We generally blame cancer on a handful of things – viruses, like human papillomavirus or hepatitis B, lifestyle choices like smoking or obesity, inherited genes, and the environment, like sunlight. We are under the impression that we can stop cancer just by living better, drinking blueberry kale shakes, or being generally healthy. According to a new study, cancer and random mutations are linked over ⅔ of the time. In other words, no matter how many of those natural health smoothies you drink, cancer might randomly occur.
Let’s take a look at cancers and the relationship between cancer and random mutations.
All about cancer
There are a lot of myths about cancer, most of which are easily debunked. But let me try to drop some facts on the reader.
Simply, cancer is a disease in which cells of the body grow in an uncontrolled way, forming a tumor that may spread to different parts of the body. There are around 250 types of cancer, though the exact number is not precisely known, since some cancers may be related to others, or may not be cancers at all. But 250 is a good average.
All cancers are caused by mutations in the DNA of cells in the body. Most of the time, cells deal with these mutations by “fixing” the DNA. Or the mutation is so serious that the cell simply dies (it’s really one cell, and cells die in your body constantly). If the mutated cell lives and divides, the body has immune defenses against most mutations–so it’s gone before you would even know that it’s there.
Technically, with 46-68 trillions (that’s 46-68,000,000,000,000) of cells in the average human body, even if a cell mutation is extraordinarily rare, the law of large numbers means that you could have literally hundreds of cancer cells living in your body, dying naturally, or being destroyed by the immune system, or not causing any problems at all. There are just so many cells in the body, and the cellular replication mechanism being slightly less than perfect, mutations will happen.
There seems to be a plausible link between cancer and random mutations. Remember, we have over 40-70 trillion cells in our body. There are complex biochemical reactions that are part of the process to replicate DNA, which is approximately the first step for cell division, a necessary part of life. This replication happens trillions of times, and despite the process being nearly perfect, it’s not absolutely perfect (nothing in nature is “perfect”). This process is amazingly accurate, only making an error approximately once every 1 billion nucleotides (a single base pair of DNA). The problem is that there are over 3 billion base pairs in the the human genome in one single human cell, and there are trillions of cells in the body.
Even though the DNA replication is 99.99999% perfect, that leaves a few thousand to a few million errors per one full replication of all the cells in the body – these numbers are so huge, even then, it’s still rare. And these errors can lead to cancers.
The odds against a cancer growing is even worse than I’m stating. For a cancer to survive from a single cell, to a mass of cells, requires nutrition (forcing the body to feed it with blood vessels). To do that, it needs another mutation of the cell. Then it needs to grow unrestricted by the normal growth control systems of the body–another couple of specific mutations. The cancer also needs to hide from the immune system, requiring more mutations.
I could go on and on, but it could take up to 10 individual and correctly placed mutations for a cell to become a cancer. Again, with trillions of cells, it becomes mathematically possible, but very hard to do. Let’s look at cancer from a strictly mathematical point of view–it’s really really really really really rare. To pile up 4 or more mutations that all are advantageous to the cancer cell is almost unimaginable.
However, outside agents, like infections, tobacco smoke, radiation (more broadly than just radioactive energy, but ultraviolet and other types of radiation), and human physiology can cause (or allow to cause) so many mutations that eventually one leads to an increase in the number of mutated cells, then a growing viable cancer. These are known causes of cancer mutations. But generally, there are just too many cells.
To reproduce, cells divide. Every time one does, there’s a chance that mistakes accumulate into the genome. Usually, these DNA mistakes don’t cause any trouble to the cell or the body. But if it happens more than once in a gene that is related to a cancer, the disease can take root and the cell can turn into the beginning of cancer.
The most important thing to realize is that there isn’t a single disease called “cancer.” There are hundreds. And the mechanisms that lead to one of those hundreds of cancers are not reliant on one mechanism, or one mistake in your life’s choices. It may just be mathematics.
One more thing. Despite the tropes out there in the world, we are not losing the war on cancer. As David Gorski, MD stated at Science Based Medicine,
Are we winning or losing the war on cancer? I know, I know, it’s a simplistic question, and I myself pointed out how cancer is not one disease near the beginning of this exploration. I also routinely point out the same thing whenever someone asks the question, “Why haven’t we cured cancer yet?” (Mainly because it’s complicated as hell.) What the evidence shows clearly is that death rates from cancer are slowly falling, driven by declines in death rates from most of the common cancers. Meanwhile, five year survival rates are climbing for most cancers, even for more advanced disease.
