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Whales and cancer

Whales and cancer



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Do whales get less cancer than they should considering they have a lot more cells and tissue? If a lot of cancer formation is random because of mutations then shouldn't whales receive a lot of cancerous growths? Is it partly because there's a lot more systems that can protect against pre-cancerous development and apoptosis degradation in the larger mammal than in a human being?


Short answer: Yes/Maybe

More detailed answer: If the rate of cancer was uniform across cells then you would expect large mammals to more frequently get cancer than small mammals, just like buying 10 lottery tickets is more likely to make you a winner than buying one ticket. However, this correlation between mass and cancer rates does not exist, and it's absence is called Peto's paradox.

Some useful quotes from that paper:

The incidence of cancer in humans stands at one in three [33%], whereas it is only 18% in beluga whales…

There are a number of different hypotheses,” says Carlo Maley, director of the Center for Evolution and Cancer at the University of California, San Francisco. “For example, rather than body mass influencing the number of tumour suppressors and oncogenes, maybe there are less reactive oxygen species in larger organisms due to their lower metabolic rate…

Some biologists question whether there is a paradox at all, saying that variations in cancer rates across species - which range between 20% and 46% - are more similar than different. “All species get cancer at about the same rate, typically in the latter part of life span,” says James DeGregori, a molecular biologist at the University of Colorado in Denver. “We simply don't have the data yet to back up the notion that larger animals have come up with a way to avoid oncogenic mutations.”


Whales and cancer - Biology

Whales, dolphins and porpoises have two properties that should not in theory go together, they have a long lifespan for mammals and they tend to be resistant to cancer.

A new study suggests that the reason is written in their genes.

In general, when a creature has more cells in its body, they are expected to be more vulnerable to random mutations that can develop into cancer.

"Given this, we would expect that large and long-lived species, such as whales, have a higher rate of cancer than in small species," said lead author Daniela Tejada-Martinez at the Austral University of Chile.

So how to explain the longevity of the bowhead whale, which can reach 60 feet in length, weigh up to around 200,000 pounds (nearly 100 tonnes) and live for more than 200 years?

A bowhead mother swims with her calf on their migration route through ocean waters. /CFP

"The way in which the different species throughout their evolutionary history managed to fight cancer remains a mystery," Tejada-Martinez told AFP.

This is known as Peto's paradox, when some species do not have an incidence of cancer that correlates with their cell count.

To investigate this, researchers tracked the evolution of 1,077 tumor suppressor genes.

The study, published in the journal Proceedings of the Royal Society B, found signs of positive genetic selection in key regulators of DNA-damage and the immune system.

The turnover rate for these tumor suppression genes was almost 2.4 times higher in cetaceans than other mammals.

Researchers also identified duplication of 11 genes linked to longevity.

But the patterns of gene evolution varied by species.

The humpback whale is a species of baleen whale. /CFP

Baleen whales, for example, had molecular variants in their tumor-suppressing genes and a fast turnover rate that may explain the evolution of their "gigantism and longevity," said Tejada-Martinez.

The bottlenose dolphin, however, had the lowest number of gene copies among the cetaceans studied.

Since this species is associated with an increased incidence of cancer, the authors hypothesized that this suggests a higher rate of tumor suppressor gene copies could mean a lower risk of developing cancer.

"The link between evolutionary biology and medicine allows a more complete understanding of how the different forms of genetic variations contribute to cancer resistance and the aging evolution in cetaceans," said Tejada-Martinez.

"The discovery of new molecular variants including additional copies of genes could be the key to reveal new biological pathways that could lead to the creation of innovative treatments for cancer and age-related diseases."


What Whales and Elephants Can Teach Us About Cancer Prevention

In the United States, the National Cancer Institute estimates that about 1.8 million new cancer diagnoses and approximately 600,000 cancer-related deaths will occur in 2020 [1]. Furthermore, about 39.5% of people can expect to receive a cancer diagnosis at some point in their life [1]. Although cancer has many possible causes, downstream genetic mutations ultimately drive the development of cancer [2].

