Researchers are actively searching for ways to extend the survival benefit of targeted cancer therapies to prevent the possibility of highly resistant tumors. A new study led by researchers at the Duke Cancer Institute describes a potential new strategy to disrupt the repair mechanism that cancer cells use after treatment, halting their ability to regenerate.
The findings are published in the journal Science Translational Medicine, in a paper titled, “Small-molecule targeted therapies induce dependence on DNA double-strand break repair in residual tumor cells.”
