When you think about getting older,  charming side effects like sore joints,   wrinkles, or a toothless smile might come to mind.

And while there are maybe some  things to look forward to,   like that AARP membership, it might  not seem to balance out entirely. There may be one other advantage, however.

At a certain point of aging, our  risk of cancer starts going down. And if you’re getting hung up on the idea that  cancer is an old folks’ disease, I mean, kinda. But keep watching.

Because just like with all things  in cancer, it is not that simple. [♪ INTRO] So cancer is one of those diseases that  can strike anyone, regardless of age,   though it tends to be more likely in older folks. And there are a lot of things that can  affect the risk of different cancers. We know that a lot of cancer risk  can be affected by genetic factors,   such as certain variants of the BRCA1  gene increasing the risk of breast cancer.

That’s why they call it brack-uh, B-R-C-A. It stands for BReast CAncer Environmental factors can also play  a role, like smoking for lung cancer. But so can plain dumb chance.

You can have no genetic risks  and avoid things like smoking   and too much sunlight, and still develop cancer. And that’s because as your cells divide,   which they’re doing all the time,  they can make some mistakes. A lot of those mistakes are harmless.

Maybe one DNA letter changed but in a  place where it didn’t make any difference,   or maybe that mutation caused the cell to die,  so it didn’t start mass producing the mistake. But the more your cells divide,  over the course of a few decades,   the more likely it is to get  one of the bad mutations,   or to accumulate enough mutations where  you start showing symptoms of a disease. That’s a big part of why cancer is  generally more likely as you age.

Plus, you have more time to be  exposed to environmental risk factors,   your immune system usually weakens, and  your body isn’t as good at repairing DNA. All of that spells more cancer for old people. So it makes sense that when you look at cancer  incidence, it pretty much increases with age. …Until you get to the very oldest people.

At some point, it looks like cancer  incidence starts to actually go back down. A paper from 2017 found that this  happened in the “oldest-old” group,   which is anyone 85 years or older. That’s a little strange because, theoretically,  that group has had the most time to hoard those   random mutations, rub shoulders with  carcinogens like tobacco or the sun,   and power down their immune  systems from regular ol’ aging.

With all those factors working  in favor of tumor development,   some researchers aren’t convinced  that the cancer decline is legit. It might be the incidence only looks like it goes   down because it isn’t being  detected in that age group. There are some good reasons  why that could be happening.

Detecting cancer isn’t always  the most comfortable experience. At 95, a colonoscopy might not  feel like it’s worth the trouble,   especially with how grueling the prep can be. Though if you are under 95,   I am here to tell you that colonoscopies  aren’t as bad as they’re made out to be.

If your doctor says do it, please do it. Additionally, if an individual is  too frail or has chronic conditions,   they might not be a candidate  for certain procedures. And if the procedure requires anesthesia,   the medical team may have to consider the  risks and benefits of detecting that cancer.

Plus, someone in their 90s might not care  to know whether they have cancer or not,   because they are adamant about not doing  intensive treatments like chemo or surgery. At that stage of life, you might want  to consider quality over quantity. It could also be that the individuals prone  to cancer already got it and succumbed to   it earlier in life, leaving most  of the oldest-old cancer-free.

A kind of natural selection bias. But even though those things could affect how  we understand cancer incidence in old folks,   the consensus among epidemiologists today   is that the decreased incidence of  cancer among the oldest-old is real. So researchers out of Stanford  and UPenn asked, what gives?

And their 2025 paper suggests  that there might be something   on the molecular level working to older  folks' advantage when it comes to cancer. But before we get to that, we need to  keep the lights on with this quick break. If you made it this far, you’re  probably the kind of person who   loves engaging with new ideas and  learning outside of a classroom.

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Brilliant’s also given our viewers 20%  off an annual Premium subscription,   which gives you unlimited daily  access to everything on Brilliant. The researchers started where a lot of  researchers do: with a bunch of mice. They split the mice into  two groups, young and old,   which translated to spry 5 month old mice  versus geriatric mice closer to 21 months old.

The oldest old mice! Then they used gene editing to give  both groups of mice lung cancer. For anyone who isn’t a molecular biologist,  that means identifying a gene that,   when changed just a smidgen, can pretty  much guarantee cancer will develop by   doing things like eliminating all the  cellular division checks and balances.

It’s like a company suddenly fired  their entire quality control team. Something would probably go  really wrong, really quickly. Genes that can easily cause  tumor-inducing disaster with   just a tiny change are called oncogenes.

And the oncogene these scientists messed with  was KRAS, whose mutations are one of the most   common linked to any cancer involving  a solid tumor, including lung cancer. So they took that cancer prone version of KRAS,   and put it in a virus, and then they  delivered the virus into the mice’s   lungs so that it would spread the mutated gene  to their lung cells and induce a lung tumor. Inducing the cancer was important so that  everyone was on a level playing field.

Rather than having the elderly mice  having a cancer built on a lifetime's   worth of mutations and the youngins’ cancer  caused by just one very unfortunate mutation,   inducing the tumors made everyone start  with genetically identical cancer. But that cancer did not stay identical for  long, because after giving the cancer 15   weeks to do its thing, the young mice  had worse tumors than the older mice. Specifically, the aged mice had 2 to 3 times  fewer tumor growths than the young mice,   and four to five times fewer  cancerous cells in general.

