Recently, I ran into a reel that one of my friends reposted, claiming it described a “herbal cure” for cancer. I watched a little more of the video, but when the creator described cancer as being “a parasite that enters your system,” my lil’ nerd brow was instantly raised. So I replied to my friends’ repost, asking her if she believed what the reel was saying. Oddly enough, to me at least, she said she did and hoped this repost reached someone who needed it. I then spent the next five to ten minutes ranting to her about how this was flagrant misinformation and explaining to her what cancer really is. A few days later, I ran into a video of a podcast where two dudes were saying matcha cures breast cancer.
We’ve all heard of cancer. But what is it, at a cellular level? Our bodies are made up of cells: inside a normal cell lies a nucleus, a little ball-like structure, whose main purpose is to protect the cell’s most basic instructions, its DNA, from the extranuclear environment, which contains an amalgam of enzymes and proteins or other structures, both extracellular and intracellular, that could possibly damage it. The cell uses these instructions to build its machinery, proteins. Some of these proteins can act as guideposts, providing the cell with the tools to detect when and how to divide.
However, sometimes the cell can make mistakes. Sometimes, external factors, such as UV radiation or tobacco smoke, can also damage the DNA, causing it to mutate. Thankfully, the cell is prepared for these kinds of scenarios and has many mechanisms to either repair the DNA or fix its mistakes. However, these mistakes may at times go under the radar. If those mistakes happen in the instructions on how to divide your cells, you get cancer. Examples of this phenomenon are what we call tumour suppressor proteins. These are a category of sub-cellular machinery responsible for telling your cell, “this is not the time to divide.” An example of this type of protein is a protein called p53 (protein number 53). When a mutation happens at the level of these proteins, they can be in a “permanently off” state, which is known as a loss-of-function mutation. When this happens, the cell loses its “no-go” signal, so it thinks it’s always the right time to divide, which is not what it’s supposed to think. This drives it to divide in unfavourable situations that could cause it to even further damage its DNA.
The aforementioned p53 protein is so crucial to this process that 60 per cent of colorectal cancer cases contain tumours with a damaged p53. On the flip side, you have oncogenes, which are the cell’s “keep going” signal and sometimes mutations on these proteins can cause them to be constantly on or even overproduced in the cell. All of these distinct damaged instructions have the same end result of producing an abnormally dividing cell. And this is a fairly boiled-down way of how a cancerous cell develops; in reality, there is much more that happens under the hood at even the most microscopic parts of your cells. Even when this happens, your body has so many failsafes in place to defend itself from these mutated cells. For instance, cells will often recognize that they’ve gone rogue and self-destruct in a process known as apoptosis. Unfortunately, these mechanisms may also fail due to a plethora of factors: genetic variance between individuals, the nature of the damage to the DNA, immune health, work environment, and so forth.
When these “mistake” cells begin to propagate, that’s when you get tumour development. Cancer happens when your cells start dividing too much and in ways they’re not supposed to.
Why has cancer been so notoriously hard to cure? The fundamental nature of cancer is what makes it so hard to treat. As tumours start, they are similar in makeup to your body’s healthy cells, and they maintain some aspects of the microscopic appearance of those cells. Targeted therapies are therefore harder to engineer since you do not want to damage your healthy cells.
What muddies the waters even more is the phenomenon of tumour heterogeneity: two tumours don’t always have the same “messed up instructions.” Sometimes, even in the same tumour, you can have the accumulation of multiple different cells, each with different “messed up instructions.” This makes it hard to produce a “one size fits all” drug for cancer.
Despite these challenges, many cancer treatments have been developed. Chemotherapy is composed of a broad range of drugs, but fundamentally, all work on the same principle: targeting and killing any cell that divides and produces other cells really quickly. Unfortunately, this also affects healthy tissues that divide rapidly, like a patient’s hair, for example, which is made of very rapidly regenerating cells. This is precisely the reason why chemotherapy patients lose their hair.
Another commonly used treatment is radiotherapy (or radiation therapy), which works by blasting cells with high-intensity radiation until they die. This could affect healthy cells in addition to the cancerous ones, yet the use of high-precision radiation beams mitigates this effect somewhat. Other treatments do exist, but they are specific to unique cases of a particular cancer.
In essence, cancer is hard to cure because cancerous cells are similar to our own cells, acting like impostors in our bodies that are very difficult to separate from healthy cells. Although treatments do exist, they either act as general “cell killers” or are often administered on a very case-by-case basis and require extensive evaluation from professionals.