A recent study suggests a more effective way to treat melanoma by using ascorbate (vitamin C) to increase DNA damage in cancer cells, leading to their death. The research, led by Marcus Cooke, professor and chair in the Department of Molecular Biosciences, indicates that melanoma cells exhibit more DNA damage and fewer antioxidant defenses than normal skin cells.
The multi-disciplinary team found that treating melanoma cells with hydrogen peroxide and vitamin C caused even more DNA damage and higher cell death rates, while normal cells were protected. Additionally, vitamin C enhanced the effectiveness of the existing melanoma drug Elesclomol.
Cooke, who also leads the Oxidative Stress Group, noted the study’s origins in long-standing research on vitamin C’s dual role as a prooxidant and antioxidant, as well as its ability to modulate DNA repair. This research was influenced by the team’s interest in skin biology and solar ultraviolet radiation, dating back to the 1990s.
The findings revealed that melanoma cells have higher levels of DNA damage than keratinocytes, with damage proportional to melanin levels. This suggests that melanin within cells can cause damage even in the absence of sunlight.
Cooke emphasized the potential for ascorbate to be included as an adjunct in existing treatments, particularly those that induce DNA damage like Elesclomol. He highlighted the need for additional clinical studies to support these findings and explore ascorbate’s role in treatment further.
“Given that ascorbate is already well-studied and known to be well-tolerated, clinicians could consider including it to enhance existing treatments,” Cooke said. “Our biomarkers of oxidative stress are particularly suitable for clinical studies, and we could support in vivo biomonitoring of patients if clinical studies are initiated.”