Once a bucket of genes linked to aging is removed, the lifespan of cells increases significantly, American scientists discovered during ten years of meticulous research, stressing that the results could be applied to humans.

An “exhaustive, ten-year effort” allowed scientists at the Buck Institute for Research on Aging and the University of Washington to identify some 238 genes which could be targeted to improve human health and possibly extend life spans by 60 percent. The paper was published on Thursday in the journal Cell Metabolism.

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The study was carried out on nearly 4,700 yeast strains, but a series of experiments involving roundworms allowed scientists to say that its results could be applied to humans, as well.

“This study looks at aging in the context of the whole genome and gives us a more complete picture of what aging is,” said lead author Brian Kennedy, Buck Institute’s president and CEO, in the press release. “It also sets up a framework to define the entire network that influences aging in this organism.”

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The researchers had to count yeast cells one by one, tracing the consequences of a single gene deletion with the help of several microscopes. The indication of success was a number of daughter cells produced before a mother cell stopped dividing.

The most “stunning” gene has turned out to be LOS1, which is in part responsible for building proteins, but also is linked to mTOR, which regulates cell growth, and Gcn4gene, which helps to manage DNA damage. The deletion of this gene was demonstrated to “robustly extended lifespan.”

“Calorie restriction has been known to extend lifespan for a long time,” Kennedy said. “The DNA damage response is linked to aging as well. LOS1 may be connecting these different processes.”

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The prolonged research, which involved advanced lab techniques and undergraduate participants, is said to be “only part of a larger process to map the relationships between all the gene pathways that govern aging,” according to the team, who hope to come up with new therapies.

“Almost half of the genes we found that affect aging are conserved in mammals,” Kennedy added. “In theory, any of these factors could be therapeutic targets to extend healthspan. What we have to do now is figure out which ones are amenable to targeting.”