With a vast analysis of genetic data, a group of scientists has shown that the genetic signature of aging tissue is very different from that of cancerous tissue.
This is important because the activity levels of certain genes can influence how the cells within tissues behave, and ultimately, whether diseases such as cancer develop.
As we age, more and more of our cells become dormant, meaning that they no longer grow, divide, and renew.
This is a process called cellular senescence, and the proportion of senescent cells in our bodies increases with age.
In the irreversible state of cell senescence, cell division ceases. Conversely, cancer is a disease defined by uncontrolled cell division that leads to the formation of tumors.
Previously, experts assumed that aging tissues are more likely to become cancerous because of an accumulation of multiple mutations in cancer causing-genes.
The team behind this research has published their findings in the journal Aging Cell.
What did the study find?
The research group — led by Prof. João Pedro de Magalhães, from the University of Liverpool, in the United Kingdom — analyzed and compared the genetic signatures of genes involved in aging. In all, they looked at the genes involved in cancer progression in nine human tissues.
Specifically, they investigated how active these genes were in each tissue to identify any patterns of activity that may link aging to the development of cancer.
In most tissues, aging and cancer gene activity patterns changed in opposite directions. In other words, while some aging genes were more active, some cancer genes were less active. This was true in all the tissues except the thyroid and uterine tissues, where both aging genes and cancer genes changed in the same direction.
In addition, gene signatures of cellular senescence changed in the same direction as the aging genes — in the opposite direction of the cancer genes.
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