A shocking study reveals a danger for people of average age!



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Researchers at the Wellcome Sanger Institute near Cambridge found that about 80% of the cells contained mutations that could cause cancer, even though they looked healthy under the microscope.

When examining oesophageal esophagus in 9 patients, the researchers found that people in their twenties already had a few hundred transitions in some cells. This number can reach more than 2,000 transitions as we age, leading to healthy tissue "full of mutations".

"We discovered that at a time when the individual is middle-aged, he may have more mutations than normal cells," said Dr. Phil Jones, lead author.

Jones stated that all deceased subjects were between the ages of 20 and 75 at the time of death and that they had no history of illness or problem in the esophagus. Under the microscope, the fabric seemed perfectly normal.

The researchers then assigned tissue-tissue genes to the study published in the journal Science.

"After studying genetics, we were shocked to see the good esophagus filled with mutations," Jones said.

A variant gene, called TP53, is associated with esophageal cancer and was found in 37% of healthy cells.

The gene that controls cell division, called NOTCH1, is modified in about 80% of cells, a rate of change greater than that observed in esophageal cancers.

The researchers believe that these mutations can protect against age-related diseases, such as cancer, in a "hidden world of mutations".

"The study may help researchers determine how cells change and evolve to colonize tissues as we get older," said lead author Inigo Martinicorina.

Cancer is caused by genetic mutations, which can be inherited or caused by smoking, exposure to radiation, obesity or viruses.

News A shocking study reveals a danger for people of average age! – You can see the source of the original news from the following link: The Al-Azhar newspaper and the website of the unit disclaim any responsibility for the content of any news, but the responsibility lies with the & # 39; 39, original publisher.

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