One-third of pancreatic cancer patients who undergo treatment die from recurrences at the primary tumor site, therefore improvement of local control could vastly increase survival from this devastating disease. Radiotherapy for pancreatic cancer is arguably effective but collateral damage to adjacent normal gastrointestinal tissues can be dose-limiting (under-dosing the tumor and tumor margin for fear of overdosing the surrounding radiosensitive normal organs) and therefore efficacy-limiting.
We propose manipulating the very mechanism that makes radiation such an effective cancer cell-killing agent – its ability to break chemical bonds in critical cellular molecules like DNA via production of free radicals, which are highly reactive molecules. Much of radiotherapy’s clinical efficacy results from ionization-induced free radical (FR) production. The presence of low-strength electromagnetic fields (EMF) – similar to what you might get from a simple refrigerator magnet – is known to change the FR recombination rates via radical pair intermediates (triplet and singlet states). FRs in cells are however, not limited to direct FR production by ionizing radiation (IR), but also to the downstream cascade of cellularly generated FR as responses to the initial FR-induced damage. Thus, changing FR interconversion rates between singlet and triplet states using weak EMFs should alter FR recombination frequency, their lifetimes, ensuing cellular responses, and therefore radiotherapy efficacy.