Researchers at UCLA's Jonsson Comprehensive Cancer Center have developed an assay that may be used to help identify new genes that can predict a predisposition to cancer.
The study, published in the April issue of Radiation Research, was done in yeast and mammalian cells.
Cancer cells show persistent genetic instability and the researchers, led by Robert Schiestl, have discovered a mechanism that switches on that genetic instability. If they can uncover and understand the molecular pathways at work in promoting genetic instability, they may be able to develop ways to switch that mechanism off, restoring stability.
"We all have several hundred cells in our body that go crazy every day, and they're taken out by our immune system," said Schiestl, a professor of pathology, radiation oncology and environmental health sciences and a Jonsson Cancer Center scientist. "What's important is that those cells don't grow and 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."
The assay determines the efficiency of the repair mechanism when DNA suffers a double-strand break, when both strands in the double helix are severed. These breaks cause genetic instability and are particularly dangerous because they can lead to genome rearrangements or deletions of certain genes that, when gone, result in cancer.
"Every cell has double strand breaks all the time," said Schiestl, senior author of the study. "It is how the cell tries to fix these breaks that is key, the capacity and the efficiency of the repair so no further harm occurs."
A cell that can't efficiently repair itself could result in cancer.
In the study, researchers irradiated cells to create double strand breaks. They wanted
|Contact: Kim Irwin|
University of California - Los Angeles