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Scientists at Van Andel Research Institute (VARI) and Cedars-Sinai have developed a computational way to measure cellular age, this may leads to simpler screening and monitoring methods for cancer and other diseases. This reveal a progressive, measurable loss of specific chemical tags that regulate gene activity and are detectable at the earliest stages of development. These changes continue throughout a person’s life, correlating with cellular rather than chronological age and foreshadowing alterations found in cancer cells.
It builds on a 2011 discovery by Berman and Laird that first determined loss of these DNA marks-called methyl groups -occurs in specific areas of the genome in cancer. However, the techniques used at that time could not detect this process occurring in normal cells. Human cellular clock starts ticking the moment the cells begin dividing, this method allows tracking the history of past divisions and measure age-related changes to the genetic code that may contribute to normal aging and dysfunction.
Each of the nearly 40 trillion cells in the human body can trace its lineage back to a single, fertilized egg cell containing the original copy of individual’s DNA. These cells divide, replacing old or damaged cells at different rates based on their function in the body, environmental insults and wound healing throughout lifespan. Despite undergoing elaborate biological quality control checks, each cell division chips away at the genome’s integrity, leaving behind an accumulating number of changes.
While loss of DNA methyl groups, known as hypomethylation, is a common feature of many cancers, the mechanisms behind this phenomenon have until now been largely unknown. It is more profound in cancers that arise in tissues with a high turnover rate, such as the skin and the epithelium, the thin layer of cells that line many organs. It also features prominently in pediatric cancers such as medulloblastoma, a rare brain tumor.
Tissues with higher turnover rates are typically more susceptible to cancer development because errors can accumulate and force the change from a normal cell to a malignant one. Analysis and data interpretation for the project were led by Wanding Zhou, Ph.D., a postdoctoral fellow in the labs of Laird, Shen and VARI Chief Scientific Officer Peter Jones, Ph.D., D.Sc., along with co-first author Huy Q. Dinh, Ph.D., at the time a project scientist in Berman’s lab at the Cedars-Sinai Center for Bioinformatics and Functional Genomics.
The study encompassed 39 diverse tumors and more than 340 human and 200 mouse datasets-the most in-depth study of its kind and would not have been possible without massive swaths of publically accessible data from large-scale sequencing projects, including The Cancer Genome Atlas.
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