Cancer: elephants have less cancer than us, unless they smoke

In theory, we should be constantly affected by cancer: our DNA is indeed a very fragile molecule. Every day, it undergoes several chemical and physical aggressions (UV rays, viruses, carcinogenic substances).

Combined with the thousands of errors that occur spontaneously every day when our cells divide, this DNA damage has the potential to cause mutations in essential genes and thus upset the cell’s balance and support its uncontrolled growth.

This is obviously not the case, and this scenario is thankfully much more of an exception than the rule. In practice, the vast majority of these errors have no adverse consequences, as they are immediately recognized and repaired using a series of very sophisticated protection mechanisms responsible for maintaining DNA integrity. This function is very important, because the risk of cancer is greatly increased when these DNA “repairers” are defective.

For example, the p53 gene is defective in more than 50% of cancers, while mutated BRCA genes, transmitted by heredity, are responsible for approximately 5% of breast cancers and 10% of ovarian cancers. . It is also to underline the importance of this phenomenon that the 2015 Nobel Prize in Chemistry was awarded to Tomas Lindahl, Paul Modrich and Aziz Sancar for their exceptional contribution to the identification and characterization of these repair mechanisms. DNA.

Large animals more protected from cancer than small ones

This careful maintenance of genetic material seems particularly important in large animals. The average cell size in animals remains quite similar. In theory, therefore, the larger an animal, the higher its risk of cancer should be, because the number of cell divisions required to reach and maintain this large size is much greater.

In addition, the life expectancy of these animals is generally longer, which increases their likelihood of developing tumors over time. However, this is not what happens: a tiny mouse weighing barely 20 g has a probability of developing cancer equivalent to that of a human being 4000 times heavier and even that of a 200 ton blue whale. , 10 million times heavier and which lives 30 times longer.

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Cancer: The Remarkable Elephant Repair System

A study suggests that this protection could involve the tumor suppressor p53. Considered as the “guardian of the genome”, this gene coordinates the response of cells to DNA damage by activating repair mechanisms or even by forcing the cell to commit suicide by apoptosis if this damage is too great.

By examining cancer mortality rates in several animal species, American scientists first observed that, despite their large size, elephants had a cancer incidence of about 5%, lower than most other animals. (including humans). By analyzing the genes of the animal, they were surprised to find that elephants have 20 copies of the p53 gene, compared to only 2 for humans! As this p53 gene plays an essential role in maintaining DNA integrity, it is very likely that this adaptation of elephants contributes to lowering their incidence of cancer.

In this sense, it is interesting to note that, in humans, the loss of a single copy of p53 causes Li-Fraumeni syndrome, a rare genetic disorder, where patients have almost a 100% risk of being affected. by several types of cancer.

If elephants smoked, they’d get as much cancer as we do

Despite their essential role, the systems that repair DNA quickly reach their limits when lifestyle habits create excess DNA damage. If elephants smoked, their cancer rates would skyrocket, regardless of the number of p53 copies present: it is estimated that a person who regularly smokes a pack of cigarettes a day accumulates almost 600 mutations in the DNA of his lung cells, many of these mutations even affecting the p53 protein.

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In short, these observations remind us that our body has a remarkable ability to protect us from cancer and that adopting healthy lifestyle habits remains the best way to get the most out of this natural protection.

Peto R: Quantitative implications of the approximate irrelevance of mammalian body size and lifespan to lifelong cancer risk. Philos Trans R Soc Lond B Biol Sci,; 370:pii:20150198.

Abegglen LM et al.: Potential mechanisms for cancer resistance in elephants and comparative cellular response to DNA damage in humans. JAMA,


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