn't like reading books. And my mother bought this book when we were at the Grand Canyon called "The Hot Zone." It was all about the outbreak of the Ebola virus. And something about it just kind of drew me towards it. There was this big sort of bumpy-looking virus on the cover, and I just wanted to read it. I picked up that book, and as we drove from the edge of the Grand Canyon to Big Sur, and to, actually, here where we are today, in Monterey, I read that book, and from when I was reading that book, I knew that I wanted to have a life in medicine. I wanted to be like the explorers I'd read about in the book, who went into the jungles of Africa, went into the research labs and just tried to figure out what this deadly virus was. So from that moment on, I read every medical book I could get my hands on, and I just loved it so much. I was a passive observer of the medical world.
事實上,我是在離這裡不遠的地方發現了這股熱誠,那年我九歲。 我們家開車到處旅遊,那時正經過大峽谷。 我從小就不愛看書, 我爸要我試著讀《哈迪男孩》,我也試過《神探俏佳人》, 全都試過,而我就是不喜歡看書。 當我們在大峽谷時,我媽買了這本書, 書名是《伊波拉浩劫》,內容是關於伊波拉病毒的爆發。 而某樣東西深深吸引著我。 書本封面上有個看起來凹凸不平的病毒, 而我就是想要讀它。我拿起那本書, 當我們從大峽谷的邊緣行駛到 Big Sur 然後到這裡 - 我們現在所在的地方,蒙特雷。 一路上我都在看那本書,當我打開那本書時, 我就知道我這輩子要從事醫學研究。 我想要像書中的探險家, 深入非洲的叢林, 身處在實驗室中,就為了查明這致命的病毒為何? 從那一刻起,我開始閱讀任何我可取得的醫學書籍, 而我真的很愛這些書。 我那時是被動地觀察著醫學世界,
It wasn't until I entered high school that I thought, "Maybe now, you know -- being a big high school kid -- I can maybe become an active part of this big medical world." I was 14, and I emailed professors at the local university to see if maybe I could go work in their lab. And hardly anyone responded. But I mean, why would they respond to a 14-year-old, anyway? And I got to go talk to one professor, Dr. Jacobs, who accepted me into the lab. At that time, I was really interested in neuroscience and wanted to do a research project in neurology -- specifically looking at the effects of heavy metals on the developing nervous system. So I started that, and worked in his lab for a year, and found the results that I guess you'd expect to find when you feed fruit flies heavy metals -- that it really, really impaired the nervous system. The spinal cord had breaks. The neurons were crossing in every which way. And from then I wanted to look not at impairment, but at prevention of impairment.
直到進入高中之後,我才開始有一個念頭, 「或許現在,身為一個高中生, 我或許能成為廣大醫學世界中主動的一員。」 那年我 14 歲,我寫了電子郵件給地區大學的教授們 看看我能否到他們的實驗室工作。幾乎沒有任何人回應。 但是話說回來,他們怎會想要回應一個才 14 歲的孩子? 最終我有機會與一位教授談話,Dr. Jacobs 他讓我進他的實驗室工作。 那時,我對神經科學極感興趣, 想要做一個與神經學相關的研究 - 著重於觀察重金屬對發育中神經系統的影響。 於是我開始在他的實驗室工作了一年, 然後得到的結果,我猜你們也會如此的預期, 當你餵食果蠅重金屬 - 真的,真的會損害神經系統。 脊髓斷裂。神經元彼此間以各種方式交叉著。 從那時開始,我不想再研究損傷,我希望研究損傷的預防方法。
So that's what led me to Alzheimer's. I started reading about Alzheimer's and tried to familiarize myself with the research, and at the same time when I was in the -- I was reading in the medical library one day, and I read this article about something called "purine derivatives." And they seemed to have cell growth-promoting properties. And being naive about the whole field, I kind of thought, "Oh, you have cell death in Alzheimer's which is causing the memory deficit, and then you have this compound -- purine derivatives -- that are promoting cell growth." And so I thought, "Maybe if it can promote cell growth, it can inhibit cell death, too." And so that's the project that I pursued for that year, and it's continuing now as well, and found that a specific purine derivative called "guanidine" had inhibited the cell growth by approximately 60 percent. So I presented those results at the International Science Fair, which was just one of the most amazing experiences of my life. And there I was awarded "Best in the World in Medicine," which allowed me to get in, or at least get a foot in the door of the big medical world.
