A simple, computational approach has been developed to evaluate cellular age by a team directed by researchers at Cedars-Sinai and VARI (Van Andel Research Institute). This can be a step forward leading to an advanced, easier diagnosing and supervising techniques for cancer as well as other diseases.
The results disclose a progressive, quantifiable loss of particular chemical tags that control the gene activity and are visible at the initial development stages. These variations carry on throughout the life of an individual, linking to cellular instead of chronological age and predicting changes found in cancer cells.
The scientist said, “Our cellular watch begins ticking the instance our cells start dividing. This technique lets us trail the records of these earlier divisions and evaluate age-related variations to the genetic code that might add to dysfunction as well as normal aging.”
Each of the almost 40 Trillion cells within the human body can mark out its lineage back to one fertilized egg cell holding the original DNA copy of a person. Throughout the lifetime of a person, these cells divide, substituting damaged or old cells at diverse rates dependent on things such as their purpose in the body, wound healing, and environmental insults.
In spite of going through complicated biological quality control tests, every cell division seeks the integrity of genome, leaving behind a compiling digit of variations. Main among these is a remarkable change in the location and number of genome’s methyl groups, division of a procedure that starts during fetal development and carries on during a lifetime.
Though DNA methyl groups’ loss, called hypomethylation, is a widespread feature of several cancers, the processes behind this occurrence are largely unidentified. It is more intense in cancers that occur in tissues with an elevated turnover rate, such as the epithelium and the skin, the cell’s thin layer that streak several organs.
The researcher said, “Tissues with elevated turnover rates are usually more prone to cancer development merely as there are more chances for faults to gather and force the alteration to a malignant cell from a normal one.”