In multicellular organisms, genetic mutations don’t just affect a single, isolated cell, but can be passed on to many cells in the organism through cell division as the organism grows. Random genetic mutations occur at every cell division, and some of these can lead to uncontrolled cell proliferation resulting in the growth of tumors that can become cancerous. As an organism grows larger and lives longer, more cell divisions will occur in its body over its lifetime. One might expect that larger organisms would accumulate more mutations due to increased numbers of cell divisions and that there should be more chances for tumor growth. However, mortality due to cancer in large animals with long lifespans is not higher than in humans: this discrepancy is known as Peto’s Paradox [3]. If organisms the size of whales had up to 1,000 times the cancer risk than humans, as we might expect given the increased number of cell divisions and random mutations, it would be very unlikely for them to reproduce before succumbing to cancer.

Several hypotheses have been proposed to account for Peto’s Paradox, using data collected from large animals such as whales and elephants [3,4]. Studying cancer in wild mammals presents unique challenges due the lack of accessibility to populations and inability to control factors such as environmental exposures. However, whales, porpoises, and dolphins are all cetaceans, which is a group of wild animals that has been extensively studied [4]. Except for a few cases linked to environmental pollution, cancer in whales rarely occurs [3,4]. This makes them a great model organism for studying Peto’s Paradox. Since these organisms do not appear to have a high risk of cancer, it is suggested that their cancer prevention mechanisms are likely more effective than those of smaller organisms. Other researchers maintain that the rate of cancer development is the same, but cancer may not be as lethal in larger organisms. Here, I will describe hypotheses explaining Peto’s Paradox involving telomeres, hypertumors, and the tumor suppressor gene p53, in the order of least to most investigated.

Telomeres may play a critical role in cancer suppression in large organisms. Similar to how shoelaces have plastic aglets to prevent fraying, telomeres are repetitive DNA sequences located on both ends of each chromosome to prevent DNA damage [5]. Telomeres protect the important stretches of the genome located in the middle of the chromosomes and have recently become a hot topic in research due to possible implications in aging and cancer [5].

Telomeres (pictured in purple) gradually shorten each time a cell divides.

Telomeres deplete with every round of DNA replication. When the telomeres become too short, the cell becomes senescent, entering a dormant state in which it doesn’t divide. Researchers hypothesize that shortened telomeres in large organisms with long lifespans could explain their reduced cancer incidence [3]. Reducing the number of times an individual cell divides would reduce the opportunities for a mutation in an oncogene or tumor suppressor gene to occur. With fewer previous divisions for mutations to accumulate, the cell has a decreased risk of developing cancer. The exploration of telomere modifications as an explanation for Peto’s Paradox has just begun, and further research is needed to investigate the possibility.

Hypertumors

Another new hypothesis proposed to explain Peto’s Paradox is promising, but has only been illustrated in silico, or through a computer simulation. Researchers suggest that in larger animals, malignant tumors have a fitness disadvantage compared to benign tumors [4]. In a population of cancer cells with various phenotypes, natural selection may favor aggressive “hypertumors” that piggyback off the vascular growth of parent tumors. Acting as parasites, these hypertumors deplete the parent tumor’s resources and eventually destroy it. Unlike in small organisms, tumors need to reach a substantial size to have consequences in large organisms. Therefore, hypertumors have plenty of time to develop and damage the original tumor before the original tumor grows to a lethal size. As a result, cancer may still be more common in large organisms, just less lethal [4]. Additional research investigating tumor growth in living whales is needed before any concrete conclusions can be drawn.

Variation in TP53 has been identified as another possible explanation for Peto’s Paradox [3,6]. As a tumor suppressor gene, TP53 helps control cell growth, and mutations in the TP53 gene have been found in up to 50% of human cancers. The p53 protein expressed by this gene has primary roles in cell cycle arrest, DNA repair, and apoptosis. Mutations in the TP53 can lead to reduced expression of p53 and the uncontrolled cell growth that is a hallmark of cancer [7].

