A subset of lung tumors known to be relatively resistant to therapy is exquisitely sensitive to a class of recently approved anti-cancer drugs, according to a study led by Ludwig Oxford’s Sebastian Nijman, who is also an adjunct Principal Investigator at the Research Center for Molecular Medicine of the Austrian Academy of Sciences where the research was conducted. The findings, published in Nature Communications, suggest a new and more personalized therapy for non-small cell lung cancers characterized by mutations to a gene known as ATM. About 10% of lung tumors—the leading cause of cancer-related deaths—carry ATM mutations, and no treatments have been approved to specifically treat such tumors.
Using systems and approaches developed in Nijman’s lab to analyze how drugs interact with genes across the human genome, the researchers discovered that cancer cells with ATM mutations are sensitive to drugs that inhibit an enzyme called MEK, which supports cell proliferation and survival. (ATM, meanwhile, plays a central role in the cell’s response to DNA damage.) Nijman’s team found that MEK inhibitors stop such cells from proliferating and induce a programmed mechanism of cell death known as apoptosis.
MEK inhibitors have so far been approved for the treatment of a type of skin cancer, but not for lung cancer. If the results of the current study are confirmed in larger clinical studies, ATM mutations could be used as a potential biomarker to identify lung cancer patients who would benefit from treatment with this class of therapies.
This statement has been adapted from a news release available here.