The Stalk Institute for Biological Studies has recently had a team studying the effects of a specific stage of reproduction for the cell, the G1 phase, and how it is different in cancer cells. In this stage, the end part of the chromosome, called telomeres, shorten after each replication. Eventually, in a healthy cell, the telomeres will become too short to replicate further and the cell dies. In cancer cells this process can be altered by the addition of an enzyme that allows for uncontrolled cellular growth even when the telomeres are shortened which causes danger with an unstable chromosome. 

To study this effect of telomeres and cell aging within the G1 phase, the scientists removed a particular protein from a telomere in a cancer cell. Removing the protein altered the behavior of the cancer cell to be more similar to a healthy cell that has the ability to age and die with a more stable chromosome. This effect of allowing the death of the cell is called telomere deprotection. When studying this process, they identified a mechanism called the p53 pathway that protects healthy cells by repairing cell damage or if the damage is too great then causing the cell to kill itself. The loss of the p53 pathway, as in cancer cells, causes the telomere deprotection to malfunction and leads to an unstable chromosome that can grow uncontrollably. In further studies, the scientists hope to better understand cellular aging and the telomere shortening process. With a better understanding of this process and understanding why cancer cells do not have the deprotection of the telomeres, they hope the discovery can lead to a treatment to stop cancer cells from growing.