Scientifically Speaking | How large animals beat cancer
Cancer is a collection of over 100 diseases that result from mutations in our DNA. Most of the mutations that cause cancer arise from mistakes made when DNA is copied during cell division. A few mutations are inherited from parents.
Cancer is mainly a disease of the elderly because mutations accumulate over time. More cell divisions means more chances of mistakes during the copying process. The DNA of an adult has been copied a whopping 30 trillion times and with each division comes an increased risk of cancer.
There is a remarkable correlation between body size and lifespan among most vertebrate animals. A small fish such as the pygmy goby lives for only 59 days. A large animal such as the bowhead whale lives for 211 years. Long-lived animals often run into the mechanical barriers of how long their organs can function. After a certain number of beats, hearts tend to give out. Long-lived animals also have to deal with cancer.
One animal that beats the odds is the naked mole rat. Mice, which are roughly the same size as naked mole rats, live for around four years; on the other hand, naked mole rats can live for more than 35 years. Researchers who study these long-lived animals have found that they have developed ways to prevent cancer.
What about large animals? Cells vary in size, but larger animals have more cells. Long-lived animals also have more cells that have undergone divisions. If the rate of mutations across cells is roughly similar for different animals, we can expect small and short-lived animals to have a lower risk of cancer than large long-lived animals. But this isn’t always the case.
To put it another way, if large animals such as whales and elephants had the same risk of getting cancer as humans, then young animals of those species would never survive into adulthood. But these animals do exist and they get quite large: in fact an adult blue can weighs 136,000 kilograms!
Also Read | The untapped green potential of agroforestry
This contradiction between observed body size in some animals and expected cancer risk is known as Peto’s Paradox. What this tells us is that large animals have found ways to beat cancer. By gleaning the biological details of how they do it, the hope is that we will find treatments for people too. Some studies have already started to show the way.
In 2015, researchers found that elephants have a much lower risk of cancer than people do, and they have 20 copies of an anti-cancer gene called TP53. This gene gives rise to a tumour suppressor protein, which causes damaged cells to destroy themselves by a process known as programmed cell death. In humans, the TP53 gene prevents cancer. Conversely, mutations that damage TP53 are some of the most common causes of cancer.
A newer study found that elephants aren’t the only large animals with many copies of the TP53 anti-cancer gene. Other large relatives such as mastodons and woolly mammoths had this gene too. Just this year, in an article in eLife, researchers looked at the entire elephant genome and found that they had many copies of other anti-cancer genes, apart from TP53. And not all large animals have many copies of TP53. Whales, for example, have other means of keeping their cancer risk low.
Taken together, we now know that large animals have evolved many different mechanisms to reduce the risk of cancer, which has helped them to increase in size.
To be sure, even though their cancer risk is reduced, large animals still succumb to other diseases. Take for example, elephants, which have six sets of teeth. If elephants live longer than the sixth, they have a hard time chewing food and are prone to starvation. In fact, loss of teeth is the leading cause of death in mature elephants.
While it might seem farfetched right now, the different biological mechanisms that animals use to reduce cancer risk might someday help in increasing lifespan and in improving human health too.
Anirban Mahapatra, a microbiologist by training, is the author of COVID-19: Separating Fact From Fiction.
The views expressed are personal
Please sign in to continue reading
- Get access to exclusive articles, newsletters, alerts and recommendations
- Read, share and save articles of enduring value