Cancer is “haywire” cells. When a random mutation turns off growth control, the self-destruct mechanism and also still gets recognized as a healthy cell by the immune system it multiplies and grows without limit.
How that happens: cells are controlled by their DNA. If the DNA gets damaged (for example by some chemical, or by radiation) there is a low chance it causes exactly the kind of effect that trigger cancerous growth.
Why big animals get it less: they have more cells and get older, so their overall cancer risk should be a lot higher. And that’s kinda the reason why it got lower, there was more evolutionary pressure to evolve cancer resistant cells (If your DNA leads to cancer after 3 years on average that’s not an issue for a rat, but for an elephant that’s the end of that bloodline, so only the most cancer resistant elephants pass on their genes)
That can happen in multiple ways. For example cells can be simply more robust to changes, I.E. cell growth being controlled by more than one DNA section. But also by the immune system being better and recognizing cells that have issues.
Cancerous cells are cells that are growing uncontrollably. They don’t listen when the body tells them to stop. This actually happens all the time, but usually the body goes “That’s not right” and tells the cell to kill itself, and it does. Except sometimes it doesn’t. And then this cell starts dividing. And now you’ve got a small cluster of cells that are growing and dividing too much and won’t self destruct. These cells can start to occupy a large amount of a tissue’s space, replacing the healthy good cells with these bad cells and organs stop performing their normal functions. Or, they can invade local tissues, causing disruption there and metastasise (or spread) to other locations, causing the same disruption all over the body, instead of in one isolated spot.
As for why bigger animals get it less is interesting. Animals have more cells and longer life spans. So they have many more cell divisions (the things that can randomly trigger the mutation that causes disobedient cells) and have much more time for these problematic cells to become large masses. So how is cancer incidence lower? This is called Peto’s paradox, and there are a number of solutions. Evolution is one. Elephants have a greater number of, what are known as, tumour suppressor genes. TP53 is a protein that, while it is formed correctly, essentially prevents a cell from becoming cancerous. When a mutation causes this gene to be dysfunctional, cancer often arises from the cell’s lack of defences. Elephants developed multiple copies of this gene, reducing the chance that a cell can be left defenceless. But this isn’t all there is to the story.
Whales didn’t develop extra copies of TP53, nor any other tumour suppressing genes. Another solution is that their DNA is less likely to get damaged in the first place. So, in the example of whales, they are in the ocean. They are much less likely to get exposed to thermal or UV radiation that can cause DNA damage that might lead to cancer. Also, there is a type of molecule called a Reactive Oxygen species. These are basically molecules that contain diatomic oxygen and as a result are extremely reactive. They can react with most other molecules that they will come into contact with. They are a perfectly normal part of body chemistry and are normal products of the metabolism, but there is always a risk of damage especially if the metabolism has been affected by some sort of pathology, and this damage can include DNA damage, which could trigger cancer. As larger animals generally have lower metabolic rates, the number and rate of production of these reactive oxygen species is lower as well, meaning they have a lower risk of damage as a result.
Another potential solution is “hypertumours”. In short, this is when a cancerous tumour grows it’s own cancerous tumour. Cancer cells, by nature, don’t follow the rules. When tumours get big, they can manipulate angiogenesis (the process by which the body makes more blood vessels) to give themselves a direct blood flow so they have easier access to nutrients. Well, sometimes a cluster of cells will basically go rogue, and start siphoning oxygen and nutrients away from the primary tumour. So there are now 2 tumours competing for the same space and nutrients, which can slow the growth and reduce the lethality of the cancer.
Other possible theories, albeit with no real research observing them in action is simply that the body’s immune system is better at detecting and killing cancerous cells, or that the DNA has a certain quality (aside from extra tumour suppressing genes) that makes it resistant to cancer.
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