Imagine the cell cycle as the process of loading laundry into your washing machine. You’ve put the clothes and detergent in and started the wash cycle when soapy water suddenly starts seeping out of the crevices. Your instinct in this situation is probably to stop and turn off the washing machine to investigate the problem. Likewise, cell cycle arrest occurs when the cell notices that something is wrong, and all duplication processes stop to identify the problem. If you notice a fraying, broken wire poking out from behind the wall, you will probably choose to call an electrician instead of risking a do-it-yourself fix. In the cell cycle, p53 recognizes DNA damage and activates DNA damage response pathways to initiate DNA repair. Sometimes, your machine might be too broken to fix, and you must resort to removing it from your house and heading out to buy a new one. In a cell, the analogous process is apoptosis, where a severely damaged cell is marked for destruction and effectively killed before it can do further damage or proliferate.

To investigate the relationship of p53 and Peto’s Paradox, genome-wide studies were conducted, synthesizing data from 61 animals with a range of sizes [6]. These animals included large species such as the Asian elephant and woolly mammoth. Researchers found that as species evolved to be bigger, they acquired more copies of TP53, the gene that encodes the p53 protein. While humans only have one copy of the TP53 gene, the elephant genome contains 20 copies of TP53, resulting in greater production of p53 protein. This increase may be responsible for protecting these large organisms from developing cancer [6,8]. The role of p53 has evolutionary implications because when p53 evolved as a way to regulate the cell cycle, it fortified the system in place to ensure DNA was replicated correctly and cells with mistakes were killed before the issue could spread.

Although many explanations have been proposed to account for Peto’s Paradox, more research is necessary to elucidate the precise molecular basis of the paradox. Mouse models currently dominate studies in cancer research, but they are small organisms with short life spans. Although these characteristics are useful when researchers want to conduct a study over an organism’s lifetime, they also mean that the mouse model is not the ideal model for studying cancer suppression. Expanding the study of cancer to a more diverse variety of organisms would allow for a more complete understanding of the underlying mechanisms.

Understanding Peto’s Paradox is not only important for conservation scientists and wildlife zoologists it also has implications in human medicine. Peto’s Paradox provides an interesting opportunity for potential research that may provide insight into cancer treatment. Determining the mechanism behind cancer resistance in large animals could reveal powerful techniques to develop novel treatments for human cancers by targeting telomere length, p53 expression, or hypertumors.

[1] Cancer Statistics. National Cancer Institute. https://www.cancer.gov/about-cancer/understanding/statistics. Accessed December 20, 2020.

[2] Griffiths AJF, Miller JH, Suzuki DT, et al. An Introduction to Genetic Analysis. 7th edition. New York: W. H. Freeman 2000. Mutation and cancer. Available from: https://www.ncbi.nlm.nih.gov/books/NBK21809/

[3] Caulin AF, Maley CC. Peto’s Paradox: evolution’s prescription for cancer prevention. Trends in Ecology & Evolution. 201126(4):175-182. doi:10.1016/j.tree.2011.01.002

[4] Nagy JD, Victor EM, Cropper JH. Why don’t all whales have cancer? A novel hypothesis resolving Peto’s paradox. Integrative and Comparative Biology. 200747(2):317-328. doi:10.1093/icb/icm062

[5] Are Telomeres the Key to Aging and Cancer. Learn.Genetics Genetic Science Learning Center. https://learn.genetics.utah.edu/content/basics/telomeres/. Accessed November 15, 2020.

