Researchers at Cornell University released a study that suggests when melanocyte stem cells (MCSCs) surpass a threshold of genetic mutations, they can contribute to the development of melanoma. Specifically, this relates to mutations that occur in the chromatin-remodelling factor gene HGMA2 and are triggered by short wave ultraviolet B (UVB) radiation.
The investigators’ findings were published in the journal Cell Stem Cell (Oct. 2017; 21(5):665–678).
“If you had mutations that were sufficient for melanoma, everything would be fine until you went out and got a sunburn,” said senior study author Andrew White, PhD, assistant professor of biomedical sciences at Cornell’s College of Veterinary Medicine in Ithaca, N.Y., in a press release. “The stimuli that would normally just give you a tanning response could in fact start a melanoma instead.”
According to the authors of the study, HGMA2 facilitates MCSCs to move from the base of skin hair follicles to the epidermis, when expressed in the skin under UVB radiation.
The researchers used mice engineered with MCSCs. One experimental group of mice was given MCSCs and HGMA2, while the other group was given MCSCs and had HGMA2 deleted. Then, the mice were given a low dose of UVB radiation to trigger a tanning response.
The mice that were given the tumour-causing mutations and the HGMA2 gene intact developed melanoma. The mice with the tumour-causing mutations and the deleted HGMA2 gene remained skin cancer-free.
“We have an actual mechanism, with HGMA2, that can be explored in the future and could be a way we can prevent melanoma from happening,” said Dr. White.
His team concluded that further investigation is needed to better understand the genetic function of HGMA2.
The study was supported by the Office of the Assistant Secretary of Defense for Health Affairs through the Peer Reviewed Cancer Research Program, the Cornell Center for Vertebrate Genomics, the Cornell Stem Cell Program and the National Institutes of Health.