When I think of “diseases”, I often think of something like the flu, COVID-19, or maybe even the bubonic plague. All of these have something in common: they’re separate organisms causing harm in our bodies. That’s what’s known as an infectious disease, and it’s one of two broad classes of diseases. Since we have diseases caused by other organisms, it makes sense that we also have diseases caused by ourselves. These are called noncommunicable or chronic diseases, think alzheimer’s, asthma, or, of course - cancer.

In many ways, that information has been really helpful. It tells us a lot about how cancer works! We know that, just like our own cells, cancer relies on DNA to grow and survive. We also know a lot about how our cells obtain nutrients and use energy, how they divide and make new cells, and, on the other end of the spectrum, how cancer has adopted those processes. But, despite all the similarities, cancer still manages to survive our treatment options, and evade our immune system… how?

Mutation or damage to a cell’s DNA leads to a loss of information. A loss of critical genes, genes that are intended to help a cell do quality control, can lead to cancer. That lack of control is hugely beneficial for cancer cells. Without its instructions, a cell is free to do things it otherwise couldn’t; there’s no more manual telling it “you have to be this, do this, act like this.” It’s no longer locked into just one identity. That means a cancer cell can change and adapt to an identity that best suits its needs.

You might wonder why that’s so important for a cancer, so let’s consider the challenges that a cancer faces. The corners of our bodies are strikingly different. Every organ varies in nutrients, has a different blood supply, and is populated by different healthy cells.

Some cancer cells can do just that. But that doesn’t just apply to travelling between organs. They can adapt to all kinds of stress. If a cancer is treated with chemotherapy or biological therapy, some cells can simply change a pathway that they rely on to alter their identity. Or, if they’re recognized by our healthy cells, cells that protect us, some cancers can essentially change outfits to become unrecognizable.

Some cells simply can’t adapt, meaning that as you treat a cancer, you’re very likely to kill quite a few cells. However, if even a few adapt and survive, they can divide and pass those changes on to more cells. Interestingly, they don’t all adapt the same. Two cells treated with the exact same thing are capable of finding different ways to avoid succumbing to treatment. As they pass these changes on, it can quickly lead to enormous variation in the types of cells present, even in the same tumour. To make it worse, those that regrow all share the identity of the first surviving cells, meaning that they’ll likely be resistant to whatever they were treated with.

New diversity can also pose an issue as you try new treatments. Many cancer therapies function in a similar manner, often by damaging DNA. Sometimes a cell can adapt to one treatment, and in doing so, can unintentionally gain resistance to multiple treatments that work in a similar way. So, adaptability in cancer can not only lead to a tumour regrowing, but it can also lead to diversity throughout the new growth, resulting in a more resistant cancer.

Despite all of our various therapies, cancer still manages to come back, sometimes even stronger than before. Adaptability and diversity are major drivers in this; they allow cancer cells to persist, even in hostile environments. With that said, it isn’t all cells, and it’s not even all cancers. Many cancers respond very well to therapy, with excellent outcomes for most patients. Take early-stage prostate cancer, for example. Prostate cancer is one of the most common cancers worldwide. Despite it being a male-only organ, it still makes up nearly 10 percent of all new cancer cases worldwide. But, with treatment, early-stage prostate cancers have nearly 100 percent survival! As new therapies are developed, the challenge now is to make them specific enough to kill cancer cells while sparing our own cells, but not so specific that all cancer cells are targeted, regardless of their diversity. It’s a tricky task, but researchers are already working on it - if only we had time to go over that today…

I hope you learned a little something today, but I also hope you’re hungry for more, because next week we’re going to talk about how our diet impacts cancer progression, and how a few specific foods play a role.

See you next week!

If you missed last week’s letter, you can read “Tumour…Der” to learn a little more about cancer therapeutics.