By Patrick Cox
November 6, 2015

I am on my way to Marrakesh, Morocco to speak to a group of investors about the importance of the many transformational technologies that you—if you have been reading me for a while—are already aware of.

One such transformational technology is located in the field of cellular repair mechanisms. An increasingly important area of research. You see, cellular life can be rough, and our cells must be able to repair themselves in response to the trauma of everyday life. We do have some amazing cellular diagnostic and reparative mechanisms, but in some cases they simply can’t keep up. There could be many factors that inhibit these mechanisms from working perfectly, but one of them is simply size.

Larger humans, those with gigantism for instance, tend to live shorter lives due to the long-term effects of having more mass for gravity to apply its force to. The joints and the hearts of those with gigantism simply take more abuse than their bodies’ repair mechanisms are designed to deal with. This is also why larger breeds of dogs, such as Great Danes and Irish Wolfhounds have shorter lifespans than their midsize cousins.

Cancer would also be expected to be more prevalent in large multicellular organisms. The reasoning behind this logic derives from a simple fact about multicellular organisms: The cells of all animals are roughly the same size. Large animals have more mass, not due to larger cells, but because there are more of them. A cell biopsied from a blue whale would look no different, under a microscope, than that of a black ant. The blue whale simply has trillions and trillions more of them.

We know cancer is simply the accumulation of certain critical mutations in genes that control vital regulatory pathways. These mutations can occur as a result of errors in the process of DNA replication during cell division or due to mutagens in the environment. The term mutagen refers to any agent that can interact with our DNA molecules and disrupt their structure such as UV radiation, hydroxyl radicals, and some heavy metals. Both internal and external sources of mutations have a certain element of randomness, as it’s impossible to predict if the mutagen will cause a harmless mutation that will be repaired or one that leads to cancer.

In the case of cancer, the mutagen may be more aptly described as a carcinogen. The probability of a carcinogenic event occurring in a cell roughly holds constant throughout the body, so it would stand to reason that the more cells you have, the higher the probability of a single carcinogenic event occurring.

Of course, biology always tends to zig when we expect it to zag. There seems to be no significant relationship between biomass and cancer. As counterintuitive as it may seem, whales have a lower cancer rate than humans. This well-known phenomenon in biology has been labeled Peto’s Paradox after Richard Peto, a statistical epidemiologist at Oxford University. He first posed the question in 1977 while writing about the multistage model of cancer,

A man has 1,000 times as many cells as a mouse… and we usually live at least 30 times as long as mice. Exposure of two similar organisms to risk of carcinoma, one for 30 times as long as the other, would give perhaps 304 or 306 (i.e., a million or a billion) times the risk of carcinoma induction per epithelial cell. However, it seems that, in the wild, the probabilities of carcinoma induction in mice and in men are not vastly different. Are our stem cells really, then, a billion or a trillion times more “cancerproof” than murine stem cells? This is biologically pretty implausible; if human DNA is no more resistant to mutagenesis in vitro than mouse DNA, why don’t we all die of multiple carcinomas at an early age?

In answer to that, Peto proposed that as multicellular organisms became larger, they must have adapted. Some mechanisms must have been put in place that counterbalance carcinogenesis among larger species. Interestingly enough, Peto’s Paradox does not hold up in populations of a single species. Long term studies have shown that among both men and women, height positively correlates with cancer risk.

Recently, some light has been shed on a piece of this puzzle due to research like that of this year’s recipients of the Nobel Prize in Chemistry. Three scientists were awarded the prize for their work mapping the molecular repair mechanisms of the cell. However, there are hundreds of pathways and mechanisms working constantly to keep our cells functional and healthy, so it is still extremely difficult to understand the significance of any one.

That being said, there exists a specific gene that has caught the attention of many, including myself. It is the TP53 gene, nicknamed the “guardian angel” gene. TP53 codes for a protein called p53, which functions as a critical tumor suppressor in our cells. If it detects a problem, p53 can exercise any of three options: activate DNA repair proteins, stop the cell from dividing, and lastly if the genomic damage is severe enough, initiate programmed cell death known as apoptosis. Our bodies detect and destroy about 1 million cancer cells every single day due to the actions of p53.

Here lies the secret behind Peto’s Paradox… at least for some of our pachyderm relatives. You see, elephants contain a staggering 20 copies of the tumor suppressor gene in their genome as opposed to humans, who contain only one copy. Elephant cells have an entire army of cancer fighting proteins, scouring their bodies for any signs of carcinogenesis. As a result, elephant cells are much more sensitive and carry out apoptosis at a much higher rate than humans.

This seems to validate the theory that if we activate the TP53 gene and upregulate the expression of p53, we could fight cancer more efficiently. There has already been plenty of research in this area, and there will continue to be more. Eventually, we could even see a gene therapy treatment that gives us cancer fighting abilities on par with the pachyderms.

I believe the discovery of p53 will stand out as one of the most significant strides in understanding how to fight cancer, and those who understand this early will have a clear advantage. If p53 is in fact a guardian angel, then it would indeed be the answer to our prayers.

This article originally appeared at Transformational Technologies.