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Spinning magnetic patterns that cause oncolysis by oxidative stress in glioma cells

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Publication Title | Spinning magnetic patterns that cause oncolysis by oxidative stress in glioma cells

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Spinning magnetic field patterns
that cause oncolysis by oxidative
stress in glioma cells
Shashank Hambarde1,2,3, Jeanne M. Manalo1,2,3, David S. Baskin1,2,3,4, Martyn A. Sharpe1,2,3 &
Santosh A. Helekar1,2,3,4*
Raising reactive oxygen species (ROS) levels in cancer cells to cause macromolecular damage and cell death is a promising anticancer treatment strategy. Observations that electromagnetic fields (EMF) elevate intracellular ROS and cause cancer cell death, have led us to develop a new portable wearable EMF device that generates spinning oscillating magnetic fields (sOMF) to selectively kill cancer cells while sparing normal cells in vitro and to shrink GBM tumors in vivo through a novel mechanism. Here, we characterized the precise configurations and timings of sOMF stimulation that produce cytotoxicity due to a critical rise in superoxide in two types of human glioma cells. We also found that the antioxidant Trolox reverses the cytotoxic effect of sOMF on glioma cells indicating that ROS play a causal role in producing the effect. Our findings clarify the link between the physics of magnetic stimulation and its mechanism of anticancer action, facilitating the development of a potential new safe noninvasive device-based treatment for GBM and other gliomas.
Reactive oxygen species (ROS) levels in cells play diverse roles in normal cellular processes such as develop- mental cell proliferation and differentiation, programmed cell death, cell motility, immune defense mechanisms, inflammation, and neuronal activity and plasticity1–8. They are also involved in cancer cell proliferation and tissue invasion, on the one hand, and cellular aging and neurodegeneration, as mediators of oxidative stress, on the other9–12. Cancer cells are known to possess high levels of ROS because of increased oxidative metabolism and dysfunctional mitochondria9–11. Previous studies have shown that abnormally high levels of ROS cause apoptosis. Therefore, it has been proposed that increasing ROS in cancer cells by drugs might have a role in the treatment of cancer13,14. Several existing anticancer drugs which have been shown to induce ROS might be acting in part through this mechanism13,15.
Besides drugs, stimulation by electromagnetic field (EMF) generating devices has been shown to raise ROS levels in cancer cells and thereby induce cell death of malignant tumor cells in vitro16–20. While some of these devices have shown safety and efficacy in mouse tumor xenograft models, to our knowledge no large patient trials have been conducted to date. In human cancer cells they produce variable results, showing both increases21–25 and decreases in ROS levels26–28, as well as a lack of change26–30 in them. This is likely due to the variability in the EMF-generating electromagnetic coils, experimental conditions, and cell types across studies31. Their underly- ing biophysical mechanism of action is not clear. Additionally, the precise range of physical parameters of EMF that produce a potentially therapeutic increase in ROS levels has not been fully characterized. Our recently developed noninvasive EMF device addresses these limitations because its stimulus parameters can be better and more precisely controlled and targeted. It generates a spinning oscillating magnetic field (sOMF or OMF) by rapidly rotating strong neodymium permanent magnets32. We have shown that this device, referred to as the “Oncomagnetic” device, substantially and consistently raises ROS in patient derived glioblastoma (GBM) cells to levels that are selectively cytotoxic to these cells, while sparing normal cells33. sOMF does not kill cultured normal human developing neurons, alveolar epithelial cells, and astrocytes33. We have also demonstrated recently that daily 2-h 3 times a day sOMF stimulation of normal wild-type mice for 4 months does not cause any adverse effects or abnormal histopathological changes in theirs tissues34. Furthermore, we have obtained evidence for the safety and efficacy of the device in mice implanted with orthotopic GBM xenografts35 and in an end-stage patient with recurrent GBM with no standard of care treatment options32. We have tested and found support for the hypothesis that the sOMF-induced increase in ROS is likely due to perturbation of the electron transfer
1Kenneth R. Peak Center for Brain and Pituitary Tumor Treatment and Research, Houston Methodist Hospital, Houston, TX, USA. 2Department of Neurosurgery, Houston Methodist Hospital, Houston, TX, USA. 3Houston Methodist Research Institute, Houston, TX, USA. 4Department of Neurosurgery, Weill Cornell Medical College, New York, NY, USA. *email:
(2023) 13:19264 | 1 Vol.:(0123456789)
Scientific Reports |

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