Feb 19, 2019 Cedars-Sinai Staff
Through advanced gene sequencing, investigators discover a new method to measure cellular age.
We measure the passage of time chronologically, but the cells inside us adhere to a different clock. They follow the timepiece of cell division—the ticking down of which can foreshadow cancer and other diseases. Better understanding of this process could help screen and monitor such conditions, but its inner workings have remained mysterious.
That is, until scientists at Cedars-Sinai and Michigan’s Van Andel Research Institute (VARI) developed a straightforward way to compute human cellular age. Their findings reveal a progressive loss of specific chemical tags that regulate gene activity. These changes continue throughout a person’s life, correlating with cellular rather than chronological age.
Although cell division is necessary for growing, living, and healing, each split chips away at the integrity of our genome. This is a natural part of aging, but, unfortunately, also plays a role in many cancers and age-related diseases.
Through advanced gene-sequencing technology, the investigators devised a method to track this process, known as hypomethylation, as a biomarker for cellular aging.
The study builds on a 2011 discovery by co-investigators Benjamin Berman, PhD, of the Cedars-Sinai Center for Bioinformatics and Functional Genomics, and Peter W. Laird, PhD, of VARI. This earlier work determined that hypomethylation occurs in specific areas of the genome in cancer. However, the techniques used at that time could not detect this process in normal cells. This new ability could track cell changes that occur before cancer first manifests.
“What is striking about the results from our new method is that they push back the start of this process to the earliest stages of fetal development,” Berman says. “That was completely surprising, given the current assumption that the process begins relatively late on the path to cancer.”