Researchers may have finally been able to explain how UV rays begin to trigger skin cancer.
A team from Cornell University have discovered that when melanocyte stem cells accumulate a sufficient number of genetic mutations, they can become the cells where melanoma—a cancer of melanocytes—originates.
Under normal conditions, UV radiation from the sun activates melanocytes to release melanin, a pigment that protects the skin from the sun’s rays.
However, if melanocyte stem cells have surpassed a threshold of genetic mutations, a tumor can begin to grow when those skin stem cells are activated by sun exposure.
“If you had mutations that were sufficient for melanoma, everything would be fine until you went out and got a sunburn,” Andrew White, assistant professor of biomedical sciences at Cornell’s College of Veterinary Medicine and senior author of the study, said in a statement. “The stimuli that would normally just give you a tanning response could in fact start a melanoma instead.”
The researchers may have also discovered a way to prevent melanomas caused by mutated stem cells. It appears that a gene called Hgma2, when expressed in the skin under UV radiation, facilitates melanocyte stem cells to move from the base of skin hair follicles to the skin’s surface where the cells release melanin.
To prove this link, the researchers used mice engineered with melanocyte stem cell mutations. One set kept the mutations intact while another set of mice with the mutations had the Hgma2 gene deleted.
They then gave the mice a very low dose of UV radiation, enough to trigger a tanning response.
The mice with tumor-causing mutations and the Hgma2 gene intact developed melanomas but the mice with the gene deleted remained healthy.
“We have an actual mechanism, with Hgma2, that can be explored in the future and could be a way we can prevent melanomas from happening,” White said.