這就是我為何開始研究阿滋海默氏症。我開始閱讀關於阿滋海默氏症的讀物, 然後試著讓自己熟悉此研究領域, 在那同時,當我 某天在醫學圖書館裡讀書,我讀到一篇文章, 提到某種叫做嘌呤衍生物的東西, 他們似乎具有促進細胞生長的特性。 由於對這整個研究領域的天真無知,我這麼想: 「喔~阿茲海默氏症是因為細胞死亡 而造成記憶力受損,然而你有這種化合物 - 可以促進細胞生長的嘌呤衍生物。」 於是我就想到:「如果它可以促進細胞生長, 或許它也可以抑制細胞死亡。」 於是那便成為我該年的研究計畫, 目前仍持續進行中。 我發現有一種特定的嘌呤衍生物,稱作「胍」(guanidine) 可以抑制細胞生長達到約 60%。 於是我在國際科學研討會上發表這些結果, 那是我人生中最棒的經驗之一。 在那邊,我獲得了「最佳世界醫藥」獎, 該獎項使我得以進入,或至少讓我得以一窺廣大的醫療世界。
And from then on, since I was now in this huge exciting world, I wanted to explore it all. I wanted it all at once, but knew I couldn't really get that. And I stumbled across something called "cancer stem cells." And this is really what I want to talk to you about today -- about cancer. At first when I heard of cancer stem cells, I didn't really know how to put the two together. I'd heard of stem cells, and I'd heard of them as the panacea of the future -- the therapy of many diseases to come in the future, perhaps. But I'd heard of cancer as the most feared disease of our time, so how did the good and bad go together? Last summer I worked at Stanford University, doing some research on cancer stem cells. And while I was doing this, I was reading the cancer literature, trying to -- again -- familiarize myself with this new medical field. And it seemed that tumors actually begin from a stem cell. This fascinated me. The more I read, the more I looked at cancer differently and almost became less fearful of it.
從那時候開始,既然我現在已經身處在這廣大刺激的世界中, 我想要探索每一個地方。我想要一次完成,但是我知道那是不可能的。 然後我碰巧遇到了某個稱作癌症幹細胞的東西。 這才是我今天真正想要跟你們談談的東西 - 關於癌症。 一開始,當我聽到癌症幹細胞時, 我並不是非常確定這兩個概念是如何湊在一起的。我聽說過幹細胞, 我聽過人們形容它是未來的萬靈丹 - 也許是很多未來疾病治療方法的依據。 但同時,我也聽說過癌症是現世最令人聞之色變的疾病, 所以,好的跟壞的東西是如何扯在一起的呢? 去年夏天,我在史丹佛大學工作,從事一些癌症幹細胞的研究。 我一面做研究,一面閱讀癌症相關文獻, 嘗試著 - 又一次 - 讓自己熟悉這一個新的醫學領域。 結果看起來腫瘤事實上是從幹細胞開始產生的。 這個發現令我著迷了。當我讀得愈多,我愈對癌症刮目相看 而且幾乎愈來愈不怕它。
It seems that cancer is a direct result to injury. If you smoke, you damage your lung tissue, and then lung cancer arises. If you drink, you damage your liver, and then liver cancer occurs. And it was really interesting -- there were articles correlating if you have a bone fracture, and then bone cancer arises. Because what stem cells are -- they're these phenomenal cells that really have the ability to differentiate into any type of tissue. So, if the body is sensing that you have damage to an organ and then it's initiating cancer, it's almost as if this is a repair response. And the cancer, the body is saying the lung tissue is damaged, we need to repair the lung. And cancer is originating in the lung trying to repair -- because you have this excessive proliferation of these remarkable cells that really have the potential to become lung tissue. But it's almost as if the body has originated this ingenious response, but can't quite control it. It hasn't yet become fine-tuned enough to finish what has been initiated. So this really, really fascinated me.
