Most people know someone who’s  faced a cancer diagnosis.

Whether it's lung, skin, breast, or  prostate, cancer is pretty common, with studies reporting an  average lifetime risk around 40%. But ask yourself: Have you ever  met anyone with heart cancer?

Probably not, because that  type of cancer is very rare. And it’s taken scientists years  to finally figure out why. [♪INTRO] In theory, heart cancer can  crop up in one of two ways. Either cells in the heart mutate  and form primary cardiac tumors, or the heart gets hit with friendly  fire from another organ that already has cancer, causing metastatic  or secondary cancer in the heart.

Primary cardiac cancer is  rare enough to land it on the American Cancer Society’s rare cancer webpage. Studies estimate the incidence to be as low as around two in every one hundred thousand people. And this is surprisingly low, since  the heart is an organ everyone has.

And even if you end up being  part of that statistic, there’s over a 75% chance  the tumor is benign anyway. Metastatic heart cancer is more  common than primary cardiac cancer, but only about 1% of cancers end up metastasizing to the heart and causing problems. Which is, again, unexpectedly  low, since cancer cells from anywhere in the body can hop right into a blood vessel and make a beeline to the heart.

And this is also not just  a human heart quirk either. Dogs, cats, and many other mammals also enjoy a suspiciously low  incidence of heart cancer. And this is why cancer doctors are right now trying to turn people into all heart.

Just one big heart– they’re not doing that. All of this has caught the interest of scientists. Cancer not happening naturally is often a hint to how to make cancer not happen on purpose.

Part of the answer is probably because heart cells rarely divide after you're born. Cancer is uncontrolled cell replication, but it’s kind of hard to  get uncontrolled replication when you don’t have replication at all. So less cell division means lower  chance of developing cancer.

But thanks to a certain heart  implant, scientists noticed that cell replication, and therefore the  possibility of cancer, can ramp back up. A ventricular assist device or VAD  is placed in a patient when the heart is too damaged and weak to  pump blood on its own anymore. It pretty much steps in to do the heavy lifting.

The thing is, some patients can  eventually get their VAD removed. And the reason they can do that is because the damaged heart tissue healed  meaning those cells divided. Having the VAD somehow triggered  the cells to start replicating, allowing the heart to regenerate  and pump on its own again.

Animal studies found the same thing. After a heart attack, if the damaged  heart got a little help, then cell division would restart, and stem  cells would start multiplying. The only difference between a  heart that can regenerate and one that can’t is whether it gets to phone  in a friend to help with the work, so researchers hypothesized that  there must be a relationship between the mechanical burden hearts are  under and their ability to regenerate.

For people with VADs, easing  that burden is good, because it increases cell replication  which translates to heart healing. But when you flip that around, it means maybe the day to day pumping stress  of being a heart decreases cell proliferation and, by  extension, the risk of cancer. If all stress worked that way, I’d  never get cancer.

Unfortunately… We’re going to learn how all  of this works really soon, but first, a quick break. Happy Learn-a-thon! Learn-a-thon is a celebration  of learning and the stuff we make at Scishow, Crash  Course, and all of Complexly!

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Thank you for supporting us, because good information is worth it. To test that hypothesis, in a  2026 paper in the journal Science, researchers did some mouse studies. Fair warning, the one I’m about  to talk about gets pretty gory, so if you’d prefer to skip it, jump  to the time code on the screen.

First, the researchers took  mice and made them super susceptible to cancer by ramping  up a cancer-promoting gene and turning off a major cancer prevention gene. Then they transplanted a healthy  heart onto each of their necks, and got the heart all wired up so that  blood went through that heart, but the actual pumping was still being  done by the mouse’s regular heart. Yeah, I know.

But there are  lots of rules in place around these sorts of experiments,  including using as few animals as you possibly can to learn the thing you need. It’s all in service of making human lives better. Anyway, this setup created two stress scenarios.

The regular hearts were under the usual amount of mechanical stress that a heart deals with when it has to pump blood through a whole body. The transplanted heart,  meanwhile, was a freeloader that had the same kinds of cells  without any of the responsibility. The researchers injected cancer cells into both hearts and waited two weeks.

What they saw was that the  transplanted hearts ended up chock full of cancer cells,  while only small portions of the stress-addled hearts became cancerous. Also the non-beating hearts  had more cell proliferation, mirroring what the VAD studies had shown. They did a similar experiment  with engineered heart tissue.

Some of the heart tissue was  exposed to ions that made it beat, while the rest wasn’t and stayed still. Then they added cancer cells to see how the movement affected cancer growth. And again, the movement of the heart  seemed to stave off the cancer.

The cancer cells stayed on the  outer layers of the beating tissue, but spread all the way through  the unbeating counterpart. They concluded that as long  as your heart is beating, cancer’s gonna have a hard  time getting a foothold. At least in that organ.

And the why for that seems  to be the protein Nesprin-2. Nesprin-2 is part of a complex that  connects a cell's cytoskeleton, its internal scaffold, to the nucleus. Nesprin-2’s main responsibility is communicating mechanical signals between the two.

If the cytoskeleton is sensing  a lot of movement from outside, Nesprin-2 will tell the nucleus about it. In response, the nucleus makes  adjustments to allow genes involved in stopping cell  proliferation to be expressed. Apparently having other cells beating down your door doesn’t scream  “great time to replicate”.

So Nesprin-2 blocks proliferation  if there’s a lot of movement… like in beating heart cells. And when scientists blocked Nesprin-2 from warning the nucleus about the pounding  outside, cancer cells were able to spread whether the  heart tissue was beating or not. So in your heart, less  Nesprin-2 means more cancer.

But nobody is really looking  for a way to get more cancer. Instead researchers think that  Nesprin-2 and related proteins could be exploited as a treatment for  cancer in other parts of the body. What exactly that might look  like is still a big TBD though.

But maybe we should keep looking  to the heart for answers here. Because it sure seems like this mighty organ might have beating cancer down to a science. [♪OUTRO]