And the size of the tumors  was noticeably different too,   with the older mice having significantly  smaller tumors than the younger mice. Fewer tumors means some of the cancer  was prevented from even starting,   while the smaller tumors means  their growth was also inhibited. It’s as if the older mice had some  sort of beneficial effect that was   basically weeding and pruning their cancer.

At first, researchers thought that maybe the virus   didn’t get into the cells of the older  mice as well as it did the young mice. So being very clever scientists, they  added a glowing marker to the virus,   injected it into the mice again, and played spot  the difference between the old and the young mice. Except it wasn’t a very good game,   because the glowiness in the tissues among  both groups was pretty much the same.

That means the virus, with its cancer-happy  version of the KRAS, was getting into the cells   equally as well, but something else was limiting  the subsequent cancer development and growth. The next idea was that there might  be a tumor suppressor gene working   better in the older mice than in the younger mice. A tumor suppressor being the opposite of an  oncogene – a gene that protects cells from cancer.

And that would make sense, but the  researchers found the opposite was true. One of the ways a mutated KRAS gene can cause  tumors is by activating the PI3K–AKT pathway. We’re getting deep in the weed now, everybody!

This is a specific signaling pathway,  which is a cascade of little chemical   messages between molecules that  trigger functions in a cell. This specific pathway tells  cells to divide and not die,   which is why it plays a big  role in tumor development. And that is where tumor suppressor  genes come in, because leaving that   pathway unchecked would be bad news for  people who prefer to not have cancer.

The scientists looked at a  bunch of tumor suppressor genes,   but the one that really caught  their eye was the PTEN gene. That gene is really good at  slowing down the PI3K-AKT pathway. The idea was that if aged mice  have smaller and fewer tumors,   then this gene was probably working  overtime to make that happen.

And they did see a difference in how effective   the tumor suppressor genes were  in old mice versus young mice. Except, not in the direction they expected. When they knocked out the PTEN gene, tumors  in the younger group grew over two times   more than those in the older group, even  though PI3K signaling increased in both.

Knocking out genes is something  molecular biologists do to find   out what goes wrong when they’re missing. So this result makes it seem like PTEN is doing  more work in younger cells compared to older ones. The effect of several other tumor  suppressor genes also decreased with age.

So those lazy tumor suppressor genes weren’t to  thank for the smaller tumors in older mice either,   since they were apparently more  active in the younger mice. But that experiment does suggest that  something in the PI3K-AKT pathway gets   less effective with age, which might  partially explain the smaller tumors. The researchers also noticed that when they  knocked out the PTEN gene in the older mice,   the cancer cells looked younger, which  is weird since no PTEN should mean more   PI3K-AKT signalling, which would force cells  to keep living even when they’re super old.

All of those surprising findings  means the researchers did not find   the answer as to why the oldest-old  have a decreased risk of cancer,   and highlights why your grandparents really  deserve to be included in more research. But those researchers aren’t the  only ones who have tried to suss   out this situationship between aging and cancer. A paper from 2003 presented  some reasons why tumors might   be at a disadvantage when they target older folks.

One idea proposed is that you’re less likely to be  exposed to carcinogens during your golden years. Somewhere between 2 and 8% of cancers are caused   by exposure to carcinogens  while you’re on the job. By the time you’re 80, there’s a pretty  good chance that you have retired,   so if you were being exposed to hazardous  substances, you probably aren’t anymore.

And if you’re in an assisted living or  nursing facility, there are probably   fewer environmental carcinogens like tobacco. A lot of the environmental changes  associated with aging could mean less   exposure to carcinogens, so a lower  incidence of cancer would make sense. But that 2003 paper clocked  some physiological reasons   why the incidence might decrease with age too.

As you age, your cells slow down in a lot of  ways, including the speed at which they divide. That goes for healthy cells and unhealthy  cells alike, such as tumor cells. So for that mouse experiment, it might not  be too surprising to see the older mice   with smaller tumors, because it might just take  longer for their tumor cells to divide and grow.

All of the cells suck when you’re old. But that only explains why the tumors would be  smaller, not why there would be fewer of them. And for that, the authors credit a  population of cells called senescent cells.

Senescent cells are cells that are  done multiplying but are not dying. They’re essentially permanent retirees, and as  you age, you build up more and more of them. The key point is that they are done replicating,  which means they can’t be compelled out of   retirement even if they’re infected with a weird  pro-cancer virus gene thingie made in a lab.

Older folks have more of these cells that  are essentially immune to becoming cancerous,   which could explain why the  older mice had fewer tumors. It’s important to note that those cells  can also release chemicals that increase   the risk of cancer, so this isn’t a clean cut  Scooby Doo mystery with a single right answer. Took his mask off. “It’s you, the Senescent Cells!

You’re so old!” Both cancer biology and aging are  complicated and deserve far more attention. But as we do learn more about the  relationship between aging and cancer,   this kind of research could guide more  tailored treatment across the lifespan. Like, perhaps treatments targeting  PTEN would be more effective in older   folks since it seems like that  gene gets a bit lazy with age.

Or maybe further research will identify a  gene or pathway that really does help older   people fight off cancer better, and it can be  used in treatment for younger cancer patients. All of that starts with including  more older people in cancer research,   especially since they have historically  been underrepresented in those studies. And in recent years, the FDA has even issued  statements telling researchers to do as much.

Not only is that a win for science in the spirit  of inclusion and learning more, but it might even   mean a few more of those golden years, if  not for meemaw, then maybe someday for you. [♪ OUTRO]