A New Understanding Of Cell Stability
Genetic instability is common for all the cells in the human body and it consists, among others, in double-strand breaks in the DNA cells. This occurs when both strands in the double helix are severed and while usually cells have the capacity to repair themselves, a cell that can’t efficiently repair itself could result in cancer.
A study conducted at UCLA’s Jonsson Comprehensive Cancer Center and led by Robert Schiestl was made trying to understand the phenomena that lead to cell instability, discovering its trigger mechanisms and opening the path for further studies that could lead to a way to reverse the process and restore stability.
According to Schiestel, professor of pathology, radiation oncology and environmental health sciences and a Jonsson Cancer Center scientist, while “several hundred cells in our body that go crazy every day, and they’re taken out by our immune system”, sometimes these unstable cells “grow, spread and invade other regions of our body. Cancer cells are able to grow, spread and invade because the continued genetic instability can disturb the cellular program and create a growth advantage. Unfortunately, the immune system is not very effective at taking cancer cells out.”
Trying to determine the efficiency of the repair mechanism when DNA suffers a double-strand break, the researchers exposed cells to radiations, creating double strand breaks. While it was thought that the genetic instability would be localized only in the breaking point, the team proved that instability could surface anywhere, trough an “in trans” effect, meaning that “DNA damage at one position in the genome causes a certain mechanism of genetic instability all over the genome”
The study proved that double strand breaks induce genetic instability in trans, that there is a pathway on which the processes of instability take place in the DNA strands and that the genes responsible for this could be identified and used as targets against cancer, also leading the way for identifying new genes that can predict a predisposition for the disease.