癌症似乎是組織或器官受傷的直接產物。 如果你抽菸,導致肺部組織損傷,就會產生肺癌。 如果你喝酒,傷害你的肝臟,就會產生肝癌。 然後非常有趣的是 - 有些文章報導到這個關聯性 如果你骨折,就容易產生骨癌。 因為幹細胞是 - 他們是這些 真正具有能分化成任何組織的能力, 不可思議的細胞。 所以,如果你的身體感覺到有某個器官損壞, 就會引發癌症,幾乎如修復機制一般。 癌症即是身體正說著,肺臟組織受傷了, 我們必需修復肺臟。因此癌症在肺臟內產生 試圖修復器官。因為你有這些過度增生, 並極有潛力成為肺臟組織的細胞。 但這幾乎就好比是身體自發性的產生這巧妙的反應, 卻不能完全控制它。 它並未受到良好調校,以完成一開始的目的。 因此這真的,真的令我著迷。
And I really think that we can't think about cancer -- let alone any disease -- in such black-and-white terms. If we eliminate cancer the way we're trying to do now, with chemotherapy and radiation, we're bombarding the body or the cancer with toxins, or with radiation, trying to kill it. It's almost as if we're getting back to this starting point. We're removing the cancer cells, but we're revealing the previous damage that the body has tried to fix. Shouldn't we think about manipulation, rather than elimination? If somehow we can cause these cells to differentiate -- to become bone tissue, lung tissue, liver tissue, whatever that cancer has been put there to do -- it would be a repair process. We'd end up better than we were before cancer. So, this really changed my view of looking at cancer. And while I was reading all these articles about cancer, it seemed that the articles -- a lot of them -- focused on, you know, the genetics of breast cancer, and the genesis and the progression of breast cancer -- tracking the cancer through the body, tracing where it is, where it goes.
而且我真的認為我們不應該用如此黑白分明的眼光, 來看待癌症,或是其他任何的疾病。 如果我們以現行的方法,例如化療和放射性療法,來消滅癌症, 我們以毒素或放射線轟炸身體或是癌症,試著殺死它。 這好像我們又回到原點了。 我們移除癌細胞,卻曝露了 身體試圖去修復的舊傷。 難道我們不應該思考如何去控制,而非殲滅癌細胞嗎? 如果我們能以某種方法引導這些細胞進行分化, 變成骨骼細胞、肺臟細胞、肝臟細胞, 任何一種該癌症應該要修補的細胞種類, 這就成為了一個修復過程。這樣我們就會比我們罹患癌症前更健康。 因此,這真的改變了我對於癌症的看法。 因此,當我閱讀這些癌症文獻的同時, 這些文章絕大多數似乎都專注在,你知道的, 乳癌的遺傳基因、發生、 與進程。 追蹤體內的癌細胞,紀錄、描繪出它在哪裡,往哪邊移動。
But it struck me that I'd never heard of cancer of the heart, or cancer of any skeletal muscle for that matter. And skeletal muscle constitutes 50 percent of our body, or over 50 percent of our body. And so at first I kind of thought, "Well, maybe there's some obvious explanation why skeletal muscle doesn't get cancer -- at least not that I know of." So, I looked further into it, found as many articles as I could, and it was amazing -- because it turned out that it was very rare. Some articles even went as far as to say that skeletal muscle tissue is resistant to cancer, and furthermore, not only to cancer, but of metastases going to skeletal muscle. And what metastases are is when the tumor -- when a piece -- breaks off and travels through the blood stream and goes to a different organ. That's what a metastasis is. It's the part of cancer that is the most dangerous. If cancer was localized, we could likely remove it, or somehow -- you know, it's contained. It's very contained. But once it starts moving throughout the body, that's when it becomes deadly. So the fact that not only did cancer not seem to originate in skeletal muscles, but cancer didn't seem to go to skeletal muscle -- there seemed to be something here. So these articles were saying, you know, "Skeletal -- metastasis to skeletal muscle -- is very rare." But it was left at that. No one seemed to be asking why.
但令我吃驚的事,我從沒聽說過心臟癌, 或者例如任何骨骼肌的癌症。 但是骨骼肌佔了我們身體組成的一半, 或一半以上。因此一開始我這樣想著: 「嗯,也許有某些顯而易見的原因, 可以說明為什麼骨骼肌不會罹患癌症,只是我不知道而已。」 因此,我深入的去調查,閱讀我所能找到的任何文獻, 結果同樣的令人吃驚,因為事實上骨骼肌癌症非常罕見。 某些文獻甚至下了結論說骨骼肌組織 對癌症有抵抗力,甚至,不只是癌症本身, 也能抵抗惡性腫瘤轉移。 惡性腫瘤轉移就是當腫瘤, 一小塊腫瘤組織,從腫瘤上脫離並沿著血管 轉移到不同的器官,這就是惡性腫瘤轉移。 這是癌症中最危險的部份。 當癌症還只是區域性的時候,我們很有可能將之移除, 或是,你知道,它是受控制的,非常受限的。 然而,一旦癌症開始在全身四處移動,它就變得非常致命。 所以,癌症似乎不只不源於骨骼肌, 也不會轉移到骨骼肌這件事,說明了 這裡面一定有文章。 所以這些文獻說,你知道的,「骨骼肌, 惡性腫瘤轉移到骨骼肌是非常罕見的。」 但是文章就這樣結束了。似乎沒有人好奇的問「為什麼」?