[6] Sulak M, Fong L, Mika K, et al. TP53 copy number expansion is associated with the evolution of increased body size and an enhanced DNA damage response in elephants. eLife. 20165. doi:10.7554/elife.11994

[7] Olivier M, Hollstein M, Hainaut P. TP53 mutations in human cancers: origins, consequences, and clinical use. Cold Spring Harb Perspect Biol. 20102(1):a001008. doi:10.1101/cshperspect.a001008

[8] Abegglen LM, Caulin AF, Chan A, et al. Potential Mechanisms for Cancer Resistance in Elephants and Comparative Cellular Response to DNA Damage in Humans. JAMA. 2015314(17):1850-1860. doi:10.1001/jama.2015.13134


Peto’s Paradox

The numbers don’t add up: animals with vastly more cells have extremely low rates of cancer, and small animals like mice can have high rates of cancer. Scientists have suggested theories about why this happens – here are two of them.

Evolution

One reason elephants and blue whales seem to have very low rates of cancer is evolution. These big animals must evolve extensive “anti-cancer” defense systems to survive, or face extinction. The African savannah elephant has 20 copies of a tumor suppressor gene called TP53. This gene instructs cells to self-destruct if they become cancerous. For comparison, humans only have one copy of TP53. It would make sense for an animal with more copies of cancer-fighting genes to be more resistant to cancer.

Metabolic rates

Another factor that may contribute to large animals’ resistance to cancer is different metabolic rates. Bigger animals tend to have lower metabolic rates, which means their cells convert nutrients to energy more slowly. They also have bigger cells, which divide more slowly compared to cells of smaller animals. The conclusion from these two observations is that the lower metabolic rate and division rate of large animals lowers their chance of developing cancer, as opposed to the rapidly-dividing cells of small mice.

Hypercancers

What may be the most interesting answer to Peto’s pardox is hypercancers. In short, hypercancers, or hypertumors, are the cancers of cancer. The theory goes that some cancer cells are so mutated that they separate from their original tumor and go rogue. The new cancer ends up competing against their original tumor for nutrients and eliminating them. This cycle can repeat indefinitely every time a new hypertumor shows up. The hypercancer theory suggests that there actually might be a ton of tumors in a blue whale, but since they’re constantly defeated by new cancers, the animal isn’t affected.

Cells Human Medical (c) qimono, CC0


AlbinoMouse

I love Carl Zimmer. I think he’s one of those people who just really get it… and not only does he get it, but he explains things in a way that makes other people get it.

Recently, he published an article on the Loom discussing whales and cancer, based around a recent review published in Trends in Ecology and Evolution. The basic premise of cancer works like this:

  • Over time, cells make mistakes in DNA replication
  • Mistakes accumulate and eventually, mistakes will affect some vital process
  • This causes cancer

This stands to reason then, that the more cells you have and the longer you live, the more mistakes you will have, and the higher likelihood that you will have cancer.

But if you looked at blue whales, they’re HUGE. They have a lot of cells and they can live a long time. Indeed, according to calculations, half of all blue whales should have colorectal cancer. By the time they reach middle age, ALL of them should be cancer-ridden. And that’s only one type of cancer!

However, this is not the case. Indeed, across all studied species, including humans with our often-poor health choices, cancer occurs at a rate of about 30%. So mice, with their rapid metabolism and short life spans, get cancer at the same rate as whales, with their much slower metabolism and longer life spans.

This suggests that larger animals have evolved mechanisms against cancer that have held it at the approximately 30% mark – regardless of cell number, age or size, which is contradictory to the current paradigms of cancer as a statistical inevitability. And if that is so, we would be better off studying how larger animals cope with cancer rather than looking at cancer in mice.

That is not to say that we should suddenly be breeding captive whales for laboratory-style research – but so little is known about the health of these animals in the first place, despite the popularity of sea mammals as aquarium entertainment. A well sequenced genome would be the first informative step – The authors suggest studying the genome to look at differences in cancer defenses among related species with a wide range of sizes, such as whales and dolphins. Learning more about their health and biology of these animals may yield interesting new avenues in both human health research and animal veterinary medicine.

