Avoiding, Treating & Curing Cancer With the Immune System | Dr. Alex Marson

We’re in a remarkable era where we can outfit T cells with lab‑built receptors that hunt tumors, then re‑infuse them like a blood transfusion to seek and destroy cancer.

Welcome to the Uberman Lab podcast; I’m Andrew Uberman, and today Dr. Alex Morrison of UCSF joins us to explain how the immune system works, what truly raises cancer risk, and how gene editing is changing prevention and treatment for kids and adults.

Big picture first: is biology about to leap forward, or are we in for a long slog?

Something fundamental has shifted—sequencing, imaging, computation, and tools like CRISPR and lipid nanoparticles let us program cells with precision rather than just observe them, so medicine is now writing instructions directly into biology.

Could you give us a quick tour of the immune system so we have the right foundation?

Innate immunity is the first alarm, while adaptive cells—T cells and B cells—deliver targeted responses; each T cell carries a unique receptor made by DNA recombination, and in the thymus they’re selected to ignore self yet react to danger, while B cells generate antibodies that circulate for protection.

What actually supports immune function in everyday life—sleep, metabolism, exposure?

We lack full answers, but lifestyle clearly matters; in our lab, obesity reshaped allergic inflammation in mice and even flipped responses to antibody drugs, showing health status can qualitatively rewire immunity.

Why do some people get sick constantly while others rarely do?

There are strong single‑gene defects and a long tail of polygenic and environmental factors, so robustness varies by genetics, exposures, and timing.

Does early exposure to foods or microbes build tolerance, like with peanuts?

Yes—there are early windows where careful exposure fosters tolerance, but it must be balanced against true allergy risk.

How do autoimmune diseases emerge, and can we calm them without shutting everything down?

Self‑reactive T cells can slip past education and later break tolerance, leading to tissue‑specific disease; the goal is precise therapies that restore tolerance to the problem target rather than blanket immunosuppression.

What makes some infections feel body‑wide while others stay local?

Local detection can trigger cytokines that flood the bloodstream and induce systemic effects like fever, which can aid defense but also drive symptoms when responses overshoot.

Antibiotics feel miraculous, but what are the trade‑offs and why so few new ones?

They’ve saved countless lives, yet overuse breeds resistance, and the pipeline for new antibiotics is underfunded despite the clear need.

Level‑set cancer for us—what it is, why it happens, and the role of mutations like BRCA.

Cancer is evolution inside tissues: replication errors and DNA damage accumulate until control is lost and cells divide, invade, and spread; smoking and UV raise mutation load, and inherited variants like BRCA sharply increase personal risk even though they cause a minority of overall cases.

How should we weigh everyday risks—lab chemicals, pesticides, X‑rays, airport scanners, charred meat, food dyes—and the confusion around nutrition?

We know the big hitters like smoking and excessive UV, but many exposures are unevenly studied and unequally borne; doses, duration, and context matter, and diet studies are messy, so hedge sensibly while recognizing cancer is probabilistic and not a moral ledger.

Treatment has long meant chemo and some targeted drugs; what changed with immunotherapy?

Checkpoint inhibitors release natural T‑cell brakes and have produced dramatic, durable responses in cancers like melanoma, and engineered CAR T cells go further by giving T cells a synthetic sensor that can eradicate certain leukemias and lymphomas.

Can you share the CAR T story that woke up the field?

In 2012, a child with refractory leukemia received her own T cells engineered with a lentiviral CAR; after intense management of immune side effects, her cancer vanished and she remains well, proving reprogrammed immunity could cure cancer.

Why does cancer risk climb with age, and how do CAR T cells avoid harming healthy tissue?

Time allows more replication errors to stack up; early CAR T cells target CD19, which is on malignant and normal B cells, and patients can tolerate losing healthy B cells, but solid tumors demand smarter logic, like requiring two tumor features before killing.

People ask about ketogenic or low‑glutamine diets for cancer—helpful or harmful?

The evidence is mixed and cancer‑type specific, so I can’t endorse a blanket strategy there.

CRISPR looms large—how does it work and how precise is it?

Borrowed from a bacterial defense system, Cas proteins plus guide RNA can cut chosen DNA sites to disable genes or paste in new code; we track off‑targets and now use base and epigenetic editors to make cleaner changes without double‑strand breaks.

How do you get CRISPR into real T cells and scale it for patients?

We mix purified Cas9 with guide RNA and use electroporation to slip it into primary T cells, enabling large DNA insertions; that platform powers clinical programs like Arsenal Biosciences, where patient T cells are edited, expanded, frozen, and returned for infusion.

Could we one day prevent cancer by supercharging T cells in advance, and can we deliver edits without removing cells?

