Furthering melanoma understanding could lead to better sunscreens

A team of researchers from the University of Kentucky found an important molecular link between MC1R signaling and DNA repair in their study, and hopes to use this information to develop new melanoma-preventive treatments.

Published in Molecular Cell​, the study looked at the receptor (melanocortin1 receptor - MC1R) on melanocytes in the skin that gets called into action following UV exposure to help the skin lay down more UV-blocking melanin to protect itself.

It found that a genetic defect in a specific hormonal pathway may make people more susceptible to developing melanoma, as they cannot make enough melanin to fully protect themselves from UV damage.

"Knowing whether people have a specific genetic predisposition for melanoma could potentially save many lives",​ says Dr. John D'Orazio, Associate Professor and the Drury Pediatric Research Endowed Chair at the university’s Markey Cancer Center.

Pathway​

"If you happen to be born with a problem in this MC1R hormonal pathway, then you need to be extra careful with respect to UV safety."​

D'Orazio says that a good indication of a person's MC1R status is what happens to the skin after sun exposure.

"If you tan well, then your MC1R probably works well,"​ he continues. "If you tend to burn, then you may have inherited a problem with your MC1R, and you probably should avoid purposeful UV exposure like tanning bed use or unprotected sun exposure."​

D'Orazio and his research team found an important molecular link between MC1R signaling and DNA repair in their study.

The team says it hopes to use this information to develop new melanoma-preventive treatments, like additives that can be included in sunblocks to ramp up the skin's ability to deal with UV damage.

Melanoma​

UV from sunlight or tanning beds is a major cause of melanoma, and inherited problems in the MC1R means that the skin lacks natural protection by melanin, which acts as a biologic sunblock.

This leads to more UV light chronically getting through to the sensitive layers of the epidermis, where it can contribute to cancer.

This study showed that MC1R defects contribute to melanoma development in ways other than melanin production.

Besides regulating the amount of melanin that gets made in the skin, MC1R also controls how well melanocytes can repair their DNA from UV damage.

Having defects in MC1R signaling delays the body's ability to clear out existing DNA damage in the ski, which researchers say can lead to an increased potential for cancerous mutations.