Zimmer ends his article eloquently:

“But such an undertaking would have to overcome a lot of inertia in the world of cancer research. Cancer biologists don’t look to big animals as models to study–which is one reason there’s not a single fully-sequenced genome of a whale or a dolphin for scientists to look at. For most cancer researchers, mice are the animals of choice.

But if we want to find inspiration for cancer-fighting medicines, mice are the last animal we’d want to consider. It’s like learning how to play baseball from a bench-cooler at a Little League game, when Willie Mays is waiting to dispense his wisdom.”


High levels of contaminants in killer whales

Little is known concerning environmental contaminants in predators at the top of a food chain. A study published in Environmental Toxicology and Chemistry has demonstrated that new types of brominated flame retardants accumulate in the tissues of killer whales near Norway and are also passed on to nursing offspring.

Investigators also detected human-made chemicals called perfluoroalkyl substances (PFAS) in the tissues of adult killer whales. Thresholds for health effects of PFAS in marine mammals are not established, but the chemical has been linked to reproductive and endocrine effects in wildlife. In addition, polychlorinated biphenyls (PCBs), which have long been banned, were detected in the blubber of 7 of the 8 killer whales in the study at levels that exceeded the proposed threshold for toxicological effects in marine mammals.

"Levels of pollutants in top predators give not only an indication of ecosystem health, but of the persistence of chemicals, passive mobility in the environment, and active biotransport with migrating animals," the authors wrote. "Our results are relevant for the continued environmental monitoring of contaminants in the Arctic."


Understanding Why Whales Don't Get Cancer

All kinds of animals are at risk of developing cancer, which has a problem since the dinosaurs. It often starts when mutations occur in DNA, which has to be copied every time cells divide, a frequent event. Those mutations can lead to unregulated cell growth - cancerous tumor formation. Weight and age also influence the risk of cancer, suggesting that large, long-lived creatures like elephants or whales should have the highest rates of cancer. But elephants and whales are actually less likely to get cancer than most animals. Assistant Professor Marc Tollis, of the School of Informatics, Computing, and Cyber Systems at Northern Arizona University, wanted to understand why. He and a team of researchers took a deep dive into cetacean genomes (which include dolphins, porpoises, and whales) to learn more.

After painstaking work collecting the material and obtaining the DNA from a humpback whale, the investigators found that some regions of the whale genome have evolved faster than they have in other mammals. Those regions contain genes that are involved in DNA repair and controlling cell division and growth these same genes are often mutated in human cancers. The whale genome also contains many copies of tumor-suppressing genes.

&ldquoThis suggests that whales are unique among mammals in that in order to evolve their gigantic sizes, these important &lsquohousekeeping&rsquo genes, that are evolutionarily conserved and normally prevent cancer, had to keep up in order to maintain the species&rsquo fitness,&rdquo Tollis said.

&ldquoWe also found that despite these cancer-related parts of whale genomes evolving faster than other mammals, on average whales have accumulated far fewer DNA mutations in their genomes over time compared to other mammals, which suggests they have slower mutation rates,&rdquo he added. The findings have been reported in Molecular Biology and Evolution.

Whales are massive and live relatively long lives. While having more cells in the body that divide for a longer period of time should make them more susceptible to cancer, in a phenomenon known as Peto&rsquos Paradox, they are not. Now that we know more about why that is, the researchers want to use their work to help develop better preventions or therapeutics for human cancers.

&ldquoNature is showing us that these changes to cancer genes are compatible with life. The next questions are, which of these changes is preventing cancer, and can we translate those discoveries into preventing cancer in humans?&rdquo said co-senior study author Carlo Maley, a cancer evolutionary biologist from ASU&rsquos Biodesign Institute.

&ldquoOur goal is not only to get nature to inform us about better cancer therapies but to give the public a new perspective of cancer,&rdquo Tollis said. &ldquoThe fact that whales and elephants evolved to beat cancer, and that dinosaurs suffered from it as well, suggests that cancer has been a selective pressure across many millions of years of evolution, and it has always been with us. Our hope is that this may change people&rsquos relationship with the disease, which can be painful and personal. It also helps provide even better appreciation for biodiversity. In our current sixth mass extinction, we need all the reasons for conservation that we can get.&rdquo


What Goes On Further?

