Researchers in California have discovered a potential new drug target, which they hope may result in… [+] new treatments for triple-negative breast cancer. Photo credit: AP Photo/Damian Dovarganes.
A new research study has identified a potential new target for therapies that could be used in triple-negative breast cancer, while sparing healthy cells.
The work published in Nature Communications by a U.S.-China team, led by researchers at Scripps Research in California, shows how a protein called Rad52 might be a new therapeutic target in some types of cancer. Rad52 participates in the repair of a certain type of DNA damage called a double-strand-break. Repairing DNA may seem like a good idea and in healthy cells it is, but in cancer cells, it can actually keep them alive in a damaged state and prevent therapies from working properly.
One cancer type that the researchers believe a Rad52-targeting drug might be useful in is that of triple-negative breast cancers, an aggressive form of the disease that affects an estimated 28,000 Americans per year. This type of breast cancer also has a lower survival than many other types, with 77% of women with triple-negative breast cancer surviving for 5 years or more, compared to 93% of women with other types of breast cancer.
Some triple-negative breast cancers have a mutation in the FANCM gene, which participates in protecting certain areas of DNA prone to breaking during cell division. The researchers found that tumors in mice without FANCM need to call in Rad52 to repair their DNA, whereas healthy cells don't need to do this. The team next stopped Rad52 from working in cells without FANCM using RNA silencing, finding that a slew of DNA damage accumulated, ultimately resulting in cell death.
A big problem with many chemotherapies is that they also affect healthy cells, giving rise to the wide range of side-effects that cancer patients experience. In this case, the scientists have reason to believe that this won't happen:
“Normal cells are fine when you remove Rad52, so we think potential therapies would have a very low toxicity,” says Xiaohua Wu, PhD, Professor at Scripps Research and senior author of the study.
The researchers suggest that any therapies developed to target Rad52 would take advantage of something called ‘synthetic lethality.' This works on the principle that a cell requir