So I decided to ask why. At first -- the first thing I did was I emailed some professors who specialized in skeletal muscle physiology, and pretty much said, "Hey, it seems like cancer doesn't really go to skeletal muscle. Is there a reason for this?" And a lot of the replies I got were that muscle is terminally differentiated tissue. Meaning that you have muscle cells, but they're not dividing, so it doesn't seem like a good target for cancer to hijack. But then again, this fact that the metastases didn't go to skeletal muscle made that seem unlikely. And furthermore, that nervous tissue -- brain -- gets cancer, and brain cells are also terminally differentiated. So I decided to ask why. And here's some of, I guess, my hypotheses that I'll be starting to investigate this May at the Sylvester Cancer Institute in Miami. And I guess I'll keep investigating until I get the answers. But I know that in science, once you get the answers, inevitably you're going to have more questions. So I guess you could say that I'll probably be doing this for the rest of my life.
因此我決定來問這個問題。一開始,我所做的第一件事是 寄電子郵件給一些 專長在骨骼肌生理學的教授們,信件內容不外忽是, 「嘿,看起來癌症不會轉移到骨骼肌上, 你知道為什麼嗎?」而我得到的回覆大多是說 肌肉是終端分化的組織。 意思是說,即使你有肌肉細胞,但因為這些細胞不會再分裂了, 所以它似乎不像是癌症會劫持的好標的。 但是話說回來, 這個理由並不能解釋為什麼癌症不會轉移到骨骼肌上。 尤有甚者,神經組織,好比大腦,也會罹患癌症, 但是腦細胞也是終端分化的細胞。 因此我決定來問為什麼。這裡是一些,我推測的,我的假說 今年五月,我將要在邁阿密的希爾維斯特癌症研究中心展開我的研究。 我猜我將會不斷的研究,直到我找到答案為止。 但是我知道在科學的世界裡,一旦你找到答案, 不可避免地,你將會有更多的問題。 所以我猜你可以說,我大概會終其一生都在做研究。
Some of my hypotheses are that when you first think about skeletal muscle, there's a lot of blood vessels going to skeletal muscle. And the first thing that makes me think is that blood vessels are like highways for the tumor cells. Tumor cells can travel through the blood vessels. And you think, the more highways there are in a tissue, the more likely it is to get cancer or to get metastases. So first of all I thought, you know, "Wouldn't it be favorable to cancer getting to skeletal muscle?" And as well, cancer tumors require a process called angiogenesis, which is really, the tumor recruits the blood vessels to itself to supply itself with nutrients so it can grow. Without angiogenesis, the tumor remains the size of a pinpoint and it's not harmful. So angiogenesis is really a central process to the pathogenesis of cancer.
我的假說包括, 首先,當你想到骨骼肌, 骨骼肌內有一大堆的血管。 而這讓我聯想到的第一件事是 血管就如同腫瘤細胞的高速公路一般, 腫瘤細胞可以經由血管移動。 然後你會想,組織內的高速公路愈多, 應該就愈有可能罹患癌症或是接受轉移。 所以首先我想到,像是 「這樣癌症應該更容易往骨骼肌轉移吧?」 同時,癌症、腫瘤需要血管增生的過程, 這過程其實就是,腫瘤在其周遭新建血管, 以供給它生長所需的養份。 去除掉血管增生,腫瘤就會維持像針珠筆尖一樣的大小且無害。 所以血管增生真的是癌症致病機制中的核心過程。
And one article that really stood out to me when I was just reading about this, trying to figure out why cancer doesn't go to skeletal muscle, was that it had reported 16 percent of micro-metastases to skeletal muscle upon autopsy. 16 percent! Meaning that there were these pinpoint tumors in skeletal muscle, but only .16 percent of actual metastases -- suggesting that maybe skeletal muscle is able to control the angiogenesis, is able to control the tumors recruiting these blood vessels. We use skeletal muscles so much. It's the one portion of our body -- our heart's always beating. We're always moving our muscles. Is it possible that muscle somehow intuitively knows that it needs this blood supply? It needs to be constantly contracting, so therefore it's almost selfish. It's grabbing its blood vessels for itself. Therefore, when a tumor comes into skeletal muscle tissue, it can't get a blood supply, and can't grow.