Sometimes, DNA gets damaged or corrupt or during the G1 phase. This G1 phase checkpoint ensures that such cells with damaged DNA do not proceed further as they can turn cancerous and are sent into a particular phase known as the G₀ phase, where cells don’t divide.

The G₀ phase cells will continue with their functions but won’t go into the cell division. Neurons are an example of cells in G₀ phase. The protein then checks if the damaged cell can be repaired and if not, then the cell is subjected to apoptosis or programmed cell death. Sometimes, such damaged DNA can go undetected by the G1 checkpoint and then malignant DNA is formed.

However, a single corrupt DNA strand won’t be enough to induce cancer. After a certain amount of damaged cells go undetected, these cells now begin to divide and grow abnormally. This is now called cancer.

Researchers previously believed that since larger animals have more cells, the incidence of getting cancer is increased. Smaller dogs are at less risk of getting cancer as compared to larger dogs. A taller person has a slightly higher risk of getting cancer than a shorter person. But the incidence of cancer in humans is a little less than that of a rat. While giant animals rarely get cancer. Why is that?


Whales Have Cancer Resistance Cells 'Written in Their Genes' Finds New Study

Whales, dolphins and porpoises have two properties that should not in theory go together — they are both large and have very long lifespans.

A new study suggests that the reason is written in their genes.

In general, when a creature has more cells in its body, they are expected to be more vulnerable to random mutations that can develop into cancer.

“Given this, we would expect that large and long-lived species, such as whales, have a higher rate of cancer than in small species," said lead author Daniela Tejada-Martinez at the Austral University of Chile.

So how to explain the longevity of the bowhead whale, which can reach 60 feet in length, weigh up to around 200,000 pounds (nearly 100 tonnes) and live for more than 200 years?

“The way in which the different species throughout their evolutionary history managed to fight cancer remains a mystery," Tejada-Martinez told AFP.

This is known as Peto’s paradox, when some species do not have an incidence of cancer that correlates with their cell count.

To investigate this, researchers tracked the evolution of 1,077 tumour suppressor genes.

The study, published in the journal Proceedings of the Royal Society B, found signs of positive genetic selection in key regulators of DNA-damage and the immune system.

The turnover rate for these tumour suppression genes was almost 2.4 times higher in cetaceans than other mammals.

Researchers also identified duplication of 11 genes linked to longevity.

But the patterns of gene evolution varied by species.

Baleen whales, for example, had molecular variants in their tumour-suppressing genes and a fast turnover rate that may explain the evolution of their “gigantism and longevity", said Tejada-Martinez.

The bottlenose dolphin, however, had the lowest number of gene copies among the cetaceans studied.

Since this species is associated with an increased incidence of cancer, the authors hypothesised that this suggests a higher rate of tumour suppressor gene copies could mean a lower risk of developing cancer.

“The link between evolutionary biology and medicine allows a more complete understanding of how the different forms of genetic variations contribute to cancer resistance and the ageing evolution in cetaceans," said Tejada-Martinez.

“The discovery of new molecular variants including additional copies of genes could be the key to reveal new biological pathways that could lead to the creation of innovative treatments for cancer and age-related diseases."


Whales are 1000 times less likely to develop cancer than human

Did you know how many people die from cancer annually? It is over 5 million. What’s worse, worldwide rates of cancer are predicted to increase by 50% compared with the current rates by 2020. What is interesting, however, is that whales rarely have cancer and they are 1000 times less likely to develop cancer than human. According to the research, it was found that their larger body size helps them be away from cancer.

large Body Size

Cells in organisms have the same probability to have a malignant transformation and to become a tumor cell. It means the large organisms with more cells have a higher cancer risk. However, as shown in the graph, mice with a smaller body size are 3 times more likely to have cancer than human. Elephants and whales with a larger body size have a relative lower cancer rate. Actually, as Peto’s paradox demonstrated, the capacity of whales to suppress cancer cells is 1000 times better than humans. The reasons behind this phenomenon are that it takes longer time for a tumor cell to reach the fatal size in whale’s body and whale has a lower metabolism rate.

