Magnetic pulses promote uptake of chemotherapy drug

Brief, localised pulses of magnetic fields have been found to increase the uptake of chemotherapy drug doxorubicin with minimal impact on healthy tissues.

The NUS team found that breast cancer cells are more vulnerable to magnetic field therapy. A 10-minute magnetic field exposure reduced the concentration of DOX – a chemotherapy drug - needed for similar amount of cancer killing by half, particularly at low doses of the drug
The NUS team found that breast cancer cells are more vulnerable to magnetic field therapy. A 10-minute magnetic field exposure reduced the concentration of DOX – a chemotherapy drug - needed for similar amount of cancer killing by half, particularly at low doses of the drug - NUS Singapore

The advance from researchers at the National University of Singapore could lead to precision-driven cancer therapies with fewer side effects. Their findings are detailed in the journal Cancers

The study, led by Associate Professor Alfredo Franco-Obregón, principal investigator at the Institute for Health Innovation & Technology (iHealthtech) at NUS and faculty member of the Department of Surgery at NUS Yong Loo Lin School of Medicine (NUS Medicine), is the first to systematically show how pulsed magnetic fields enhance DOX uptake in cancer cells. The team also showed that this approach could suppress tumours at lower drug doses.

DOX works by binding to DNA components and disrupting cell replication and respiration, which then kills off cancer cells. Despite its efficacy, it is a non-selective drug that can damage healthy tissues, leading to side effects ranging from mild to severe, including cardiomyopathy and muscle atrophy.

To address these challenges, the NUS researchers developed a novel approach that uses brief pulses of magnetic fields to selectively increase DOX uptake into breast cancer cells. Their study revealed the role of a calcium ion channel called TRPC1, which is often found in aggressive cancers, including breast cancer. Magnetic field exposure activates TRPC1, enhancing its ability to facilitate the entry of DOX into cancer cells.

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