Why elephants rarely get cancer

·3 min read
Mother elephant with her calf.
Elephants are cancer-resistant despite their large frame and lengthy lifespan. (Stock, Getty Images)

Scientists may have discovered why elephants rarely develop cancer.

The risk of the disease tends to increase alongside life expectancy and body size, as there are more cells to become malignant.

Elephants – the world’s largest land mammal with a lifespan of up to 70 years – have puzzled experts by rarely being struck down with the illness.

Scientists from the University at Buffalo have now revealed elephants have multiple copies of tumour-suppressing genes, all of which “contribute probably a little bit to cancer resistance”.

Read more: Humans carry proportionately more fat than elephants

The replication of these genes is thought to have “facilitated the evolution of increased body size by compensating for decreasing intrinsic cancer risk”.

Better understanding natural cancer resistance may help in the development of new treatments, the scientists hope.

Medical 3D illustration of a dividing cancer cell with a cell surface
Tumours develop when cells grow in an uncontrolled way. (Stock, Getty Images)

One in two people born after 1960 in the UK will statistically develop cancer at some point in their life.

The disease arises when genetic mutations cause individual cells to grow in an uncontrolled way.

A longer life creates more opportunities for these mutations to take place, hence why cancers are more common among the elderly.

Elephants – with their lengthy lifespan and gargantuan frame – rarely develop the disease, however.

Read more: Why naked mole rats are cancer resistant

To better understand why this occurs, the Buffalo scientists analysed Asian, African savanna and African forest elephants, as well as their living and extinct relatives.

Perhaps surprisingly, elephants are related to small mammals like Cape golden moles, which also express multiple tumour-suppressing genes.

This genetic advantage may therefore have come about before, or while, today’s elephants evolved their exceptionally large frame, the scientists wrote in the journal eLife.

“One of the expectations is as you get a really big body, your burden of cancer should increase because things with big bodies have more cells,” said study author Dr Vincent Lynch.

“The fact this isn’t true across species, a long-standing paradox in evolutionary medicine and cancer biology, indicates evolution found a way to reduce cancer risk.”

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The scientists have previously focused on the tumour-suppressing gene TP53.

“This time, we said, ‘Let’s just look at whether the entire elephant genome includes more copies of tumour suppressors than what you’d expect’,” said Dr Lynch.

“Is the trend general? Or is the trend specific to one gene? We found it was general.

“Elephants have lots and lots and lots of extra copies of tumour-suppressor genes, and they all contribute probably a little bit to cancer resistance.”

These genes are involved in DNA repair and internal stress resistance, as well as in the growth, ageing and death of cells.

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“If you pick a weird mammal, there’s a good chance it will be in these groups – the Afrotherians and Xenarthrans: armadillos, aardvarks, sloths, anteaters, all of these weird mammals,” said Dr Lynch.

“We found within these groups of organisms, the ones we studied all seem to have extra copies of tumour-suppressor genes.

“That may be why in the last Ice Age, there were giant sloths and ancient mega-armadillos.

“There’s even an extinct species of manatee relative called the Steller’s sea cow that was elephant-big.

“Extra copies of tumor-suppressors may have helped all of these animals get really, really big.”

The scientists hope their results will lead to the development of new cancer treatments.

“By determining how big, long-lived species evolved better ways to suppress cancer we can learn something new about how evolution works and hopefully find ways to use that knowledge to inspire new cancer treatments,” said co-author Dr Juan Manuel Vazquez from the University of California, Berkeley.

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