Cancer, Ralph Stein Rockefeller University, Nobel Prize discussed on On Point with Tom Ashbrook | Podcasts

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I look at it but take it apart. It's actually not all that complicated. But what we do is just is developed a way to take the brakes off the immune system. There's a, it's it's fairly complicated process, but now that the first step is a thing called a t cell antigen receptor. It's a molecule service of of these t. cells that go all over the body, looking for things that shouldn't be there and try to eliminate them. But this antigen receptors wet allows the t. cell the know something you know is wrong. You know. And gives a signal that's kind of just like the ignition switch in a car. You know, every tesol has a different one, but turning it onto, I'd make it go anywhere. There's a nother molecule. Another signal co stimulatory signal that we showed the late eighties is given by molecule CD twenty eight. And this can really only be provided by very specialized cells called in genetic sales that that Ralph Stein Rockefeller University gut the Nobel prize several years ago. And so one of the things that we've found was that tumor cells can't give that signal and so they're kind of invisible to the moon system. But, but it's actually more complex than that because there's another molecule but is very much like CD twenty eight, but it it acts like the brakes. And so because when you turn T-cells on, they start dividing very, very fast reproducing themselves to give you, you know, hundreds of thousands to millions and you've got to do that within about a week or so, you know, deal with virus infections or cancer or whatever, but you've gotta stop that process. And that's seeps like four's job is to stop that before it can cause any harm to normal cells. And since the tumors had a head start because they as it turns out, T-cells against tumors don't don't get primes, don't get get to see twenty eight six until they die for some reason and cause inflammation and immune system and gets alert in starts to process. But, but if they start growing in, I mean, they've been growing for a while. So they've had a head start so secretly. I just reason that maybe know therapies hadn't worked very well reason that maybe the thing was is that if you tumor gets too big for to get enough T-cells cells to eliminate them before seats, four inches off, then that tumor win. So we just disabled the brakes for while figured out a way just disable the break. So if I, if I may just jump in here with a sort of a lay person summary of what you said and tell me telling me from doing this right that essentially, part of the reason why immunotherapy is beforehand perhaps weren't as affective, is that as you were saying, there's something about tumor cells themselves that allowed the immune or in inhibited t. cells in the immune system from from working and you figured out a way to sort of turn on those t cells so that they could help essentially attack the tumors. Is that right? Most sensually. I mean, we figured out how to how to keep them from turning off. Keep them from turning off. Okay. So so so so how I mean, how revolutionary was this? This shift in thinking about what you could do with t. cells did ha- did it has it really opened the door in terms of thinking about using the immune system as as a primary means of of attacking cancers or. Yes, it was. It was quite revolutionary at the time because what it involves trying to target a molecule on the surface of t cells and had nothing to do with cancer, the cancer. So and so when I started talking about this, all we gotta do is unleash the t. cells by blocking. You know this molecule people said, well, how can you treat cancer bag knowing the cancer. And I said, because the immune system doesn't know that it's necessarily can't..

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