We finally know why very old people are protected from cancer

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The older a person gets, the more their risk of getting cancer increases. This is at least true until the age of 80, because once this threshold is crossed, the risks of having cancer decrease. Scientists have long sought to know how such a thing was possible and it seems that the answer to this question has finally been found.

How does cancer risk change with age?

As individuals age, their risk of developing cancer increases. Research has shown that older adults – particularly those aged 65 and over – are 11 times more likely to develop cancer compared to younger people. Age is one of the main risk factors for cancer, partly because over time, DNA damage gradually accumulates in cells due to multitude of factors, such as exposure to UV rays, chronic inflammation, environmental toxins or alcohol consumption.

As we age, cells become less effective at repairing this damage, leading to an accumulation of DNA mutations in a tissue-specific manner. The more mutations accumulate in our bodies, the greater the risk of uncontrolled cell division, or cancer. Although it seems obvious that the risk of cancer only increases with age, in reality, this risk decreases from the age of 80. Indeed, as surprising as it may be, studies have shown that the risk of developing cancer is low among octogenarians.

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It is linked to the evolution of cellular regeneration in the elderly

For a long time, scientists were unable to explain how such a phenomenon was possible. A recent study carried out by researchers at the New York institution Memorial Sloan Kettering Cancer Center has finally provided the solution to this enigma. According to the results of the study published in the journal Natureif octogenarians are less likely to get cancer, it is because their cellular activity is also declining, and this hinders the growth of cancer. Indeed, aging cells do not regenerate sufficiently to allow cancer to develop, which makes the disease less threatening.

To reach their conclusions, the researchers studied genetically modified mice predisposed to developing lung cancer. This allowed scientists to discover that as mice age, they produce more of a protein called NUPR1. An increase in NUPR1 protein makes lung cells function as if they are iron deficient, although this is not really the case. In fact, aging cells contain more iron.

But because these cells function as if they lack iron, they lose their ability to regenerate. And because the cells’ ability to regenerate is directly linked to increased cancer risks, the older mice developed far fewer tumors than their younger counterparts. Note that this effect can be reversed by giving the mice an additional supply of iron or by reducing the amount of NUPR1 in their cells. These findings are particularly important because it could give researchers the opportunity to explore treatments targeting iron metabolism for various diseases. Furthermore, this form of cancer is increasing among people under 50 throughout the world.

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