At its core, DNA is a way of storing information. It stores all of the instructions required to make us… us. It does that in a really complicated way, using billions of molecules called nucleotides. To be precise, humans have around 6 billion of these molecules in every single cell. Four primary nucleotides are mixed and matched, placed in different orders. As they’re put in different orders, we get unique sequences, called genes. Genes are specific instructions that lead to the creation of a specific proteins that fulfill a specific function.

In total, the average human cell has roughly 20,000 different genes. Each cell can then turn genes on and off, making whatever it needs in different situations, giving itself an identity.

Well, that’s because even though the genes are the same, sometimes the sequence changes. Over time, our DNA can be altered and mutated, which can influence the end product. Take hair colour, for example. What’s the difference between red and brown hair? Well, it really comes down to one gene: MC1R. The MC1R gene, when “scanned”, makes a protein which leads to melanin production. In people with brown hair, their genes are unaltered, meaning they actively produce melanin, which gives hair a darker colour.

So, as DNA is passed down from our parents, we get the same genes, but the sequences can vary, leading to differences in the product… us.

Well, cancer is a disease caused by DNA damage. When DNA is damaged in certain genes, we can lose information that’s essential to our cells’ regulation. That includes all of our checks and balances that prevent our cells from over-dividing or migrating when they’re not supposed to. Importantly, cancer is never caused by a single damaged gene. It can vary, but usually, there are a handful of mutations needed to get a full-blown cancer. Typically, that would be a good thing, but that also means that someone can carry some cancer-causing DNA damage without having cancer.

That’s important because just having damaged DNA in essential genes brings us one step closer to cancer, even if it’s not all the way yet. 

Something we need to consider is what DNA we actually get from our parents. We don’t inherit all of our parents’ DNA. We really only get something called the “germline DNA”. That DNA is only found in our parents’ reproductive cells, and it’s what’s passed down through generations. That’s the master blueprint that all of our other cells are based on. So, when we’re talking about diseases, that’s usually a good thing. If, for example, our DNA is damaged in our skin and we develop cancer, that won’t be passed down to our children because it’s not in our germline. But what happens when someone carries damaged DNA in their germline?

When that information is passed down, it means that someone is already one step closer to having cancer and needs less new DNA damage to get that full-blown cancer. On top of that, germline DNA from our parents is carried in every cell in our bodies, meaning that, when passed down, every single cell already has damaged DNA. Having that cancer-causing DNA damage in every single cell, even if by itself it’s not enough to cause cancer, greatly increases the risk of developing cancer long-term.

One example of this is the poster child of hereditary cancers: the BRCA gene. This gene is one of those essential genes that help regulate our cells. In fact, BRCA actually functions to repair damaged DNA. When it’s functional, BRCA actively fixes cancer-causing DNA damage. Inheriting a damaged BRCA gene increases the chances of developing both breast and ovarian cancer, with an increased risk of around 60 percent and 50 percent, respectively. It even increases the risk of breast cancer in men.

Well, without inherited DNA damage, you can still certainly develop cancer. Interestingly, only around 5 to 10 percent of cancers are hereditary; the rest are spontaneous. Spontaneous cancers are caused by the accumulation of DNA damage from various sources. It could be UV rays from the sun or even chemotherapeutics. Any exposure to DNA-damaging agents can damage our essential genes. With that said, without inherited DNA damage, it’s harder for cancers to develop. That’s because mutations are random. With 20,000 genes per cell and roughly 37 trillion cells in our body, the likelihood that the same cell gets DNA damage in all of the required genes is actually exceptionally low. And even if one cell happens to get all the necessary mutations, our bodies have regular quality checks to get rid of those damaged cells. In fact, we destroy and regrow around 330 billion cells every single day. The difference between hereditary and spontaneous cancers is reflected in the ages at which they appear. Hereditary cancers generally appear much earlier because they require fewer mutations. Spontaneous cancers usually appear later in life. But over time, cells can amass more mutations, eventually leading to cancer.

Despite how common cancer is, the odds of getting all of the DNA damage necessary to cause cancer are actually exceptionally low. We have over 20,000 genes in each of our cells, 37 trillion cells in our body, and we destroy and regrow over 330 billion cells every single day. But, with enough time and enough exposure to DNA-damaging agents in the world around us, cancer still happens. For those who inherit damaged genes, the likelihood of developing cancer is significantly higher. Thankfully, modern medicine makes it possible to test for these mutations. Genetic tests can search your DNA, locate specific genes, and identify mutations at the scale of a single molecule that increase your risk of cancer before it has the chance to develop. This helps us to be proactive in our fight against cancer, which is one of the best possible options we have.

I hope you learned a little something today, but now it’s time to put on our best outfits, because next week we’re talking about how our clothes affect cancer.

See you next week!

If you missed last week’s letter, you can read “You Can’t Outrun Cancer, But You Sure Can Try” to learn a little more about the role exercise plays in cancer.