有一篇文章,非常的與眾不同,引起了我的注意, 當我在閱讀這篇文章,嘗試找出癌症不會轉移到骨骼肌的原因時, 我看到這篇文章指出,解剖發現,16% 的骨骼肌 具有微型癌症轉移的跡象。 16% ! 意味著骨骼肌中的確可以發現這些鋼珠筆尖大小般的腫瘤, 但是真正惡性腫瘤轉移發生的機率只有 0.16%, 意味著也許骨骼肌可以控制血管增生的過程, 可以控制腫瘤周遭的血管新生。 我們無時無刻不在使用骨骼肌。它是我們身體的一部分, 我的的心臟總在跳動,我們的肌肉也一直在運動, 是不是有可能,肌肉不知怎的,直覺性的知道 它需要大量的血液供給?它常常在收縮, 所以它幾乎是極端自私的。它為了它自己霸佔住了所有血管。 因此,當腫瘤來到了骨骼肌組織中, 它無法取得血液供給,不能生長。
So this suggests that maybe if there is an anti-angiogenic factor in skeletal muscle -- or perhaps even more, an angiogenic routing factor, so it can actually direct where the blood vessels grow -- this could be a potential future therapy for cancer. And another thing that's really interesting is that there's this whole -- the way tumors move throughout the body, it's a very complex system -- and there's something called the chemokine network. And chemokines are essentially chemical attractants, and they're the stop and go signals for cancer. So a tumor expresses chemokine receptors, and another organ -- a distant organ somewhere in the body -- will have the corresponding chemokines, and the tumor will see these chemokines and migrate towards it. Is it possible that skeletal muscle doesn't express this type of molecules? And the other really interesting thing is that when skeletal muscle -- there's been several reports that when skeletal muscle is injured, that's what correlates with metastases going to skeletal muscle.
因次這暗示著,也許骨骼肌中有一種反血管新生的物質存在, 尤有甚者,甚至有可能有 一種血管新生導引的物質,因此它可以引導血管該向何處生長。 這有潛力成為未來治療癌症的方法之一。 又一個非常令人感興趣的是 這整個,腫瘤在體內四處移動的方法, 是一個非常複雜的系統,我們稱之為趨化因子網路。 趨化因子基本上就是化學性的吸引物, 它們就是癌症停止與移動的訊號。 腫瘤細胞的表面會表現許多驅化因子受器, 而其他的器官,在體內某處較遠距離的器官, 就會擁有相對應的驅化因子, 而腫瘤將會感應到這些趨化因子,而開始朝它移動。 有可能骨骼肌不表達這些分子嗎? 最後一個非常有趣的是 當骨骼肌,許多報告指出 在骨骼肌受傷的同時,也伴隨惡性腫瘤轉移到骨骼肌內的現象。
And, furthermore, when skeletal muscle is injured, that's what causes chemokines -- these signals saying, "Cancer, you can come to me," the "go signs" for the tumors -- it causes them to highly express these chemokines. So, there's so much interplay here. I mean, there are so many possibilities for why tumors don't go to skeletal muscle. But it seems like by investigating, by attacking cancer, by searching where cancer is not, there has got to be something -- there's got to be something -- that's making this tissue resistant to tumors. And can we utilize -- can we take this property, this compound, this receptor, whatever it is that's controlling these anti-tumor properties and apply it to cancer therapy in general? Now, one thing that kind of ties the resistance of skeletal muscle to cancer -- to the cancer as a repair response gone out of control in the body -- is that skeletal muscle has a factor in it called "MyoD." And what MyoD essentially does is, it causes cells to differentiate into muscle cells. So this compound, MyoD, has been tested on a lot of different cell types and been shown to actually convert this variety of cell types into skeletal muscle cells. So, is it possible that the tumor cells are going to the skeletal muscle tissue, but once in contact inside the skeletal muscle tissue, MyoD acts upon these tumor cells and causes them to become skeletal muscle cells? Maybe tumor cells are being disguised as skeletal muscle cells, and this is why it seems as if it is so rare.
