0439 GMT April 22, 2021
Lead researcher, Professor David Thomas from Australia's Garvan Institute of Medical Research told Xinhua on Saturday that those errors can change the shape of the proteins that cancer drugs target, resulting in the drugs no longer working.
"Such changes are called mutations. The faster the rate of mutations, the more likely a cancer cell will discover a way to survive the drug treatment," Thomas said.
First author of the study, Dr. Arcadi Cipponi from Garvan Institute of Medical Research found cancer cells had a much higher mutation rate when they were exposed to cancer treatments compared with those which weren't.
"Our experiments revealed that cancer cells exposed to targeted therapies undergo a process called stress-induced mutagenesis — they generate random genetic variation at a much higher rate than cancer cells not exposed to anti-cancer drugs," Cipponi said.
On top of that, cancer cells can switch back to a normal high-quality DNA duplicating process after developing a resistance to cancer treatments, therefore ensuring its survival.
"The concept is that although an increased mutation rate increases the chance of becoming resistant to the drug, it also damages randomly other parts of cells, which can have a harmful effect on cancer cells," Thomas explained.
Based on their findings, researchers said that combining conventional targeted cancer therapy, with drugs specifically designed to disable cancer cells' ability to make higher mutation rates, may lead to more effective therapeutic strategies.
"Our findings have opened up new potential strategies that either prevent stress-induced mutagenesis in cancers, or are more effective in cancers that have already developed resistance," Thomas said.