Joe Rogan Experience #2372 - Garry Nolan

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Gary, very nice to meet you, sir.

Nice to meet you as well.

Thank you for doing this. I really appreciate it. Um, tell everybody what you do. Tell everybody what your official position is. You- you're a professor at the School of Medicine at Stanford. What- what do you do?

So, my day job is in cancer research and cancer biology, mostly immunology and cancer. Much of what my laboratory does is not so much the biology of cancer, but developing instruments that create the data that allow us to analyze the complexities of how the immune system interfaces with tumors, and how tumors basically re-enable, uh, the immune system to help the cancer itself. So the problem's been we don't have the ability to collect enough data, or not until recently, to collect and understand what all of that means, so we've been kind of poking in the dark for decades. And so probably for the last 20 years, I've developed a number of instruments and turned them into companies that allow everybody to access a level of information they couldn't get before.

So, uh, ex- ex- explain that. The- the immune system allows the tumors? Ex- wh- wh- wh- wh-

So what happens is that there's sort of a, there's a dance between the mutations that initiate a tumor and then, uh, sort of an evolution of how the tumor eventually learns how to trick the immune system to not recognize it. So we have all kinds-

Hmm.

... of inter- I mean, literally every day, uh, every person, you'll develop five cancer-like objects inside of your body, but the immune system, uh, and your body has a way of shutting it down very quickly. But with enough time and with enough variation, tumors will eventually evolve in a way that trick the immune system, not only to- to not recognize them, but in fact, to help them and feed them in a way, to create an inflammatory environment that actually then the tumor uses to propagate its own cell division and then metastasize.

So it's a normal function of natural human biology to create tumors?

It's not so much a normal function. It's a byproduct of what evolution is, that when the genes mutate when a cell divides, or if you go out and, you know, stand in the- in the sun, uh, too much for instance, you get skin cancers because you're getting ionizing radiation that's changing the DNA, making a mutation, and some of those random mutations will initiate a cancer. So for instance, I have, um, a mutation called MIDF E318K. It's, uh, a mutation that I was born with. It didn't- it wasn't in my family, and it causes both melanoma and kidney cancer, which I've had both. I've had a dozen, uh, melanomas alone. Um, you know, we didn't find that out until a couple of years ago, but I've been following it over the years and we basically figured out, okay, it's gonna have to be this. So we had my sequ- my genome sequenced. But there's... That's just one of hundreds of different kinds of mutations that can occur that are on a path towards creating a cancer. But the cancer can't survive if the immune system recognizes it. So eventually what happens is there's this detente that is reached between the immune system and the cancer, where the immune system basically ignores the cancer. So Jim Allison here in Houston, uh, won the Nobel Prize back in 2018, uh, for understanding one of these turn-off signals about the immune system u- that the cancers use to turn off the immune system, and that by showing he could block it, his wife, Pam Sharma, ran a bunch of clinical trials at MD Anderson that showed in fact that this could actually turn a 5% survival disease in melanoma to a 50% survival. And that then created the whole immunotherapy field that the world is, uh, taking advantage of today.