James P. Allison
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Podcast Appearances
They get a lot of polyps, you know. They eventually go on and develop colon cancer. It's definitely a predisposition you can predict. But there are mutations, common mutations associated with that, that I think if you immunized early enough, you could protect those people from ever developing the disease. by immunizing them later. Maybe the same will happen with BRCA.
They get a lot of polyps, you know. They eventually go on and develop colon cancer. It's definitely a predisposition you can predict. But there are mutations, common mutations associated with that, that I think if you immunized early enough, you could protect those people from ever developing the disease. by immunizing them later. Maybe the same will happen with BRCA.
BRCA mutations are associated in women with breast cancer and ovarian cancer and men also with certain kinds of cancer, but it may be possible to prepare vaccines there. But most of the times the mutations are so individual individually specific to you that there's no way you're going to have a vaccine. You can prophylactically treat the population.
BRCA mutations are associated in women with breast cancer and ovarian cancer and men also with certain kinds of cancer, but it may be possible to prepare vaccines there. But most of the times the mutations are so individual individually specific to you that there's no way you're going to have a vaccine. You can prophylactically treat the population.
For most cancers, you're going to have to come up with something that's really powerful and allows you to jumpstart a response as soon as you detect it. And I think we're getting close. We're not there yet.
For most cancers, you're going to have to come up with something that's really powerful and allows you to jumpstart a response as soon as you detect it. And I think we're getting close. We're not there yet.
Yeah, I mean, we're still there, although it's better now. We could guess. We can make educated guesses now. We can't get exactly there.
Yeah, I mean, we're still there, although it's better now. We could guess. We can make educated guesses now. We can't get exactly there.
Yeah. Well, again, it's because one of them is big and largely they're individual. So your tumor has mutations that nobody else has had. So you got to tailor it to the individual. And secondly, there are ways that the tumor can lose. For example, the peptide has to be from containing the mutation has to get on the cell surface by these MHC molecules.
Yeah. Well, again, it's because one of them is big and largely they're individual. So your tumor has mutations that nobody else has had. So you got to tailor it to the individual. And secondly, there are ways that the tumor can lose. For example, the peptide has to be from containing the mutation has to get on the cell surface by these MHC molecules.
And if you lose expression of MHC molecules, then they're invisible to the immune system. The tumor will still be there. The mutation will still be being made, but the immune system can't see it because it doesn't get to the surface of the cell. There are ways around that that we've got to have them, but that's what happens.
And if you lose expression of MHC molecules, then they're invisible to the immune system. The tumor will still be there. The mutation will still be being made, but the immune system can't see it because it doesn't get to the surface of the cell. There are ways around that that we've got to have them, but that's what happens.
It's been shown in melanoma, for example, patients just quit making the molecule that carries it. But there are other ways around that that we're beginning to come up with. But that's one easy mechanism. Another one is that one of the main ways that tumors kill tumor cells is by making gamma interferon.
It's been shown in melanoma, for example, patients just quit making the molecule that carries it. But there are other ways around that that we're beginning to come up with. But that's one easy mechanism. Another one is that one of the main ways that tumors kill tumor cells is by making gamma interferon.
which is a cytokine that, I mean, you've heard of, but one of its activities, besides helping protect you against viruses, it causes tumor cells to quit dividing and can kill many of them. But if you lose anything along the receptor downstream of the gamma interferon, the thing that detects gamma interferon and tells the cell it's around,
which is a cytokine that, I mean, you've heard of, but one of its activities, besides helping protect you against viruses, it causes tumor cells to quit dividing and can kill many of them. But if you lose anything along the receptor downstream of the gamma interferon, the thing that detects gamma interferon and tells the cell it's around,
If you mutate anything in that pathway, then that doesn't work anymore either. And so the T cells can make all the gamma interferon they want, and the tumor won't. respond to it. So there's that too.
If you mutate anything in that pathway, then that doesn't work anymore either. And so the T cells can make all the gamma interferon they want, and the tumor won't. respond to it. So there's that too.
Well, first it's just to get the T cells. And then secondly, in importance, is do something about the myeloid cells, which were not there yet. We're getting close on the T cells. The myeloid cells, we're only beginning there. But ultimately, it's how do we deal with these things that comes down.
Well, first it's just to get the T cells. And then secondly, in importance, is do something about the myeloid cells, which were not there yet. We're getting close on the T cells. The myeloid cells, we're only beginning there. But ultimately, it's how do we deal with these things that comes down.