Cancer and random mutations
A new study published in the journal Science makes a strong case for random chance as the most important factor in cancer development. According to the study, the vast majority of cancers are just a simple error in DNA replication. If this is so, developing one of the 250 different cancers may be unavoidable, despite a “healthy lifestyle” or attempting to “boost” your immune system.
Geneticist Bert Vogelstein and mathematician Cristian Tomasetti, at the Johns Hopkins Sidney Kimmel Comprehensive Cancer Center, conducted the study, a follow-up to an earlier one, which arrived at the same conclusion. The researchers wanted to know whether replications errors were behind most cancers, versus other factors, such as tobacco.
What they found gives us important information on the causes of cancer:
- After examining 32 different kinds of cancer, Vogelstein and Tomasetti determined that 66% were a result of chance mutations in cells, 29% resulted from the environment, and 5% from inheriting a mutation.
- For lung cancer, 65% were caused by the environment (tobacco smoking mostly), with only 35% caused by replication errors.
- For prostate cancer, over 95% of cases were caused from replication errors.
Now you might think with such a high rate of cancers being caused by replication errors, why bother worrying about a healthy lifestyle (except for stopping smoking, of course) or why bother avoiding environmental issues (other than smoking) that might induce cancer. Well, the main reason for trying is that the researchers still found that 42% of all cancers are preventable.
These researchers also determined that the actual number of stem cell divisions in a given organ that’s associated with risk. Those organs with more stem cell divisions are at higher risk for cancer – one such location is the colon. On the other hand, those organs with fewer stem cell divisions, such as the brain, exhibit lower risk for cancer development.
This study seemed to avoid some issues that other research of this type encountered. Mainly, they examined databases from 70 different countries, not just the US based data.
According to the researchers, we might conclude that the case for environmental factors in cancer may have been overemphasized. Volgelstein told Nature,
If we think of the mutations as the enemies, and all the enemies are outside of our border, it’s obvious how to keep them from getting inside. But if a lot of the enemies — in this case close to two-thirds — are actually inside our borders, it means we need a completely different strategy.
Vogelstein told NPR, “We’re not saying the only thing that determines the seriousness of the cancer, or its aggressiveness, or its likelihood to cause the patient’s death, are these mutations. We’re simply saying that they are necessary to get the cancer.”
The point here is not to say “it doesn’t matter,” it’s just simple math that drives cancer and random mutations. It’s still more complex than that – on one hand, it’s not all about mutations, but on the other hand, preventing cancer isn’t all about having a kale smoothie every day.
Yes there are methods to prevent cancers. Quit smoking. Stay out of the sun. Lose weight. Get vaccinated against HPV and HepB. Get exercise. But these prevent very specific kinds of cancer, not all of them.
As for cancer and random mutations? There are no miracle substances that will increase or decrease the risk of these replication errors. You can never change your cell’s replication accuracy to 100% – you just don’t have that sort of control over your cellular biochemistry.
If you quit smoking (or haven’t ever smoked), you immediately cut your cancer risk by a whole bunch, considering the fact that 14% of all new cancers are lung cancers. This is much more important than worrying about your genetic errors. Worry about the 42% of cancers that are preventable – and try not to think about those trillions of dividing cells that probably won’t lead to cancer.
- McCulloch SD, Kunkel TA. The fidelity of DNA synthesis by eukaryotic replicative and translesion synthesis polymerases. Cell Res. 2008 Jan;18(1):148-61. doi: 10.1038/cr.2008.4. Review. PubMed PMID: 18166979; PubMed Central PMCID: PMC3639319.
- Tomasetti C, Li L, Vogelstein B. Stem cell divisions, somatic mutations, cancer etiology, and cancer prevention. Science. 2017 Mar 24;355(6331):1330-1334. doi: 10.1126/science.aaf9011. PubMed PMID: 28336671.
- Tomasetti C, Vogelstein B. Cancer etiology. Variation in cancer risk among tissues can be explained by the number of stem cell divisions. Science. 2015 Jan 2;347(6217):78-81. doi: 10.1126/science.1260825. PubMed PMID: 25554788; PubMed Central PMCID: PMC4446723.
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