The pre-clinical work has already shown promise in killing ovarian cancer cells. Researchers hope the approach, which stems drug resistance, might also prove effective in treating other forms of cancers.
“When we use drugs to kill cancer, we almost never kill all of it,” said OMRF scientist Amit Maiti, Ph.D. “And when the cancer comes back, it’s resistant to the drug, which makes it harder to kill.”
In a paper published in the online edition of Pharmacogenomics Journal, Maiti has identified genes that could be manipulated to keep cancer cells from surviving drug treatment. “If we could prevent cancers from becoming drug-resistant, it could improve treatment outcomes,” said Maiti.
When cells in our body produce energy, they create a byproduct called reactive oxygen species (ROS). Cancer cells, which grow continuously, have higher levels of these byproducts. When anti-cancer drugs are used, the level of byproducts in those cells decreases, and the cells become drug-resistant.
Maiti suspected that if he could keep ROS levels high in cancer cells, they might not become drug-resistant. So in the culture medium, he took drug-resistant ovarian cancer cells and treated them with an anti-cancer drug and a small dose of ROS.
“It killed them all, 100 percent,” he said. “So we know that by increasing ROS levels in drug-resistant cancer cells, we make them vulnerable to drugs again.”
In humans or other living creatures, injecting ROS into cells is extremely challenging. So Maiti is looking at ways to alter gene function that would achieve the same results.
The next step will be testing the approach in laboratory mice.
“There’s lots of work to be done, but there’s a lot to be hopeful for, too,” Maiti said. “If this works in ovarian cancer, there’s no reason it couldn’t also work in other types of recurring cancer, like breast and colon cancers.”