而且不只這樣,當骨骼肌受傷時, 也導致趨化因子,這些訊號發出: 「癌症,現在你可以過來了。」這種通行的訊號給腫瘤, 這導致它們開始大量的表達這些趨化因子。 所以,這邊實在是有太多會相互影響的事情了。 我是說,有這麼多種可能性 可以解釋為什麼腫瘤不會轉移到骨骼肌。 但是看起來藉由研究、攻擊癌症 與尋找癌症所不存在的地方,一定有某些東西, 肯定有某些東西,使這組織對腫瘤具有抵抗力。 我們能夠利用,如果我們能夠利用這特性, 這種化合物,這種受器,任何控制這個 抗腫瘤特性的東西,並將之應用在大眾化的癌症療法中嗎? 現在我們知道,在骨骼肌中,有個可能跟抗癌能力密切相關的物質, 能控制癌症—也就是體內失去控制的修補機制。 那是一個稱為 MyoD 的因子。 MyoD 的基本作用是,它導致細胞分化成 骨骼細胞。所以 MyoD 這種化合物 已經在很多不同種類的細胞上測試過,並已經被證明 真正能夠將這些各式不同種類的細胞,轉換為骨骼肌細胞。 所以,是不是有可能,腫瘤細胞的確會進入骨骼肌組織, 但是一旦它接觸到骨骼肌組織的內部, MoyD 便開始對這些腫瘤細胞作用,導致它們 轉變為骨骼肌細胞? 或許腫瘤細胞偽裝為骨骼肌細胞, 這也是為什麼它看起來這麼罕見。
It's not harmful; it has just repaired the muscle. Muscle is constantly being used -- constantly being damaged. If every time we tore a muscle or every time we stretched a muscle or moved in a wrong way, cancer occurred -- I mean, everybody would have cancer almost. And I hate to say that. But it seems as though muscle cell, possibly because of all its use, has adapted faster than other body tissues to respond to injury, to fine-tune this repair response and actually be able to finish the process which the body wants to finish. I really believe that the human body is very, very smart, and we can't counteract something the body is saying to do.
它對人體沒有傷害。它只是修復肌肉。 肌肉無時無刻不被使用,也不斷的被損害。 如果每次我們肌肉撕裂傷 或是每次我們錯誤的運動或伸展肌肉, 就會導致癌症。我是說,這樣的話,幾乎所有人都會罹患癌症了。 雖然我討厭這麼說。但是看起來肌肉細胞, 可能因為它的功能, 能比其他組織,更快適應身體對組織受損的反應, 並微調這修復過程,而確實完成 身體想要完成的過程。我真誠的相信人類的身體非常、非常的聰明, 我們無法對抗身體想要做的事。
It's different when a bacteria comes into the body -- that's a foreign object -- we want that out. But when the body is actually initiating a process and we're calling it a disease, it doesn't seem as though elimination is the right solution. So even to go from there, it's possible, although far-fetched, that in the future we could almost think of cancer being used as a therapy. If those diseases where tissues are deteriorating -- for example Alzheimer's, where the brain, the brain cells, die and we need to restore new brain cells, new functional brain cells -- what if we could, in the future, use cancer? A tumor -- put it in the brain and cause it to differentiate into brain cells?
這跟細菌進入人體不同, 細菌是外來物,我們希望排除它。 但是當身體啟動某種過程, 我們卻把這種過程稱之為疾病,殲滅看起來並不是一個好的解決辦法。 所以從那個角度來看,雖然仍舊很遙遠,但是 未來將癌症視為是一種療法來使用是有可能的。 如果那些組織退化的疾病, 例如:阿茲海默氏症,其腦部,腦細胞面臨死亡 而我們需要重建新的腦細胞,新的腦細胞功能, 也許我們可以,在未來使用癌症來治療? 將一個腫瘤放進腦部,並引導它分化成為腦細胞?
That's a very far-fetched idea, but I really believe that it may be possible. These cells are so versatile, these cancer cells are so versatile -- we just have to manipulate them in the right way. And again, some of these may be far-fetched, but I figured if there's anywhere to present far-fetched ideas, it's here at TED, so thank you very much.
這是一個天馬行空的想法,但我真的相信是有可能的。 這些細胞這樣的變化多端,這些癌症細胞非常多變, 我們只需要用正確來方法來操控它們。 我再強調,這些想法有部份是天馬行空, 但是我想,如果有什麼場合可以公開發表天馬行空的點子,唯有在 TED, 非常謝謝大家。
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