Whales are less likely to have cancer because it takes a long time for tumors in whale’s bodies to reach the lethal size. In large organisms such as whales, Nagy, Victor, & Cropper. (2007) argued that tumors must be larger to become lethal. In order to become lethal tumors, cancer cells need to collect aggressive cells to make themselves stronger. These aggressive cells then grow and gradually become lethal. However, this process takes long time for tumors in large body size organisms to evolve and then reach the large enough lethal size. The longer time to reach the lethal size allows more time for organisms to repair cells so whales are able to repair the cancer cells before they becoming lethal. Therefore, even though it is more likely for whales to have cancer cells, these cancer cells are less lethal while cancer cells in human being’s body are more easily become lethal.

Lower Metabolism Rate

Whales have lower risk of having cancer because of the lower metabolism rate compared with humans. Metabolism proceeds in organism by generating a kind of destructive chemically species-reactive oxygen. The reactive oxygen can damage the DNA by breaking the bonds between DNA and inducing chromosome mutations. Once the DNA is damaged, the risk of cancer increases. What’s worse, the damaged DNA, as junk in the organism, can also induce cancer. It means the rate of metabolism has a positive correlation with the possibility of having cancer.

Based on the previous study, larger organism tends to have a lower metabolism rate. Hence a larger organism has an overall lower risk of having cancer. Consequently, whales, as large organisms, are less likely to have cancer compared with human beings whose body size are smaller.

To summarize, a large body size of whales explains why the cancer rate of whales are lower. Meanwhile, these findings could also be applied to prevent and treat cancer. Though humans cannot change body size easily, humans could try to lower the metabolism rate to achieve the same effect as whales have.


Why don’t whales get cancer?

Whales, dolphins and porpoises are the world’s largest and longest-living mammals – and they can resist cancer.

Why these cetaceans and other large animals evade this scourge has long perplexed scientists, who reason that organisms with more cells should have a higher risk of cancerous mutations – a dilemma known as Peto’s paradox.

A molecular study, published in the Proceedings of the Royal Society B, has now found cetaceans have rapidly evolving genes that suppress tumours.

A team of international scientists from Chile, the UK and the US explored how natural selection drove the evolution of 1077 tumour suppressor genes in cetacean ancestors and compared them with those of 15 other mammal species, including humans.

Key Research points

  • Whales and dolphins are less susceptible to cancer than humans.
  • Molecular analysis showed they had a high rate of gene mutation.
  • This led to a high number of tumour suppressor genes.

The turnover of the genes – the rate at which they were gained and lost through mutation– was nearly 2.4 times higher in cetaceans than most other mammals, and highest in baleen whales (filter-feeding species that include blue, humpback and right whales).

The gene variants found in those mammals “could have favoured the evolution of their particular traits of anti-cancer resistance, gigantism and longevity,” write Daniela Tejada-Martinez, from the Universidad Austral de Chile, and co-authors.

The study found signs of positive selection in genes regulating DNA-damage, tumour spreading and immunity. It also found 71 genes with duplications associated with fighting cancer, such as DNA repair, metabolism, cell death and ageing and 11 duplicate genes associated with longevity.

“Overall, these results provide evolutionary evidence that natural selection in tumour suppressor genes could act on species with large body sizes and extended lifespan,” the authors write, “providing novel insights into the genetic basis of disease resistance.”

Natalie Parletta

Natalie Parletta is a freelance science writer based in Adelaide and an adjunct senior research fellow with the University of South Australia.

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