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While cancer therapies that target specific genes or disease pathways extend life, when small reservoirs of cancer cells survive, grow and spread during treatment, they can also lead to highly drug-resistant tumors
In their search for ways to prolong the survival benefit of targeted therapy, a team led by researchers at the Duke Cancer Institute has discovered a potential new strategy for disrupting the repair mechanisms that cancer cells use after treatment.
The research team's findings were published March 30 in the journal Science Translational Medicine
"We urgently need to find ways to make targeted therapies work better and longer," said senior author Kris Wood, Ph.
Wood and his colleagues found that targeted therapy caused DNA strands to break in cancer cells that survived the treatment
"We were surprised to find that the ATM pathway is often activated by surviving cancer cells," Wood said
The researchers used ATM inhibitors, which are currently being studied, and the answer is yes
In real-world cases, further confirmation is evident
"Taken together, these findings provide a rationale for the mechanistic integration of ATM inhibitors with existing targeted therapies," Wood said