We start in advanced disease for safety, then move earlier as precision improves; in vivo delivery is rising fast with engineered viruses and lipid nanoparticles that can home to T cells and even transiently express a CAR inside the body.

Many worried about mRNA vaccines persisting too long—what turned them off, and how do you see the wider context?

mRNA is a short‑lived template that degrades after making protein for a limited time, and while mandates and shutdowns amplified social fracture, the vaccine itself was a rapid, targeted instruction set delivered at scale using LNPs.

What about directing toxins or T cells to tumors with precision, and where does AI fit?

Antibody–drug conjugates and bispecific T‑cell engagers tether payloads or T cells to tumor markers, and AI is now designing synthetic binders that recognize chosen targets, making these Lego‑like systems even more modular.

Before we pause, what happened in the high‑profile case of gene‑edited babies?

At an international meeting, a researcher announced embryo edits intended to disrupt CCR5 for HIV resistance in twins, triggering a global outcry and a reckoning on ethics and boundaries.

It was framed as HIV prevention, but sperm washing already drives transmission risk to nearly zero, so the need looked manufactured. Embryos were made by IVF, CRISPR was used on CCR5 with unpredictable edits, nothing was peer reviewed, and consent raised red flags.

The announcement sparked immediate horror, he was later punished with house arrest, and, as I understand it, he is now free and trying to restart a lab outside China.

I draw a hard line against edits that pass to future generations. I work on somatic edits in immune cells, but germline changes invite disease‑prevention claims today and enhancement pressures tomorrow.

People dream about boosting memory or strength with receptor tweaks like those super‑learning mouse studies once hinted at, but we do not even know if that would help a life; forgetting can be healthy.

Selecting embryos to avoid severe disease in IVF is categorically different from rewriting them. Designing offspring risks fad chasing, loss of human diversity, and a society shaped by trends rather than chance.

Given companies now offering deeper embryo sequencing for those who can pay, how do you view algorithmic risk scores that hint at disease yet cannot claim causality?

I get the wish to spare kids from suffering, but beyond clear, high‑impact mutations, most calls become probabilistic and oversold, creating a false axis of desirability that DNA alone cannot define because life emerges from genes meeting environment. For a thoughtful lens, Michael Sandel’s The Case Against Perfection wrestles with what we lose when we chase engineered ideals instead of embracing chance.

In my experience, every highly successful person grapples with something they once hated about themselves, and that friction becomes fuel; being treated as flawless can breed fragility.

I agree; hardship often deepens empathy and strength, while the illusion of perfection can box us in.

What are you most excited about right now in your lab, and what breakthrough feels just over the horizon?

I’m energized by trials now moving from decades of work into the clinic, including efforts in prostate cancer and multiple myeloma. Even more striking, the same CAR T cells that clear B cells in leukemia are showing remarkable early responses in lupus and other autoimmune diseases.

Could these approaches extend to conditions like rheumatoid arthritis, type one diabetes, or multiple sclerosis, and what about fibromyalgia, which crushes people I know?

Fibromyalgia remains poorly understood, so it is its own challenge, but engineered T cells and related immunotherapies are being explored for lupus, rheumatoid arthritis, type one diabetes, multiple sclerosis, and more, and that near future already looks promising.

The next wave is even bigger: we can now deliver tens of thousands of CRISPR perturbations into primary human T cells, let them compete in tumor‑like settings, and read which edits build staying power. With single‑cell RNA sequencing tied to each edit, we’ve mapped around 22 million cells to build a functional sequel to the genome project, a practical roadmap for tuning or silencing genes to give T cells precision and endurance.

Should I bank T cells now, just in case?

I would not recommend it for most people; aside from edge cases like chemo depleting T cells, we’re getting better at re‑engineering the cells already in you.

What about banking skin cells or induced pluripotent stem cells so they can be turned into whatever tissue I might need later?

iPS cells can, in principle, generate limitless T cells, which could make personal banking unnecessary, and teams are building immune‑compatible iPS cell banks for off‑the‑shelf use while we also aim to make patient‑matched lines on demand. I moved my lab to Gladstone to sit with Shinya Yamanaka and Jennifer Doudna because epigenetic reprogramming plus CRISPR lets us imagine programmable cells for regeneration and immune surveillance, which is the intersection that keeps me up in the best way.

How do you even sleep with tools like these within reach; this has been a master class, and I’m grateful for the clarity and heart you bring to it, so please come back when the next wave lands.

I’d be honored to return, and thank you for creating a place where we can linger in the details and share real science with depth.

Thanks for listening; you can find links to Dr. Marson’s work in the show notes, subscribe on YouTube, follow on Spotify and Apple, and leave a five‑star review with comments. Follow Huberman Lab across social platforms and get our free monthly newsletter with summaries and protocols at hubermanlab.com.