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Grantee in the News: Judith Campisi shares insights on senescent cells and healthspan on Smithsonian.com

May 31
2017

Grantee in the News: Judith Campisi shares insights on senescent cells and healthspan on Smithsonian.com View MoreBACK

In the June 2017 issue of Smithsonian Magazine, 1990 AFAR Research Award recipient, Judith Campisi, PhD shared insights on the role senescent cells play in aging and cancer, and the possible evolutionary reasons senescent cells remain in our bodies.

While the article, Can Human Mortality Really Be Hacked?, focuses on the nonprofit SENS—Strategies for Engineered Negligible Senescence, Dr. Campisi shares that senescent cells originally act as a tumor suppressant mechanism, but later develops into a risk factor for all age-related diseases, including cancer.

She explains: “One thing evolution had to select for was protection from cancer, because we are complex organisms, we have lots of cells in our body that divide, and cell division is a very risky time for a cell because it’s easy to pick up a mutation when you are replicating three billion base pairs of DNA. So evolution put into place these very powerful tumor suppressant mechanisms—senescent cells—but they only had to last for 40 years at the most.”

Dr. Campisi stresses that, unlike SENS, the focus of most aging research organizations isn’t living forever, but rather to understand how to increase human healthspan.

The full article can be read here.

Judith Campisi, PhD is a Professor at the Buck Institute for Research on Aging.


For more information on senescent cells, we encourage you to explore our expert-edited Infoaging Guide to Cellular Senescence here.





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