Almost every cell in the human body contains what researchers have dubbed as “death clocks.” Death clocks can be used to count down how fast humans are aging and whether they will develop cancer.

Researchers have found a distinct patter of mutations in DNA that build up at a constant rate through a person’s life. The mutation damage health genes and lead to cells turning cancerous. These mutations appear to occur at specific rates in different tissue.

This finding could also provide a new way of treating cancer by slowing the rate at which these mutation clocks “tick” in order to help reduce the spread of cancer.

Researchers believe that it may even be possible to develop ways of altering the rate at which humans age by slowing the rate of the mutations down.

Different mutational processes may be a contributing factor to the mutations accumulated in a cell. Each mutational process imprints a mutational signature on the cell’s genome.

Some processes generate mutations throughout lie at a constant rate in all individuals. The number of mutations in a cell attributable to these processes will be proportional to the chronological age of the person.

Researchers studied the DNA sequences of 36 different cancers from 10,000 individuals and searched for complex patters of mutations known as signatures.

Researchers discovered 30 different signatures and looked at the rate at which they appeared. Some cancers are caused by bursts of mutation as a result of smoking or overexposure to the sun while others are caused by DNA damage that builds up gradually over decades.

The study found that two mutation signature that appeared to build up at a steady rate caused more damage the more they accumulated.

One of the mutations was found to be linked to when cells divide and multiply as they grow and the other may be linked to the repair mechanisms in the cell that fix DNA damage.

These two mutation clocks tick at different rates in different tissues around the body.

These finding could allow researchers to read the rates and predict the time it may take for mutations to become cancerous.

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Gerry Oginski
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