Scientifically, the arsenic-based agent the researchers have identified is known as As2O3.
During a study, the researchers found that a tumour suppressor protein called PML enables LICs to maintain their quiescence, and thereby protects them from being destroyed by cancer therapies.
They also observed that inhibiting this protein with the help of As2O3 successfully disrupted LICs, and increased the efficacy of the anti-cancer therapy by sensitising such cells to pro-apoptopic stimuli.
"It's actually a very simple concept. Ninety percent of existing cancer treatments are antiproliferative agents - they target the pool of proliferative cells, leaving behind the dormant LICs," Nature magazine quoted senior author Pier Paolo Pandolfi, Director of the Cancer Genetics Program in BIDMC's Cancer Center, as saying.
"But in determining that PML serves to guard the LICs that have been left behind, we also discovered that if we knock out PML (through pharmacologic means), the LICs will lose their braking abilities and run out of gas, thereby commiting the fatal error of proliferation -- and exposing themselves to the deadly effects of cancer therapies," Pandolfi added.
His team is now trying to determine whether PML exerts a similar role in the stem cells of other tissues, as well as in the cancer initiating cells of solid tumours.
"If this turn out to be the case, the transient use of As2O3 may represent a more global strategy to target CICs in other forms of cancer," he said.